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  1. Cell therapy attenuates cardiac dysfunction post myocardial infarction: effect of timing, routes of injection and a fibrin scaffold.

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    Juliana S Nakamuta

    Full Text Available BACKGROUND: Cell therapy approaches for biologic cardiac repair hold great promises, although basic fundamental issues remain poorly understood. In the present study we examined the effects of timing and routes of administration of bone marrow cells (BMC post-myocardial infarction (MI and the efficacy of an injectable biopolymer scaffold to improve cardiac cell retention and function. METHODOLOGY/PRINCIPAL FINDINGS: (99mTc-labeled BMC (6 x 10(6 cells were injected by 4 different routes in adult rats: intravenous (IV, left ventricular cavity (LV, left ventricular cavity with temporal aorta occlusion (LV(+ to mimic coronary injection, and intramyocardial (IM. The injections were performed 1, 2, 3, or 7 days post-MI and cell retention was estimated by gamma-emission counting of the organs excised 24 hs after cell injection. IM injection improved cell retention and attenuated cardiac dysfunction, whereas IV, LV or LV* routes were somewhat inefficient (<1%. Cardiac BMC retention was not influenced by timing except for the IM injection that showed greater cell retention at 7 (16% vs. 1, 2 or 3 (average of 7% days post-MI. Cardiac cell retention was further improved by an injectable fibrin scaffold at day 3 post-MI (17 vs. 7%, even though morphometric and function parameters evaluated 4 weeks later displayed similar improvements. CONCLUSIONS/SIGNIFICANCE: These results show that cells injected post-MI display comparable tissue distribution profile regardless of the route of injection and that there is no time effect for cardiac cell accumulation for injections performed 1 to 3 days post-MI. As expected the IM injection is the most efficient for cardiac cell retention, it can be further improved by co-injection with a fibrin scaffold and it significantly attenuates cardiac dysfunction evaluated 4 weeks post myocardial infarction. These pharmacokinetic data obtained under similar experimental conditions are essential for further development of these

  2. Aldosterone blockade in post-acute myocardial infarction heart failure

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    Pitt, Bertram; Ferrari, Roberto; Gheorghiade, Mihai; van Veldhuisen, Dirk J.; Krum, Henry; McMurray, John; Lopez-Sendon, Jose

    2006-01-01

    Development of heart failure (HF) or left ventricular systolic dysfunction (LVSD) significantly increases mortality post acute myocardial infarction (AMI). Aldosterone contributes to the development and progression of HF post AMI, and major guidelines now recommend aldosterone blockade in this setti

  3. Peri-infarct dysfunction in post-myocardial infarction: assessment of 3-T tagged and late enhancement MRI

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    Inoue, Yuma; Nagao, Michinobu; Higashino, Hiroshi; Hosokawa, Kohei; Kido, Teruhito; Kurata, Akira; Mochizuki, Teruhito [Ehime University Graduate School of Medicine, Department of Diagnostic and Therapeutic Radiology, Toon-city, Ehime (Japan); Yang, Xiaomei [Sichuan University, College of Electrical Engineering and Information Technology, Sichuan (China); Okayama, Hideki; Higaki, Jitsuo [Ehime University Graduate School of Medicine, Department of Integrated Medicine and Informatics, Matsuyama City (Japan); Murase, Kenya [Osaka University Medical School, Department of Medical Engineering Division of Allied Health Sciences, Osaka (Japan)

    2010-05-15

    To determine LV function at different distances from myocardial infarction (MI) by using 3-T tagged MRI and late gadolinium enhancement (LGE). Cardiac MR images were acquired from 21 patients with previous MI. The harmonic phase (HARP) method was used to calculate radial and circumferential strain (RS, CS). The two strains were synchronised by subtracting the CS from the RS at the same time, and this was defined as the efficient strain (ES). Peak strain (P-RS, P-CS, P-ES) and time to peak strain (T-RS, T-CS, T-ES) were used as estimates of contractile function. Based on the presence of LGE, myocardium was classified into infarct, border zone, adjacent and remote areas. P-RS and P-ES were significantly greater for remote than for adjacent and infarct areas. P-CS values were significantly greater for remote and border zone than for infarct areas. T-RS and T-ES were significantly shorter for remote and border zone than for infarct areas. T-CS was significantly shorter for border zone than for infarct areas. Contractile dysfunction demonstrated by peak strain was correlated with location at different distances from the infarct. In the border zone, contractile deformation was characterised as earlier T-RS, T-CS and T-ES and greater P-CS than in the infarct area. (orig.)

  4. Direct Evidence that Myocardial Insulin Resistance following Myocardial Ischemia Contributes to Post-Ischemic Heart Failure

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    Fu, Feng; Zhao, Kun; Li, Jia; Xu, Jie; Zhang, Yuan; Liu, Chengfeng; Yang, Weidong; Gao, Chao; Li, Jun; Zhang, Haifeng; Li, Yan; Cui, Qin; Wang, Haichang; Tao, Ling; Wang, Jing; Quon, Michael J; Gao, Feng

    2015-01-01

    A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its association with HF are inadequately investigated. This study aims to determine the role of myocardial insulin resistance in ischemic HF and its underlying mechanisms. Male Sprague-Dawley rats subjected to myocardial infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk post-MI. Of note, myocardial insulin sensitivity was decreased as early as 1 wk after MI, which was accompanied by increased production of myocardial TNF-α. Overexpression of TNF-α in heart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI. Treatment of rats with a specific TNF-α inhibitor improved myocardial insulin signaling post-MI. Insulin treatment given immediately following MI suppressed myocardial TNF-α production and improved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling. Moreover, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with controls. In conclusion, MI induces myocardial insulin resistance (without systemic insulin resistance) mediated partly by ischemia-induced myocardial TNF-α overproduction and promotes the development of HF. Our findings underscore the direct and essential role of myocardial insulin signaling in protection against post-ischemic HF. PMID:26659007

  5. Myocardial dysfunction in ankylosing spondylitis.

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    Gould, B A; Turner, J.; Keeling, D H; Hickling, P; Marshall, A J.

    1992-01-01

    Echocardiographic evidence has suggested abnormalities of the myocardial function in patients with ankylosing spondylitis. In this work the cardiac function in patients with ankylosing spondylitis and in normal volunteers was evaluated. Twenty four normal volunteers and 21 patients with ankylosing spondylitis aged 18-45 were studied. None had overt cardiac disease. Cardiac function was assessed at rest with echocardiography, at rest and during supine bicycle exercise using radionuclide angiog...

  6. TOWARD THE QUESTION OF ISCHEMIC MYOCARDIAL DYSFUNCTION

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    V. V. Kalyuzhin

    2014-01-01

    Full Text Available The authors of the review have analyzed papers published on the problem of ischemic myocardial dysfunction. They begin with a definition of the term “ischemia” (derived from two Greek words: ischō, meaning to hold back, and haima, meaning blood - a condition at which the arterial blood flow is insufficient to provide enough oxygen to prevent intracellular respiration from shifting from the aerobic to the anaerobic form. The poor rate of ATP generation from this process causes a decrease in cellular ATP, a concomitant rise in ADP, and ultimately, to depression inotropic (systolic and lusitropic (diastolic function of the affected segments of the myocardium. But with such simplicity of basic concepts, the consequences of ischemia so diverse. Influence of an ischemia on myocardial function so unequally at different patients, which is almost impossible to find two identical cases (as in the case of fingerprints. It depends on the infinite variety of lesions of coronary arteries, reperfusion (time and completeness of restoration of blood flow and reactions of a myocardium which, apparently, has considerable flexibility in its response. Ischemic myocardial dysfunction includes a number of discrete states, such as acute left ventricular failure in angina, acute myocardial infarction, ischemic cardiomyopathy, stunning, hibernation, pre- and postconditioning. There are widely differing underlying pathophysiologic states. The possibility exists that several of these states can coexist.

  7. Myocardial dysfunction in malnourished children

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    Faddan Nagla Hassan

    2010-01-01

    Full Text Available Background : Malnourished children suffer several alterations in body composition that could produce cardiac abnormalities. Aim : The aim of the present study was to detect the frequency of myocardial damage in malnourished children as shown by echocardiography and cardiac troponin T (cTnT level. Methods : Forty-five malnourished infants and young children (mean±SD of age was 11.24 ±7.88 months were matched with 25 apparently healthy controls (mean±SD of age was 10.78±6.29 months. Blood sample was taken for complete blood picture, liver and kidney function tests, serum sodium, potassium, calcium levels and cTnT. All the malnourished children were subjected to echocardiographic evaluation. Results : Malnourished children showed a significantly lower left ventricular (LV mass than the control group. The LV systolic functions were significantly impaired in patients with severe malnutrition. The cTnT level was higher than the upper reference limits in 11 (24.44% of the studied malnourished children and all of them had a severe degree of malnutrition. The cTnT level was significantly higher in patients with anemia, sepsis and electrolyte abnormalities and it correlated negatively with LV ejection fraction (EF. Six of the studied children with high cTnT levels (54.5% died within 21 days of treatment while only one case (2.9% with normal level of cTnT died within the same period. Conclusions: LV mass is reduced in malnourished children. Children with severe malnutrition have a significant decrease in LV systolic functions. Elevated cTnT levels in malnourished children has both diagnostic and prognostic significance for cardiomyocyte damage.

  8. CADUCEUS, SCIPIO, ALCADIA: Cell therapy trials using cardiac-°©‐derived cells for patients with post myocardial infarction LV dysfunction, still evolving

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    Magdi H Yacoub

    2012-03-01

    Full Text Available The early results of the CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction study were recently published in the Lancet [1]. This study is a phase 1 prospective randomised study, performed at two centres. The study was designed to test the hypothesis that intracoronary infusion of autologous cardiac-derived cells following myocardial infarction can reduce the size of the infarct and increase the amount of viable myocardium. The eligible patients were randomised in a 2:1 ratio to receive CDCs or standard care. In all, 17 patients were randomised to cell therapy and 8 to standard care. The cell therapy consisted of an infusion of 25 million cells into the infarct related artery, 1.5–3 months after successful primary angioplasty in patients who developed LV dysfunction (EF less than 37 per cent. The cells were derived from RV endomyocardial biopsies performed within the previous 37 days. The number of cells was determined from previous experimental studies of the maximum number of cells which can be injected without inducing infarction. The study was not blinded because of ethical considerations regarding performing right ventricular biopsy on the controls. The exclusion criteria included patients who had evidence of right ventricular infarction, or could not have an MRI examination because of claustrophobia or prior insertion of devices. There was no death, myocardial infarction or serious arrhythmia reported in either group during the period of follow up, which was between 6-12 months. Serious adverse events were observed in 24 percent of the intervention group versus 12 per cent in the controls (p not significant.

  9. Low-Level Vagus Nerve Stimulation Reverses Cardiac Dysfunction and Subcellular Calcium Handling in Rats With Post-Myocardial Infarction Heart Failure.

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    Zhang, Yunhe; Chen, Ao; Song, Lei; Li, Min; Luo, Zhangyuan; Zhang, Wenzan; Chen, Yingmin; He, Ben

    2016-05-25

    Vagus nerve stimulation (VNS), targeting the imbalanced autonomic nervous system, is a promising therapeutic approach for chronic heart failure (HF). Moreover, calcium cycling is an important part of cardiac excitation-contraction coupling (ECC), which also participates in the antiarrhythmic effects of VNS. We hypothesized that low-level VNS (LL-VNS) could improve cardiac function by regulation of intracellular calcium handling properties. The experimental HF model was established by ligation of the left anterior descending coronary artery (LAD). Thirty-two male Sprague-Dawley rats were divided into 3 groups as follows; control group (sham operated without coronary ligation, n = 10), HF-VNS group (HF rats with VNS, n = 12), and HF-SS group (HF rats with sham nerve stimulation, n = 10). After 8 weeks of treatment, LL-VNS significantly improved left ventricular ejection fraction (LVEF) and attenuated myocardial interstitial fibrosis in the HF-VNS group compared with the HF-SS group. Elevated plasma norepinephrine and dopamine, but not epinephrine, were partially reduced by LL-VNS. Additionally, LL-VNS restored the protein and mRNA levels of sarcoplasmic reticulum Ca(2+) ATPase (SERCA2a), Na(+)-Ca(2+) exchanger 1 (NCX1), and phospholamban (PLB) whereas the expression of ryanodine receptor 2 (RyR2) as well as mRNA level was unaffected. Thus, our study results suggest that the improvement of cardiac performance by LL-VNS is accompanied by the reversal of dysfunctional calcium handling properties including SERCA2a, NCX1, and PLB which may be a potential molecular mechanism of VNS for HF.

  10. Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction.

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    Wang, Wei; Zhang, Fuyang; Xia, Yunlong; Zhao, Shihao; Yan, Wenjun; Wang, Helin; Lee, Yan; Li, Congye; Zhang, Ling; Lian, Kun; Gao, Erhe; Cheng, Hexiang; Tao, Ling

    2016-11-01

    Cardiac metabolic remodeling is a central event during heart failure (HF) development following myocardial infarction (MI). It is well known that myocardial glucose and fatty acid dysmetabolism contribute to post-MI cardiac dysfunction and remodeling. However, the role of amino acid metabolism in post-MI HF remains elusive. Branched chain amino acids (BCAAs) are an important group of essential amino acids and function as crucial nutrient signaling in mammalian animals. The present study aimed to determine the role of cardiac BCAA metabolism in post-MI HF progression. Utilizing coronary artery ligation-induced murine MI models, we found that myocardial BCAA catabolism was significantly impaired in response to permanent MI, therefore leading to an obvious elevation of myocardial BCAA abundance. In MI-operated mice, oral BCAA administration further increased cardiac BCAA levels, activated the mammalian target of rapamycin (mTOR) signaling, and exacerbated cardiac dysfunction and remodeling. These data demonstrate that BCAAs act as a direct contributor to post-MI cardiac pathologies. Furthermore, these BCAA-mediated deleterious effects were improved by rapamycin cotreatment, revealing an indispensable role of mTOR in BCAA-mediated adverse effects on cardiac function/structure post-MI. Of note, pharmacological inhibition of branched chain ketoacid dehydrogenase kinase (BDK), a negative regulator of myocardial BCAA catabolism, significantly improved cardiac BCAA catabolic disorders, reduced myocardial BCAA levels, and ameliorated post-MI cardiac dysfunction and remodeling. In conclusion, our data provide the evidence that impaired cardiac BCAA catabolism directly contributes to post-MI cardiac dysfunction and remodeling. Moreover, improving cardiac BCAA catabolic defects may be a promising therapeutic strategy against post-MI HF.

  11. Sildenafil and diastolic dysfunction after acute myocardial infarction trial

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    Andersen, Mads J; Gustafsson, Finn; Hassager, Christian

    2013-01-01

    Diastolic dysfunction following myocardial infarction is an important predictor of outcome, irrespective of left ventricular systolic function. Previous studies suggest that phosphordiesterase-5 inhibition has a favorable effect on the myocardium as well as on the pulmonary and systemic vasculature....

  12. Severe postpartum sepsis with prolonged myocardial dysfunction: a case report

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    Chen Katherine T

    2010-10-01

    Full Text Available Abstract Introduction Severe sepsis during pregnancy or in the postpartum period is a rare clinical event. In non obstetric surviving patients, the cardiovascular changes seen in sepsis and septic shock are fully reversible five to ten days after their onset. We report a case of septic myocardial dysfunction lasting longer than ten days. To the best of our knowledge, this is the first report of prolonged septic myocardial dysfunction in a parturient. Case presentation A 24 year old Hispanic woman with no previous medical history developed pyelonephritis and severe sepsis with prolonged myocardial dysfunction after a normal spontaneous vaginal delivery. Conclusions Septic myocardial dysfunction may be prolonged in parturients requiring longer term follow up and pharmacologic treatment.

  13. Cardiac remodeling and physical training post myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Michael; A; Garza; Emily; A; Wason; John; Q; Zhang

    2015-01-01

    After myocardial infarction(MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts. Due to the degree of difficulty to study a viable human heart at both protein and molecular levels, most of the detailed studies have been performed by using animal models. Although there are some negative reports indicating that post-MI exercise may further cause deterioration of the wounded hearts, a growing body of research from both human and animal experiments demonstrates that post-MI exercise may beneficially alter the course of wound healing and improve cardiac function. Furthermore, the improved function is likely due to exercise training-induced mitigation of reninangiotensin-aldosterone system, improved balance between matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1, favorable myosin heavy chain isoform switch, diminished oxidative stress, enhanced antioxidant capacity, improved mitochondrial calcium handling, and boosted myocardial angiogenesis. Additionally, meta-analyses revealed that exercise-based cardiac rehabilitation has proven to be effective, and remains one of the least expensive therapies for both the prevention and treatment of cardiovascular disease, and prevents re-infarction.

  14. Myocardial steatosis as a possible mechanistic link between diastolic dysfunction and coronary microvascular dysfunction in women.

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    Wei, Janet; Nelson, Michael D; Szczepaniak, Edward W; Smith, Laura; Mehta, Puja K; Thomson, Louise E J; Berman, Daniel S; Li, Debiao; Bairey Merz, C Noel; Szczepaniak, Lidia S

    2016-01-01

    Women with coronary microvascular dysfunction (CMD) and no obstructive coronary artery disease (CAD) have increased rates of heart failure with preserved ejection fraction (HFpEF). The mechanisms of HFpEF are not well understood. Ectopic fat deposition in the myocardium, termed myocardial steatosis, is frequently associated with diastolic dysfunction in other metabolic diseases. We investigated the prevalence of myocardial steatosis and diastolic dysfunction in women with CMD and subclinical HFpEF. In 13 women, including eight reference controls and five women with CMD and evidence of subclinical HFpEF (left ventricular end-diastolic pressure >12 mmHg), we measured myocardial triglyceride content (TG) and diastolic function, by proton magnetic resonance spectroscopy and magnetic resonance tissue tagging, respectively. When compared with reference controls, women with CMD had higher myocardial TG content (0.83 ± 0.12% vs. 0.43 ± 0.06%; P = 0.025) and lower diastolic circumferential strain rate (168 ± 12 vs. 217 ± 15%/s; P = 0.012), with myocardial TG content correlating inversely with diastolic circumferential strain rate (r = -0.779; P = 0.002). This study provides proof-of-concept that myocardial steatosis may play an important mechanistic role in the development of diastolic dysfunction in women with CMD and no obstructive CAD. Detailed longitudinal studies are warranted to explore specific treatment strategies targeting myocardial steatosis and its effect on diastolic function.

  15. Myocardial Dysfunction in Sepsis: A Large, Unsolved Puzzle

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    Constantino Jose Fernandes Jr.

    2012-01-01

    Full Text Available Sepsis has high incidence and mortality rates around the world. The role of cardiac depression in myocardial dysfunction during sepsis remains to be elucidated. This review attempts to summarize our understanding of the anatomical, histopathological, and pathophysiological mechanisms behind cardiac dysfunction. Biomarkers to detect cardiac depression have been used to recognize developing problems, but the actual impact of these tools remains unclear.

  16. Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats

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    Luiz Henrique Marchesi Bozi

    2013-04-01

    Full Text Available OBJECTIVES: The present study was performed to investigate 1 whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2 whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. METHODS: Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM, sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05. RESULTS: Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. CONCLUSION: Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.

  17. Polybiomarker approach in myocardial dysfunction assessment in senile patients

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    Malinova L.I.

    2015-03-01

    Full Text Available Purpose: to evaluate interaction of obesity, inflammation and myocardial dysfunction in senile myocardial infarction survivors. Material and Methods. Patients aged 70 and older were involved in the study (n=108 and divided into 2 groups according to the history of myocardial infarction (Ml — 5 years before involvement: senile Ml survivors (n=26 vs senile patients without history of Ml (n=82. Measurements of serum levels of adipokines (leptin, adiponectin, myocardial dysfunction markers (BNP, NT proBNP, proANP, galectin 3 and inflammatory cytokines (TNF, interleukin 6 were performed. Results. Both groups were comparable by age and major clinical characteristics. Ejection fraction was preserved in both groups under the study (67 (64; 70 %vs67 (64; 68 %, p=0,655. Frequency of diastolic dysfunction was comparable in both groups. However it was more severe in Ml survivors. BNP and NT proBNP levels were significantly lower in patients without the history of Ml (p=0,021; 0,004, respectively. On the contrary serum levels of proANP had tendency to increase in patients with the history of Ml, but not significantly: p=0,821. Adiponectin and galectin-3 were significantly higher in patients with the history of Ml (p=0,019and p=0,011. Conclusion. Pathogenetic peculiarities of chronic heart failure with preserved ejection fraction in senile patients with and without myocardial infarction history were revealed. More expedient biomarker panel appropriate for senile patients with probable heart failure should include NT-proBNP, galectin-3 and adiponectin.

  18. Behavioral disorders in rats with chronic myocardial dysfunction

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    Rodinskiy A.G.

    2014-09-01

    Full Text Available Observation of cardiologists and psychiatrists suggest that cardiovascular diseases and depression are the most common and frequent comorbid conditions. Therefore the aim of the study was to identify behavioral disorders in rats on the background of myocardial dysfunction in the experiment. Material of the research: 60 adult male rats of Wistar line, weighing 200-220 g, divided into 2 groups - control and experimental. Myocardial dysfunction was modeled by intraperitoneal injection of doxorubicin by 5 mg/kg of animal weight. To verify the model of myocardial dysfunction ECG and histological examination of the myocardium were performed. Evaluation of higher divisions of the CNS reactions was performed using the "open field" method by such indicators: vertical and horizontal motor activity (decreased by 71,4%, acts and defecation boluses (down by 85-88%, the number of burrows (decreased by 57-90%, grooming (decreased by 23%, all parameters were reliable (in p<0,05. There was a gradual decline of rats’ emotionality, CNS depression and increased anxiety. It was found that behavioral disorders in the experiment were typical for anxiety and depression states.

  19. Post myocardial infarction cardiogenic shock: a review of current therapies.

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    Ng, Ramford; Yeghiazarians, Yerem

    2013-01-01

    Cardiogenic shock is often a devastating consequence of acute myocardial infarction (MI) and portends to significant mortality and morbidity. Despite improvements in expediting the time to treatment and enhancements in available medical therapy and reperfusion techniques, cardiogenic shock remains the most common cause of mortality following MI. Post-MI cardiogenic shock most commonly occurs as a consequence of severe left ventricular dysfunction. Right ventricular (RV) MI must also be considered. Mechanical complications including acute mitral regurgitation, ventricular septal rupture, and ventricular free-wall rupture can also lead to cardiogenic shock. Rapid diagnosis of cardiogenic shock and its underlying cause is pivotal to delivering definitive therapy. Intravenous vasoactive agents and mechanical support devices may temporize the patient's hemodynamic status until definitive therapy by percutaneous or surgical intervention can be performed. Despite prompt management, post-MI cardiogenic shock mortality remains high.

  20. Central autonomic control of the heart, angina, and pathogenic mechanisms of post-myocardial infarction depression

    NARCIS (Netherlands)

    Ter Horst, GJ

    1999-01-01

    Depression can develop in 20% of the patients with a myocardial infarction (MI). Pathobiological mechanisms underlying the development of mood disorders in these patients are unknown. Since post-MI depression has been associated with increased risk of mortality we hypothesized that dysfunction of li

  1. Myocardial dysfunction and cardiovascular disease in type 2 diabetes.

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    Ofstad, Anne Pernille

    2016-07-01

    Type 2 diabetes mellitus (T2DM) is strongly associated with increased risk of myocardial dysfunction and cardiovascular disease (CVD), two separate conditions which often co-exist and influence each other's course. The prevalence of myocardial dysfunction may be as high as 75% in T2DM populations but is often overlooked due to the initial asymptomatic nature of the disease, complicating co-morbidities such as coronary artery disease (CAD) and obesity, and the lack of consensus on diagnostic criteria. More sensitive echocardiographic applications are furthermore needed to improve detection of early subclinical changes in myocardial function which do not affect conventional echocardiographic parameters. The pathophysiology of the diabetic myocardial dysfunction is not fully elucidated, but involves hyperglycemia and high levels of free fatty acids. It evolves over several years and increases the risk of developing overt HF, and is suggested to at least in part account for the worse outcome seen in T2DM individuals after cardiac events. CAD and stroke are the most frequent CV manifestations among T2DM patients and relate to a large degree to the accelerated atherosclerosis driven by inflammation. Diagnosing CAD is challenging due to the lower sensitivity inherent in the diagnostic tests and there is thus a need for new biomarkers to improve prediction and detection of CAD. It seems that a multi-factorial approach (i.e. targeting several CV risk factors simultaneously) is superior to a strict glucose lowering strategy in reducing risk for macrovascular events, and recent research may even support an effect also on HF outcomes.

  2. Myocardial Viability and Survival in Ischemic Left Ventricular Dysfunction

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    Bonow, Robert O.; Maurer, Gerald; Lee, Kerry L.; Holly, Thomas A.; Binkley, Philip F.; Desvigne-Nickens, Patrice; Drozdz, Jaroslaw; Farsky, Pedro S.; Feldman, Arthur M.; Doenst, Torsten; Michler, Robert E.; Berman, Daniel S.; Nicolau, Jose C.; Pellikka, Patricia A.; Wrobel, Krzysztof; Alotti, Nasri; Asch, Federico M.; Favaloro, Liliana E.; She, Lilin; Velazquez, Eric J.; Jones, Robert H.; Panza, Julio A.

    2012-01-01

    BACKGROUND The assessment of myocardial viability has been used to identify patients with coronary artery disease and left ventricular dysfunction in whom coronary-artery bypass grafting (CABG) will provide a survival benefit. However, the efficacy of this approach is uncertain. METHODS In a substudy of patients with coronary artery disease and left ventricular dysfunction who were enrolled in a randomized trial of medical therapy with or without CABG, we used single-photon-emission computed tomography (SPECT), dobutamine echocardiography, or both to assess myocardial viability on the basis of pre-specified thresholds. RESULTS Among the 1212 patients enrolled in the randomized trial, 601 underwent assessment of myocardial viability. Of these patients, we randomly assigned 298 to receive medical therapy plus CABG and 303 to receive medical therapy alone. A total of 178 of 487 patients with viable myocardium (37%) and 58 of 114 patients without viable myocardium (51%) died (hazard ratio for death among patients with viable myocardium, 0.64; 95% confidence interval [CI], 0.48 to 0.86; P = 0.003). However, after adjustment for other baseline variables, this association with mortality was not significant (P = 0.21). There was no significant interaction between viability status and treatment assignment with respect to mortality (P = 0.53). CONCLUSIONS The presence of viable myocardium was associated with a greater likelihood of survival in patients with coronary artery disease and left ventricular dysfunction, but this relationship was not significant after adjustment for other baseline variables. The assessment of myocardial viability did not identify patients with a differential survival benefit from CABG, as compared with medical therapy alone. (Funded by the National Heart, Lung, and Blood Institute; STICH ClinicalTrials.gov number, NCT00023595.) PMID:21463153

  3. Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization.

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    Canton, Marcella; Skyschally, Andreas; Menabò, Roberta; Boengler, Kerstin; Gres, Petra; Schulz, Rainer; Haude, Michael; Erbel, Raimund; Di Lisa, Fabio; Heusch, Gerd

    2006-04-01

    We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins. Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38 +/- 7% of baseline and a 2.62 +/- 0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r = -0.68; P = 0.015) and was associated with increased TNF-alpha content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-alpha. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8+/-10% of baseline and DCB in MEA was 1.48+/-0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r = -0.83; P = 0.005). Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.

  4. Early Myocardial Dysfunction is Not Caused by Mitochondrial Abnormalities in a Rat Model of Peritonitis

    NARCIS (Netherlands)

    Smeding, Lonneke; van der Laarse, Willem J.; van Veelen, Toke A.; Lamberts, Regis R.; Niessen, Hans W. M.; Kneyber, Martin C. J.; Groeneveld, A. B. Johan; Plotz, Frans B.

    2012-01-01

    Background. Patients with complicated intra-abdominal infections are prone to develop multiple organ failure, including myocardial dysfunction. We hypothesized that early dysfunction during sepsis is associated with inflammation, mitochondrial injury, impaired mitochondrial function, and activation

  5. Galectin-3 and post-myocardial infarction cardiac remodeling

    NARCIS (Netherlands)

    Meijers, Wouter C.; van der Velde, A. Rogier; Pascual-Figal, Domingo A.; de Boer, Rudolf A.

    2015-01-01

    This review summarizes the current literature regarding the involvement and the putative role(s) of galectin-3 in post-myocardial infarction cardiac remodeling. Post-myocardial infarction remodeling is characterized by acute loss of myocardium, which leads to structural and biomechanical changes in

  6. Galectin-3 and post-myocardial infarction cardiac remodeling

    NARCIS (Netherlands)

    Meijers, Wouter C.; van der Velde, A. Rogier; Pascual-Figal, Domingo A.; de Boer, Rudolf A.

    2015-01-01

    This review summarizes the current literature regarding the involvement and the putative role(s) of galectin-3 in post-myocardial infarction cardiac remodeling. Post-myocardial infarction remodeling is characterized by acute loss of myocardium, which leads to structural and biomechanical changes in

  7. Myocardial ultrasonic tissue characterization in patients with thyroid dysfunction

    Directory of Open Access Journals (Sweden)

    Schmidt André

    2010-04-01

    Full Text Available Abstract Background Structural myocardial abnormalities have been extensively documented in hypothyroidism. Experimental studies in animal models have also shown involvement of thyroid hormones in gene expression of myocardial collagen. This study was planned to investigate the ability of ultrasonic tissue characterization, as evaluated by integrated backscatter (IBS, to early identify myocardial involvement in thyroid dysfunction. Patients and Methods We studied 15 patients with hyperthyroidism (HYPER, 8 patients with hypothyroidism (HYPO, 14 patients with subclinical hypothyroidism (SCH and 19 normal (N subjects, who had normal LV systolic function. After treatment, 10 HYPER, 6 HYPO, and 8 SCH patients were reevaluated. IBS images were obtained and analyzed in parasternal short axis (papillary muscle level view, at left ventricular (LV posterior wall. The following IBS variables were analyzed: 1 the corrected coefficient (CC of IBS, obtained by dividing IBS intensity by IBS intensity measured in a rubber phantom, using the same equipment adjustments, at the same depth; 2 cardiac cyclic variation (CV of IBS - peak-to-peak difference between maximal and minimal values of IBS during cardiac cycle; 3 cardiac cyclic variation index (CVI of IBS - percentual relationship between the cyclic variation (CV and the mean value of IBS intensity. Results CC of IBS was significantly larger (p Conclusions CC of IBS was able to differentiate cardiac involvement in patients with overt HYPO and HYPER who had normal LV systolic function. These early myocardial structural abnormalities were partially reversed by drug therapy in HYPER group. On the other hand, although mean IBS intensity tended to be slightly larger in patients with SCH as compared to N, this difference was not statistical significant.

  8. Cardiac remodeling and myocardial dysfunction in obese spontaneously hypertensive rats

    Directory of Open Access Journals (Sweden)

    Linz Dominik

    2012-09-01

    Full Text Available Abstract Background The additive effects of obesity and metabolic syndrome on left ventricular (LV maladaptive remodeling and function in hypertension are not characterized. Methods We compared an obese spontaneously hypertensive rat model (SHR-ob with lean spontaneously hypertensive rats (SHR-lean and normotensive controls (Ctr. LV-function was investigated by cardiac magnetic resonance imaging and invasive LV-pressure measurements. LV-interstitial fibrosis was quantified and protein levels of phospholamban (PLB, Serca2a and glucose transporters (GLUT1 and GLUT4 were determined by immunohistochemistry. Results Systolic blood pressure was similar in SHR-lean and SHR-ob (252 ± 7 vs. 242 ± 7 mmHg, p = 0.398 but was higher when compared to Ctr (155 ± 2 mmHg, p  Conclusion In addition to hypertension alone, metabolic syndrome and obesity adds to the myocardial phenotype by aggravating diastolic dysfunction and a progression towards systolic dysfunction. SHR-ob may be a useful model to develop new interventional and pharmacological treatment strategies for hypertensive heart disease and metabolic disorders.

  9. TIME COURSE OF MYOCARDIAL INTERSTITIAL EDEMA RESOLUTION AND ASSOCIATED LEFT VENTRICULAR DYSFUNCTION

    Science.gov (United States)

    Dongaonkar, Ranjeet M.; Stewart, Randolph H.; Quick, Christopher M.; Uray, Karen L.; Cox, Charles S.; Laine, Glen A.

    2012-01-01

    Objective Although the causal relationship between acute myocardial edema and cardiac dysfunction has been established, resolution of myocardial edema and subsequent recovery of cardiac function have not. The time to resolve myocardial edema and the degree that cardiac function is depressed after edema resolves are not known. We therefore characterized temporal changes in cardiac function as acute myocardial edema formed and resolved. Methods Acute myocardial edema was induced in the canine model by elevating coronary sinus pressure for three hours. Myocardial water content and cardiac function were determined before and during coronary sinus pressure elevation, and after coronary sinus pressure restoration. Results Although no change in systolic properties was detected, accumulation of water in myocardial interstitium was associated with increased diastolic stiffness. When coronary sinus pressure was relieved, myocardial edema resolved within 180 min. Diastolic stiffness, however, remained significantly elevated compared to baseline values, and cardiac function remained compromised. Conclusions The present work suggests that the cardiac dysfunction caused by the formation of myocardial edema may persist after myocardial edema resolves. With the advent of new imaging techniques to quantify myocardial edema, this insight provides a new avenue for research to detect and treat a significant cause of cardiac dysfunction. PMID:22708850

  10. Exercise hemodynamics in patients with and without diastolic dysfunction and preserved ejection fraction after myocardial infarction

    DEFF Research Database (Denmark)

    Andersen, Mads J; Ersbøll, Mads; Bro-Jeppesen, John

    2012-01-01

    Left ventricular diastolic dysfunction (DD) is common after myocardial infarction (MI) despite preservation of left ventricular ejection fraction, yet it remains unclear how or whether DD affects cardiac hemodynamics with stress....

  11. Increased myocardial fibrosis and left ventricular dysfunction in Cushing's syndrome.

    NARCIS (Netherlands)

    Yiu, K.H.; Marsan, N.A.; Delgado, V.; Biermasz, N.R.; Holman, E.R.; Smit, J.W.A.; Feelders, R.A.; Bax, J.J.; Pereira, A.M.

    2012-01-01

    OBJECTIVE: Active Cushing's syndrome (CS) is associated with cardiomyopathy, characterized by myocardial structural, and ultrastructural abnormalities. The extent of myocardial fibrosis in patients with CS has not been previously evaluated. Therefore, the objective of this study was to assess myocar

  12. Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality

    DEFF Research Database (Denmark)

    Thomas, Kevin L; Al-Khatib, Sana M; Lokhnygina, Yuliya;

    2008-01-01

    BACKGROUND: We sought to assess the association of amiodarone use with mortality during consecutive periods in patients with post-acute myocardial infarction with left ventricular systolic dysfunction and/or HF treated with a contemporary medical regimen. METHODS: This study used data from VALIAN...

  13. Comparison between primary angioplasty and thrombolytic therapy on erectile dysfunction after acute ST elevation myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Ramazan Akdemir; Ekrem Yeter; (O)zlem Karakurt; Salih Orcan; Nihat Karakoyunlu; Mustafa Mucahit Balci; Levent Sa(g)nak; Hamit Ersoy; Mehmet Bulent Vatan; Harun Kilic

    2012-01-01

    Acute ST elevation myocarclial infarction has high mortality and morbidity rates.The majority of patients with this condition face erectile dysfunction in addition to other health problems,In this study,we aimed to investigate the effects of two different reperfusion strategies,primary angioplasty and thrombolytic therapy,on the prevalence of erectile dysfunction after acute myocardial infarction.Of the 71 patients matching the selection criteria,45 were treated with primary coronary angioplasty with stenting,and 26 were treated with thrombolytic agents.Erectile function was evaluated using the International Index of Erectile Function in the hospital to characterize each patient's sexual function before the acute myocardial infarction and 6 months after the event.The time required to restore blood flow to the artery affected by the infarct was found to be associated with the occurrence of erectile dysfunction after acute myocardial infarction.The increase in the prevalence of erectile dysfunction after acute myocardial infarction was 44.4% in the angioplasty group and 76.9% in the thrombolytic therapy group (P=0.008).In conclusion,this study has shown that reducing the time of reperfusion decreases the erectile dysfunction prevalence,and primary angioplasty is superior to thrombolytic therapy for decreasing the prevalence of erectile dysfunction after acute myocardial infarction.

  14. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.

    Science.gov (United States)

    Soraya, Hamid; Clanachan, Alexander S; Rameshrad, Maryam; Maleki-Dizaji, Nasrin; Ghazi-Khansari, Mahmoud; Garjani, Alireza

    2014-08-15

    Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium.

  15. Protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats.

    Science.gov (United States)

    Roy, Subhro Jyoti; Stanely Mainzen Prince, Ponnian

    2012-11-01

    In the pathology of myocardial infarction, lysosomal lipid peroxidation and resulting enzyme release play an important role. We evaluated the protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats. Male Wistar rats were treated with sinapic acid (12 mg/kg body weight) orally daily for 10 days and isoproterenol (100 mg/kg body weight) was injected twice at an interval of 24 h (9th and 10th day). Then, lysosomal lipid peroxidation, lysosomal enzymes in serum, heart homogenate, lysosomal fraction and myocardial infarct size were measured. Isoproterenol induced myocardial infarcted rats showed a significant increase in serum creatine kinase-MB and lysosomal lipid peroxidation. The activities of β-glucuronidase, β-galactosidase, cathepsin-B and D were significantly increased in serum, heart and the activities of β-glucuronidase and cathepsin-D were significantly decreased in lysosomal fraction of myocardial infarcted rats. Pre-and-co-treatment with sinapic acid normalized all the biochemical parameters and reduced myocardial infarct size in myocardial infarcted rats. In vitro studies confirmed the free radical scavenging effects of sinapic acid. The possible mechanisms for the observed effects are attributed to sinapic acid's free radical scavenging and membrane stabilizing properties. Thus, sinapic acid has protective effects on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats.

  16. A peptide vaccine targeting angiotensin II attenuates the cardiac dysfunction induced by myocardial infarction

    Science.gov (United States)

    Watanabe, Ryo; Suzuki, Jun-ichi; Wakayama, Kouji; Maejima, Yasuhiro; Shimamura, Munehisa; Koriyama, Hiroshi; Nakagami, Hironori; Kumagai, Hidetoshi; Ikeda, Yuichi; Akazawa, Hiroshi; Morishita, Ryuichi; Komuro, Issei; Isobe, Mitsuaki

    2017-01-01

    A peptide vaccine targeting angiotensin II (Ang II) was recently developed as a novel treatment for hypertension to resolve the problem of noncompliance with pharmacotherapy. Ang II plays a crucial role in the pathogenesis of cardiac remodeling after myocardial infarction (MI), which causes heart failure. In the present study, we examined whether the Ang II vaccine is effective in preventing heart failure. The injection of the Ang II vaccine in a rat model of MI attenuated cardiac dysfunction in association with an elevation in the serum anti-Ang II antibody titer. Furthermore, any detrimental effects of the Ang II vaccine were not observed in the rats that underwent sham operations. Treatment with immunized serum from Ang II vaccine-injected rats significantly suppressed post-MI cardiac dysfunction in MI rats and Ang II-induced remodeling-associated signaling in cardiac fibroblasts. Thus, our present study demonstrates that the Ang II vaccine may provide a promising novel therapeutic strategy for preventing heart failure. PMID:28266578

  17. Correlation between myocardial dysfunction and perfusion impairment in diabetic rats with velocity vector imaging and myocardial contrast echocardiography.

    Science.gov (United States)

    Wei, Zhangrui; Zhang, Haibin; Su, Haili; Zhu, Ting; Zhu, Yongsheng; Zhang, Jun

    2012-11-01

    The purpose of this study was to investigate whether myocardial systolic dysfunction and perfusion impairment occur in diabetic rats, and to assess their relationship using velocity vector imaging (VVI) and myocardial contrast echocardiography (MCE). Forty-six rats were randomly divided into either control or the diabetes mellitus (DM) groups. DM was induced by intraperitoneal administration of streptozotocin. Twelve weeks later, 39 survival rats underwent VVI and MCE in short-axis view at the middle level of the left ventricle, both at rest and after dipyridamole stress. VVI-derived contractile parameters included peak systolic velocity (Vs ), circumferential strain (εc ), strain rate (SRc ), and their reserves. MCE-derived perfusion parameters consisted of myocardial blood flow (MBF) and myocardial flow reserve (MFR). At rest, SRc in the DM group was significantly lower than in the control group, Vs , εc , and MBF did not differ significantly between groups. After dipyridamole stress, all VVI parameters and their reserves in the DM group were significantly lower than those in the control group, MBF and MFR were substantially lower than those in the control group, too. Meanwhile, significant correlations between VVI parameter reserves and MFR were observed in the DM group. Both myocardial systolic function and perfusion were impaired in DM rats. Decreased MFR could be an important contributor to the reduction in myocardial contractile reserve.

  18. Heart dysfunction and fibrosis in rat treated with myocardial ...

    African Journals Online (AJOL)

    use

    2011-11-16

    Nov 16, 2011 ... 2Department of Veterinary Medicine, National Chia Yi University, Chiayi, 60004, Taiwan. 3Animal Science ... inflammation, and millions of marrow-derived leukocytes ... repair process of myocardial infarction in humans.

  19. Discrepancy between myocardial perfusion and fatty acid metabolism following acute myocardial infarction for evaluating the dysfunctional viable myocardium.

    Science.gov (United States)

    Biswas, Shankar K; Sarai, Masayoshi; Toyama, Hiroshi; Hishida, Hitoshi; Ozaki, Yukio

    2012-01-01

    Following acute myocardial infarction (AMI) the area of myocardial perfusion and metabolism mismatch is designated as dysfunctional viable myocardium. (123)I-beta-methyl iodophenyl pentadecanoic acid (BMIPP) is clinically very useful for evaluating myocardial fatty acid metabolism, and (99)mTc-Tetrofosmin (TF) is a widely used tracer for myocardial perfusion. This study was designed to evaluate the degree of discrepancy between BMIPP and TF at the subacute state of AMI. Fifty-two patients (aged 59 ± 10 years; mean 46 years) with AMI were enrolled, and all of them underwent percutaneous coronary intervention (PCI). Patients were classified according to ST-T change and PCI timing. (123)I-beta-methyl iodophenyl pentadecanoic acid and TF cardiac scintigraphy were performed on 7 ± 3.5 days of admission using a dual headed gamma camera. Perfusion and fatty acid metabolism defect were scored on a 17 segments model. The mean BMIPP defect score on early and delayed images were 16.67 ± 10.19 and 16.25 ± 10.40, respectively. The mean TF defect score was 10 ± 7.69. Defect score of BMIPP was significantly higher than that of the TF (P TF), and 5 (10%) patients showed matched defect (BMIPP = TF). Mismatched defect score (MMDS) was significantly higher in patients with ST-segment elevation myocardial infarction (STEMI) than that of non-ST-segment elevation myocardial infarction (NSTEMI) (P < 0.041; 95% CI 0.11-5.19). At the subacute state of AMI, most of the patients showed perfusion-metabolism mismatch, which represents the dysfunctional viable myocardium, and patients with STEMI showed higher mismatch. Copyright © 2012 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.

  20. Mechanical ventilation with high tidal volumes attenuates myocardial dysfunction by decreasing cardiac edema in a rat model of LPS-induced peritonitis

    NARCIS (Netherlands)

    Smeding, Lonneke; Plotz, Frans B.; Lamberts, Regis R.; van der Laarse, Willem J.; Kneyber, Martin C. J.; Groeneveld, A. B. Johan

    2012-01-01

    Background: Injurious mechanical ventilation (MV) may augment organ injury remote from the lungs. During sepsis, myocardial dysfunction is common and increased endothelial activation and permeability can cause myocardial edema, which may, among other factors, hamper myocardial function. We investiga

  1. Mechanical ventilation with high tidal volumes attenuates myocardial dysfunction by decreasing cardiac edema in a rat model of LPS-induced peritonitis

    NARCIS (Netherlands)

    Smeding, Lonneke; Plotz, Frans B.; Lamberts, Regis R.; van der Laarse, Willem J.; Kneyber, Martin C. J.; Groeneveld, A. B. Johan

    2012-01-01

    Background: Injurious mechanical ventilation (MV) may augment organ injury remote from the lungs. During sepsis, myocardial dysfunction is common and increased endothelial activation and permeability can cause myocardial edema, which may, among other factors, hamper myocardial function. We investiga

  2. AT2 Receptors Targeting Cardiac Protection Post-Myocardial Infarction

    DEFF Research Database (Denmark)

    Kaschina, Elena; Lauer, Dilyara; Schmerler, Patrick

    2014-01-01

    The angiotensin AT2-receptor mediates tissue protective actions. Its regenerative potential has been tested in multiple disease models including models of myocardial infarction. These studies used different experimental approaches in order to detect AT2-receptor-related effects such as AT2-receptor...... is preserved over periods of up to four months. Depending on the experimental protocol, the AT2R also attenuates post-MI left ventricular remodeling or protects the heart from early left ventricular thinning and rupture. In combination with AT1-receptor blockade or deficiency, post-MI cardiac hypertrophy...... is reduced. This article reviews studies on the role of the AT2-receptor in myocardial infarction with an emphasis on the most recent data obtained in studies using AT2-receptor agonists....

  3. Pre- and postconditioning effect of Sevoflurane on myocardial dysfunction after cardiopulmonary resuscitation in rats.

    Science.gov (United States)

    Knapp, Jürgen; Bergmann, Greta; Bruckner, Thomas; Russ, Nicolai; Böttiger, Bernd W; Popp, Erik

    2013-10-01

    Post-resuscitation myocardial dysfunction is an important cause of death in the intensive care unit after initially successful cardiopulmonary resuscitation (CPR) of pre-hospital cardiac arrest (CA) patients. Volatile anaesthetics reduce ischaemic-reperfusion injury in regional ischaemia in beating hearts. This effect, called anaesthetic-induced pre- or postconditioning, can be shown when the volatile anaesthetic is given either before regional ischaemia or in the reperfusion phase. However, up to now, little data exist for volatile anaesthetics after global ischaemia due to CA. Therefore, the goal of this study was to clarify whether Sevoflurane improves post-resuscitation myocardial dysfunction after CA in rats. Following institutional approval by the Governmental Animal Care Committee, 144 male Wistar rats (341±19g) were randomized either to a control group or to one of the 9 interventional groups receiving 0.25 MAC, 0.5 MAC or 1 MAC of Sevoflurane for 5min either before resuscitation (SBR), during resuscitation (SDR) or after resuscitation (SAR). After 6min of electrically induced ventricular fibrillation CPR was performed. Before CA (baseline) as well as 1h and 24h after restoration of spontaneous circulation (ROSC), continuous measurement of ejection fraction (EF), and preload adjusted maximum power (PAMP) as primary outcome parameters and end systolic pressure (ESP), end diastolic volume (EDV) and maximal slope of systolic pressure increment (dP/dtmax) as secondary outcome parameters was performed using a conductance catheter. EF was improved in all Sevoflurane treated groups 1h after ROSC in comparison to control, except for the 0.25 MAC SDR and 0.25 MAC SAR group (0.25 MAC SBR: 38±8, p=0.02; 0.5 MAC SBR: 39±7, p=0.04; 1 MAC SBR: 40±6, p=0.007; 0.5 MAC SDR: 38±7, p=0.02; 1 MAC SDR: 40±6, p=0.006; 0.5 MAC SAR: 39±6, p=0.01; 1 MAC SAR: 39±6, p=0.002, vs. 30±7%). Twenty-four hours after ROSC, EF was higher than control in all interventional groups

  4. Liposome encapsulated berberine treatment attenuates cardiac dysfunction after myocardial infarction

    NARCIS (Netherlands)

    Allijn, Iris E.; Czarny, Bertrand M.S.; Wang, Xiaoyuan; Chong, Suet Yen; Weiler, Marek; Eduardo Da Silva, Acarilia; Metselaar, Josbert M.; Lam, Carolyn Su Ping; Pastorin, Giorgia; Kleijn, de Dominique P.V.; Storm, Gert; Wang, Jiong-Wei; Schiffelers, Raymond M.

    2017-01-01

    Inflammation is a known mediator of adverse ventricular remodeling after myocardial infarction (MI) that may lead to reduction of ejection fraction and subsequent heart failure. Berberine is a isoquinoline quarternary alkaloid from plants that has been associated with anti-inflammatory, anti-oxidati

  5. Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction

    DEFF Research Database (Denmark)

    Anavekar, Nagesh S; McMurray, John J V; Velazquez, Eric J;

    2004-01-01

    BACKGROUND: The presence of coexisting conditions has a substantial effect on the outcome of acute myocardial infarction. Renal failure is associated with one of the highest risks, but the influence of milder degrees of renal impairment is less well defined. METHODS: As part of the Valsartan in A...

  6. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both

    DEFF Research Database (Denmark)

    Pfeffer, Marc A; McMurray, John J V; Velazquez, Eric J;

    2003-01-01

    BACKGROUND: Angiotensin-converting-enzyme (ACE) inhibitors such as captopril reduce mortality and cardiovascular morbidity among patients with myocardial infarction complicated by left ventricular systolic dysfunction, heart failure, or both. In a double-blind trial, we compared the effect of the...

  7. Myocardial infarction and transient ventricular dysfunction in an adolescent with sickle cell disease.

    Science.gov (United States)

    Deymann, Andreas J; Goertz, Kenneth K

    2003-02-01

    We report a case of an adolescent who had sickle cell disease and previous evidence of myocardial damage and presented with abdominal pain and rapid progression to cardiogenic shock and subsequent development of myocardial infarction. To our knowledge, this represents only the second report of a case of acute myocardial ischemia and subsequent infarction resulting transient ventricular dysfunction reported in a child with sickle cell disease successfully treated with exchange transfusion. The pathophysiology of this complication remains unclear, and cardiac complications may remain undetected as lung, bone, and brain infarcts are more common and the pain associated with sickle cell crisis may mask the ischemic symptoms. Multiple factors may contribute to ischemia in addition to the presence of a vaso-occlusive crisis or infection. Acute or chronic myocardial ischemia are probably more prevalent than currently known.

  8. Preventive effects of p-coumaric acid on lysosomal dysfunction and myocardial infarct size in experimentally induced myocardial infarction.

    Science.gov (United States)

    Jyoti Roy, Abhro; Stanely Mainzen Prince, P

    2013-01-15

    The present study was designed to evaluate the preventive effects of p-coumaric acid on lysosomal dysfunction and myocardial infarct size in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days after which isoproterenol (100mg/kg body weight) was injected subcutaneously into rats twice at an interval of 24h (8th and 9th day).The activity/levels of serum cardiac diagnostic markers, heart lysosomal lipid peroxidation products and the activities of lysosomal enzymes (β-glucuronidase, β-galactosidase, cathepsin-B and cathepsin-D) were significantly (Plysosomal fraction. The pretreatment with p-coumaric acid significantly (Plysosomal lipid peroxidation products and the activities of lysosomal enzymes. In addition, p-coumaric acid greatly reduced myocardial infarct size. p-Coumaric acid pretreatment (8 mg/kg body weight) to normal rats did not show any significant effect. Thus, this study showed that p-coumaric acid prevents lysosomal dysfunction against cardiac damage induced by isoproterenol and brings back the levels of lipid peroxidation products and activities of lysosomal enzymes to near normal levels. The in vitro study also revealed the free radical scavenging activity of p-coumaric acid. Thus, the observed effects are due to p-coumaric acid's free radical scavenging and membrane stabilizing properties.

  9. Post Operative Cognitive Dysfunction (POCD in Geriatric Population

    Directory of Open Access Journals (Sweden)

    Rajesh MC

    2015-10-01

    Full Text Available Post-operative mental dysfunction and confusion in aged patients is a well recognized entity. Commonly known as post-operative delirium and cognitive dysfunction (POCD, these are important for any peri-operative physician dealing with geriatric population. The incidence is more in older patients with pre-existing impairment. Impact of POCD is grave. This can result in poor rehabilitation outcome and increased hospital stay. Incidence ranges from 15-50% with ˂5% for cataract surgery and as high as 60% after hip replacement procedures.

  10. Endothelial cells overexpressing IL-8 receptor reduce cardiac remodeling and dysfunction following myocardial infarction.

    Science.gov (United States)

    Zhao, Xiangmin; Zhang, Wei; Xing, Dongqi; Li, Peng; Fu, Jinyan; Gong, Kaizheng; Hage, Fadi G; Oparil, Suzanne; Chen, Yiu-Fai

    2013-08-15

    The endothelium is a dynamic component of the cardiovascular system that plays an important role in health and disease. This study tested the hypothesis that targeted delivery of endothelial cells (ECs) overexpressing neutrophil membrane IL-8 receptors IL8RA and IL8RB reduces acute myocardial infarction (MI)-induced left ventricular (LV) remodeling and dysfunction and increases neovascularization in the area at risk surrounding the infarcted tissue. MI was created by ligating the left anterior descending coronary artery in 12-wk-old male Sprague-Dawley rats. Four groups of rats were studied: group 1: sham-operated rats without MI or EC transfusion; group 2: MI rats with intravenous vehicle; group 3: MI rats with transfused ECs transduced with empty adenoviral vector (Null-EC); and group 4: MI rats with transfused ECs overexpressing IL8RA/RB (1.5 × 10⁶ cells post-MI). Two weeks after MI, LV function was assessed by echocardiography; infarct size was assessed by triphenyltetrazolium chloride (live tissue) and picrosirus red (collagen) staining, and capillary density and neutrophil infiltration in the area at risk were measured by CD31 and MPO immunohistochemical staining, respectively. When compared with the MI + vehicle and MI-Null-EC groups, transfusion of IL8RA/RB-ECs decreased neutrophil infiltration and pro-inflammatory cytokine expression and increased capillary density in the area at risk, decreased infarct size, and reduced MI-induced LV dysfunction. These findings provide proof of principle that targeted delivery of ECs is effective in repairing injured cardiac tissue. Targeted delivery of ECs to infarcted hearts provides a potential novel strategy for the treatment of acute MI in humans.

  11. Usefulness of C-reactive protein as a marker of early post-infarct left ventricular systolic dysfunction

    OpenAIRE

    Świątkiewicz, Iwona; Koziński, Marek; Magielski, Przemysław; Gierach, Joanna; Fabiszak, Tomasz; Kubica, Aldona; Sukiennik, Adam; Navarese, Eliano Pio; Odrowąż-Sypniewska, Grażyna; Kubica, Jacek

    2012-01-01

    Objective To assess the usefulness of in-hospital measurement of C-reactive protein (CRP) concentration in comparison to well-established risk factors as a marker of post-infarct left ventricular systolic dysfunction (LVSD) at discharge. Materials and methods Two hundred and four consecutive patients with ST-segment-elevation myocardial infarction (STEMI) were prospectively enrolled into the study. CRP plasma concentrations were measured before reperfusion, 24 h after admission and at dischar...

  12. Abnormal Calcium "Sparks" in Cardiomyocytes of Post-myocardial Infarction Heart

    Institute of Scientific and Technical Information of China (English)

    Kai HUANG; Dan HUANG; Shengquan FU; Chongzhe YANG; Yuhua LIAO

    2008-01-01

    In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alphalc, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant.It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes,which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.

  13. Utilization of 3 amplatzer occluders for closure of post-myocardial infarction ventricular septal defect.

    Science.gov (United States)

    Kar, Saibal; Ibebuogu, Uzoma N; Conte, Antonio Hernandez

    2012-05-01

    This case report describes a patient who sustained a post-myocardial infarction ventricular septal defect (VSD) with an associated left ventricular aneurysm who developed cardiogenic shock and required an intra-aortic balloon pump for hemodynamic stabilization. After deployment of a single Amplatzer occluder (AGA Medical), a residual VSD measuring 0.5 cm was noted. Therefore, a second Amplatzer occluder was deployed and a minimal residual VSD remained. The patient remained hemodynamically stable throughout the procedure and was subsequently extubated with removal of intra-aortic balloon pump. Post-discharge, the patient was readmitted with congestive heart failure. A third Amplatzer device was deployed to ameliorate the recurrent VSD shunt. At 9-week follow-up, transthoracic echocardiogram was performed and findings included: 1) left ventricular ejection fraction of 62%; 2) appearance of 3 Amplatzer devices along the interventrcular septum seated well with no motion and residual shunt; 3) moderate diastolic dysfunction with pseudonormal left ventricular filling pattern; and 4) no valvular abnormalities. The patient had increased exercise tolerance with no shortness of breath at rest or with exertion. This case demonstrates the utility and viability of multiple Amplatzer device deployment as a means of repairing a large post-myocardial infarction VSD and recurrent VSDs.

  14. Use of Valsartan in Post-Myocardial Infarction and Heart Failure Patients

    Directory of Open Access Journals (Sweden)

    Peter P Liu

    2006-03-01

    Full Text Available Left ventricular (LV dysfunction and/or heart failure (HF are frequent complications of hypertension and myocardial infarction (MI, placing affected patients at increased risk of significant morbidity and premature death. Given that the renin-angiotensin-aldosterone system (RAAS is activated and of pathophysiological importance in such patients, a strong therapeutic rationale exists to target the main effector mechanism (that is, angiotensin II [Ang II] in order to lessen the associated morbidity and mortality burden.Angiotensin-converting enzyme (ACE inhibitors have been shown to reduce mortality and LV dysfunction and to slow disease progression in patients with HF, including high-risk, post-MI patients. However, ACE inhibitors (ACE-Is may not provide optimal long-term RAAS blockade (a finding that is associated with a worse prognosis such and many patients are unable to tolerate such therapy (because of troublesome dry cough, for example. In contrast, Ang II receptor blockers (ARBs may block the RAAS more completely than ACE-Is and appear to be better tolerated. Several large-scale trials have evaluated the efficacy of ARBs in patients with LV dysfunction and/or HF (including high-risk, post-MI patients, and have confirmed their utility as an R efficacious and well-tolerated alternative to ACE-Is in this setting.

  15. Depth of anaesthesia and post-operative cognitive dysfunction

    DEFF Research Database (Denmark)

    Steinmetz, J; Funder, K S; Dahl, B T

    2010-01-01

    A deep level of anaesthesia measured by the bispectral index has been found to improve processing speed as one aspect of cognitive function after surgery. The purpose of the present study was to assess the possible effect of the level of anaesthesia on post-operative cognitive dysfunction (POCD) 1...

  16. Depth of anaesthesia and post-operative cognitive dysfunction

    DEFF Research Database (Denmark)

    Steinmetz, J; Funder, K S; Dahl, B T;

    2010-01-01

    A deep level of anaesthesia measured by the bispectral index has been found to improve processing speed as one aspect of cognitive function after surgery. The purpose of the present study was to assess the possible effect of the level of anaesthesia on post-operative cognitive dysfunction (POCD) 1...

  17. Berberine attenuates adverse left ventricular remodeling and cardiac dysfunction after acute myocardial infarction in rats: role of autophagy.

    Science.gov (United States)

    Zhang, Yao-Jun; Yang, Shao-Hua; Li, Ming-Hui; Iqbal, Javaid; Bourantas, Christos V; Mi, Qiong-Yu; Yu, Yi-Hui; Li, Jing-Jing; Zhao, Shu-Li; Tian, Nai-Liang; Chen, Shao-Liang

    2014-12-01

    The present study aimed to test the hypothesis that berberine, a plant-derived anti-oxidant, attenuates adverse left ventricular remodelling and improves cardiac function in a rat model of myocardial infarction (MI). Furthermore, the potential mechanisms that mediated the cardioprotective actions of berberine, in particular the effect on autophagy, were also investigated. Acute MI was induced by ligating the left anterior descending coronary artery of Sprague-Dawley rats. Cardiac function was assessed by transthoracic echocardiography. The protein activity/levels of autophagy related to signalling pathways (e.g. LC-3B, Beclin-1) were measured in myocardial tissue by immunohistochemical staining and western blot. Four weeks after MI, berberine significantly prevented cardiac dysfunction and adverse cardiac remodelling. MI rats treated with low dose berberine (10 mg/kg per day) showed higher left ventricular ejection fraction and fractional shortening than those treated with high-dose berberine (50 mg/kg per day). Both doses reduced interstitial fibrosis and post-MI adverse cardiac remodelling. The cardioprotective action of berberine was associated with increased LC-3B II and Beclin-1 expressions. Furthermore, cardioprotection with berberine was potentially related to p38 MAPK inhibition and phospho-Akt activation. The present in vivo study showed that berberine is effective in promoting autophagy, and subsequently attenuating left ventricular remodelling and cardiac dysfunction after MI. The potential underlying mechanism is augmentation of autophagy through inhibition of p38 MAPK and activation of phospho-Akt signalling pathways.

  18. Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

    Energy Technology Data Exchange (ETDEWEB)

    Watanabe, Tomoyuki [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Saotome, Masao, E-mail: msaotome@hama-med.ac.jp [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Nobuhara, Mamoru; Sakamoto, Atsushi; Urushida, Tsuyoshi; Katoh, Hideki; Satoh, Hiroshi [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Funaki, Makoto [Clinical Research Center for Diabetes, Tokushima University Hospital, 2-50-1 Kuramoto-cho, Tokushima 770-8503 (Japan); Hayashi, Hideharu [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan)

    2014-05-01

    Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ{sub m}) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H{sub 2}O{sub 2}), they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ{sub m} depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H{sub 2}O{sub 2}-induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ{sub m} depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin

  19. Percutaneous coronary intervention for acute myocardial infarction in elderly patients with renal dysfunction: results from the Korea Acute Myocardial Infarction Registry.

    Science.gov (United States)

    Lim, Sang Yup; Bae, Eun Hui; Choi, Joon Seok; Kim, Chang Seong; Ma, Seong Kwon; Ahn, Youngkeun; Jeong, Myung Ho; Kim, Weon; Woo, Jong Shin; Kim, Young Jo; Cho, Myeong Chan; Kim, Chong Jin; Kim, Soo Wan

    2013-07-01

    This study aimed to evaluate the effects of percutaneous coronary intervention (PCI) on short- and long-term major adverse cardiac events (MACE) in elderly (>75 yr old) acute myocardial infarction (AMI) patients with renal dysfunction. As part of Korea AMI Registry (KAMIR), elderly patients with AMI and renal dysfunction (GFRrenal dysfunction, PCI therapy yields favorable in-hospital and short-term and long-term MACE-free survival.

  20. Anaemia is an independent predictor of mortality in patients with left ventricular systolic dysfunction following acute myocardial infarction

    DEFF Research Database (Denmark)

    Valeur, Nana; Nielsen, Olav Wendelboe; McMurray, John J V;

    2006-01-01

    BACKGROUND: In patients with chronic heart failure (HF), mortality is inversely related to haemoglobin (hgb) concentration. We investigated the prognostic importance of anaemia in patients with acute myocardial infarction (AMI) and left ventricular systolic dysfunction (LVSD) with and without HF...

  1. Early detection of myocardial dysfunction in children with mitochondrial disease: An ultrasound and two-dimensional strain echocardiography study

    NARCIS (Netherlands)

    Marcus, K.A.; Barends, M.; Morava, E.; Feuth, T.; Korte, C.L. de; Kapusta, L.

    2011-01-01

    BACKGROUND: Myocardial dysfunction in children diagnosed with mitochondrial disease is an ominous sign and has been associated with substantial increased mortality rates. Early detection of cardiac involvement would therefore be desirable. Two dimensional strain echocardiography (2DSTE) has proven t

  2. NOS3 Protects Against Systemic Inflammation and Myocardial Dysfunction in Murine Polymicrobial Sepsis

    OpenAIRE

    Bougaki, Masahiko; Searles, Robert J.; Kida, Kotaro; Yu, JiaDe; Buys, Emmanuel; Ichinose, Fumito

    2010-01-01

    NO has been implicated in the pathogenesis of septic shock. However, the role of NO synthase 3 (NOS3) during sepsis remains incompletely understood. Here, we examined the impact of NOS3 deficiency on systemic inflammation and myocardial dysfunction during peritonitis-induced polymicrobial sepsis. Severe polymicrobial sepsis was induced by colon ascendens stent peritonitis (CASP) in wild-type (WT) and NOS3-deficient (NOS3KO) mice. NOS3KO mice exhibited shorter survival time than did WT mice af...

  3. Use of Statins by Medicare Beneficiaries Post Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Mary C. Schroeder PhD

    2015-02-01

    Full Text Available Even though guidelines strongly recommend that patients receive a statin for secondary prevention after an acute myocardial infarction (MI, many elderly patients do not fill a statin prescription within 30 days of discharge. This paper assesses whether patterns of statin use by Medicare beneficiaries post-discharge may be due to a mix of high-quality and low-quality physicians. Our data come from the Centers for Medicare & Medicaid Services (CMS Chronic Condition Data Warehouse (CCW and include 100% of Medicare beneficiaries hospitalized for an acute myocardial infarction in 2008 or 2009. Our study sample included physicians treating at least 10 Medicare fee-for-service beneficiaries during their MI institutional stay. Physician-specific statin fill rates (the proportion of each physician’s patients with a statin within 30 days post-discharge were calculated to assess physician quality. We hypothesized that if the observed statin rates reflected a mix of high-quality and low-quality physicians, then physician-specific statin fill rates should follow a u-shaped or bimodal distribution. In our sample, 62% of patients filled a statin prescription within 30 days of discharge. We found that the distribution of statin fill rates across physicians was normal, with no clear distinctions in physician quality. Physicians, especially cardiologists, with relatively younger and healthier patient populations had higher rates of statin use. Our results suggest that physicians were engaging in patient-centered care, tailoring treatments to patient characteristics.

  4. Post-stroke cognitive dysfunctions: A clinical and neuroimaging study

    Directory of Open Access Journals (Sweden)

    Andrei Yuryevich Emelin

    2013-01-01

    Full Text Available Clinical, neuropsychological, and neuroimaging examinations were made in 65 patients (52 men and 13 women aged 65.6±10.1 years who had experienced ischemic stroke. Cognitive impairments (CI were heterogeneous; regulatory functions, attention, and counting were most significantly affected in moderate CI. In mild dementia, mainly poor attention and regulatory dysfunctions were added by clearly-cut impairments of memory, orientation, and visual-spatial function. Brain atrophy, white matter changes, and small focal gray matter damages along with focal post-stroke changes were revealed by neuroimaging in most patients. It was found that besides the volume and location of a damage focus, the signs of impaired integrated mental activity of the brain, regulatory dysfunctions in particular, should be a necessary condition for the verification of post-stroke CI.

  5. MYOCARDIAL REVASCULARIZATION IN PATIENTS WITH LEFT VENTRICULAR SYSTOLIC DYSFUNCTION: PROBLEM STATEMENT

    Directory of Open Access Journals (Sweden)

    A. B. Mironkov

    2013-01-01

    Full Text Available Outcomes of myocardium revascularization in patients with chronic left ventricular systolic dysfunction due to coronary artery disease are still unclear. The identification of dysfunctional myocardial with residual viability that can improve after revascularization are very important for further patient treatment. Hibernating myocardium can be identified by different methods and its presence and extent can predict functional and structural recovery after revascularization. New medical treatments and devices, have improved the prognosis of this patients and their use is supported by a number of clinical trials. The prognostic benefits of coronary revascularization for patients with chronic left ventricular dysfunction on optimal medical therapy and novel devices a randomized trial is still needed. 

  6. Myocardial dysfunction occurs prior to changes in ventricular geometry in mice with chronic kidney disease (CKD).

    Science.gov (United States)

    Winterberg, Pamela D; Jiang, Rong; Maxwell, Josh T; Wang, Bo; Wagner, Mary B

    2016-03-01

    Uremic cardiomyopathy is responsible for high morbidity and mortality rates among patients with chronic kidney disease (CKD), but the underlying mechanisms contributing to this complex phenotype are incompletely understood. Myocardial deformation analyses (ventricular strain) of patients with mild CKD have recently been reported to predict adverse clinical outcome. We aimed to determine if early myocardial dysfunction in a mouse model of CKD could be detected using ventricular strain analyses. CKD was induced in 5-week-old male 129X1/SvJ mice through partial nephrectomy (5/6Nx) with age-matched mice undergoing bilateral sham surgeries serving as controls. Serial transthoracic echocardiography was performed over 16 weeks following induction of CKD. Invasive hemodynamic measurements were performed at 8 weeks. Gene expression and histology was performed on hearts at 8 and 16 weeks. CKD mice developed decreased longitudinal strain (-25 ± 4.2% vs. -29 ± 2.3%; P = 0.01) and diastolic dysfunction (E/A ratio 1.2 ± 0.15 vs. 1.9 ± 0.18; P ventricular hypertrophy was not apparent until 4 weeks. Hearts from CKD mice developed progressive fibrosis at 8 and 16 weeks with gene signatures suggestive of evolving heart failure with elevated expression of natriuretic peptides. Uremic cardiomyopathy in this model is characterized by early myocardial dysfunction which preceded observable changes in ventricular geometry. The model ultimately resulted in myocardial fibrosis and increased expression of natriuretic peptides suggestive of progressive heart failure.

  7. Prevalence and distribution of regional scar in dysfunctional myocardial segments in Duchenne muscular dystrophy

    Directory of Open Access Journals (Sweden)

    Crawford Thomas O

    2011-03-01

    Full Text Available Abstract Background The segmental relationship between cardiovascular magnetic resonance (CMR peak circumferential strain (Ecc and myocardial scar has not been well characterized in Duchenne muscular dystrophy (DMD, and it is unknown whether echocardiography accurately measures Ecc in DMD. We assessed segmental Ecc and scar using CMR with myocardial tissue tagging and late gadolinium enhancement (LGE in patients with DMD, then compared CMR with echocardiographic velocity vector imaging (VVI for regional Ecc based on independent observer assessments. Results Participants enrolled (n = 16; age 8-23 had median left ventricular (LV ejection fraction of 0.52 (range 0.28-0.69, and 156 basal and mid-cavity myocardial segments from the 13 patients completing the LGE protocol were analyzed for strain and scar. Segmental CMR Ecc in the most negative quartile (quartile 4 ruled out scar in that segment, but scar was present in 46% of segments in the least negative (most dysfunctional Ecc quartile 1, 33% of Ecc quartile 2 segments, and 15% of Ecc quartile 3 segments. Overall scar prevalence in inferior, inferolateral, and anterolateral segments was eight times higher than in inferoseptal, anteroseptal, and anterior segments (p Conclusions The relationship between scar and Ecc in DMD is complex. Among myocardial segments with depressed Ecc, scar prevalence was much higher in inferior, inferolateral, and anterolateral segments, indicating a regionally dependent association between abnormal Ecc and scar, with free wall segments commonly developing dysfunction with scar and septal segments developing dysfunction without scar. Although normal echocardiographic Ecc predicted absence of scar, regional echocardiographic Ecc by VVI has only a limited association with CMR Ecc in DMD.

  8. Nos3 protects against systemic inflammation and myocardial dysfunction in murine polymicrobial sepsis.

    Science.gov (United States)

    Bougaki, Masahiko; Searles, Robert J; Kida, Kotaro; Yu, JiaDe; Buys, Emmanuel S; Ichinose, Fumito

    2010-09-01

    NO has been implicated in the pathogenesis of septic shock. However, the role of NO synthase 3 (NOS3) during sepsis remains incompletely understood. Here, we examined the impact of NOS3 deficiency on systemic inflammation and myocardial dysfunction during peritonitis-induced polymicrobial sepsis. Severe polymicrobial sepsis was induced by colon ascendens stent peritonitis (CASP) in wild-type (WT) and NOS3-deficient (NOS3KO) mice. NOS3KO mice exhibited shorter survival time than did WT mice after CASP. NOS3 deficiency worsened systemic inflammation assessed by the expression of inflammatory cytokines in the lung, liver, and heart. Colon ascendens stent peritonitis markedly increased the number of leukocyte infiltrating the liver and heart in NOS3KO but not in WT mice. The exaggerated systemic inflammation in septic NOS3KO mice was associated with more marked myocardial dysfunction than in WT mice 22 h after CASP. The detrimental effects of NOS3 deficiency on myocardial function after CASP seem to be caused by impaired Ca handling of cardiomyocytes. The impaired Ca handling of cardiomyocytes isolated from NOS3KO mice subjected to CASP was associated with depressed mitochondrial ATP production, a determinant of the Ca cycling capacity of sarcoplasmic reticulum Ca-ATPase. The NOS3 deficiency-induced impairment of the ability of mitochondria to produce ATP after CASP was at least in part attributable to reduction in mitochondrial respiratory chain complex I activity. These observations suggest that NOS3 protects against systemic inflammation and myocardial dysfunction after peritonitis-induced polymicrobial sepsis in mice.

  9. Stem cell mechanisms during left ventricular remodeling post-myocardial infarction:Repair and regeneration

    Institute of Scientific and Technical Information of China (English)

    Rogelio; Zamilpa; Mary; M; Navarro; Iris; Flores; Sy; Griffey

    2014-01-01

    Post-myocardial infarction(MI),the left ventricle(LV)undergoes a series of events collectively referred to as remodeling.As a result,damaged myocardium is replaced with fibrotic tissue consequently leading to contractile dysfunction and ultimately heart failure.LV remodeling post-MI includes inflammatory,fibrotic,and neovascularization responses that involve regulated cell recruitment and function.Stem cells(SCs)have been transplanted post-MI for treatment of LV remodeling and shown to improve LV function by reduction in scar tissue formation in humans and animal models of MI.The promising results obtained from the application of SCs post-MI have sparked a massive effort to identify the optimal SC for regeneration of cardiomyocytes and the paradigm for clinical applications.Although SC transplantations are generally associated with new tissue formation,SCs also secrete cytokines,chemokines and growth factors that robustly regulate cell behavior in a paracrine fashion during the remodeling process.In this review,the different types of SCs used for cardiomyogenesis,markers of differentiation,paracrine factor secretion,and strategies for cell recruitment and delivery are addressed.

  10. Sildenafil and diastolic dysfunction after acute myocardial infarction in patients with preserved ejection fraction: the Sildenafil and Diastolic Dysfunction After Acute Myocardial Infarction (SIDAMI) trial

    DEFF Research Database (Denmark)

    Andersen, Mads Jønsson; Ersboll, M; Axelsson, Anders

    2013-01-01

    BACKGROUND: Diastolic dysfunction is frequently seen after myocardial infarction and is characterized by a disproportionate increase in filling pressure during exercise to maintain stroke volume. We hypothesized that sildenafil would reduce filling pressure during exercise in patients...... weeks of treatment patients underwent simultaneous echocardiography and right heart catheterization at rest and during exercise. Primary end point was pulmonary capillary wedge pressure, and secondary end points comprised cardiac index and pulmonary arterial pressure at rest and during exercise after 9...... weeks. After 9 weeks there were no differences in pulmonary capillary wedge pressure at rest (13+/-4 versus 13+/-3 mm Hg, P=0.25) or at peak exercise (35+/-8 mm Hg versus 31+/-7 mm Hg, P=0.07). However, with treatment cardiac index increased at rest (P=0.006) and peak exercise (P=0.02) in the sildenafil...

  11. Quantitative proteomic changes during post myocardial infarction remodeling reveals altered cardiac metabolism and Desmin aggregation in the infarct region.

    Science.gov (United States)

    Datta, Kaberi; Basak, Trayambak; Varshney, Swati; Sengupta, Shantanu; Sarkar, Sagartirtha

    2017-01-30

    Myocardial infarction is one of the leading causes of cardiac dysfunction, failure and sudden death. Post infarction cardiac remodeling presents a poor prognosis, with 30%-45% of patients developing heart failure, in a period of 5-25years. Oxidative stress has been labelled as the primary causative factor for cardiac damage during infarction, however, the impact it may have during the process of post infarction remodeling has not been well probed. In this study, we have implemented iTRAQ proteomics to catalogue proteins and functional processes, participating both temporally (early and late phases) and spatially (infarct and remote zones), during post myocardial infarction remodeling of the heart as functions of the differential oxidative stress manifest during the remodeling process. Cardiac metabolism was the dominant network to be affected during infarction and the remodeling time points considered in this study. A distinctive expression pattern of cytoskeletal proteins was also observed with increased remodeling time points. Further, it was found that the cytoskeletal protein Desmin, aggregated in the infarct zone during the remodeling process, mediated by the protease Calpain1. Taken together, all of these data in conjunction may lay the foundation to understand the effects of oxidative stress on the remodeling process and elaborate the mechanism behind the compromised cardiac function observed during post myocardial infarction remodeling.

  12. Patients without myocardial accumulation of {sup 123}I-metaiodobenzylguanidine. Does it always reflect cardiac adrenergic dysfunction?

    Energy Technology Data Exchange (ETDEWEB)

    Narita, Michihiro; Kurihara, Tadashi; Honda, Minoru; Hohjoh, Osamu [Sumitomo Hospital, Osaka (Japan)

    1994-12-01

    Since December 1992 to March 1994, we have performed myocardial imaging with {sup 123}I-metaiodobenzylguanidine ({sup 123}I-MIBG) in 110 patients to examine myocardial sympathetic integrity. Among them 11 patients (10%) showed no accumulation of {sup 123}I-MIBG in the heart. So we have examined the mechanisms of no myocardial {sup 123}I-MIBG accumulation. {sup 123}I-MIBG imaging was obtained at 20 min and 3 h after intravenous injection of {sup 123}I-MIBG (148 MBq) at rest. In addition to routine tomography, anterior planar imaging of the heart and the whole body imaging were performed. Eleven patients without myocardial {sup 123}I-MIBG accumulation consisted of 5 patients with orthostatic hypotension (including 3 patients with diabetic neuropathy). four patients with hypertrophic cardiomyopathy (HCM), one patient with hypertension and one normal subject. In patients with orthostatic hypotension, standing test showed cardiac sympathetic dysfunction. In addition to no myocardial {sup 123}I-MIBG accumulation, accumulation of {sup 123}I-MIBG in the salivary glands was not found in all them. These indicated that in patients with orthostatic hypotension, generalized sympathetic dysfunction caused no myocardial {sup 123}I-MIBG accumulation. But in other 6 patients there was no evidence which suggested the cardiac sympathetic nerve dysfunction. Age, sex, serum norepinephrine level, myocardial perfusion and the medication were not different between the patients with and without myocardial {sup 123}I-MIBG accumulation. So the mechanism of no myocardial {sup 123}I-MIBG accumulation was not clear in these patients. But it was noteworthy that in patients with HCM, no myocardial {sup 123}I-MIBG accumulation appeared in 17% (4/24), and the frequency of no myocardial {sup 123}I-MIBG accumulation in HCM was significantly (p<0.05) higher than in other disease entities when patients with orthostatic hypotension were excluded. (author).

  13. Ischemic Left Ventricular Dysfunction: Severity of Remodeling, Myocardial Viability and Survival After Surgical Revascularization

    Science.gov (United States)

    Bonow, Robert O.; Castelvecchio, Serenella; Panza, Julio A.; Berman, Daniel S.; Velazquez, Eric J.; Michler, Robert E.; She, Lilin; Holly, Thomas A.; Desvigne-Nickens, Patrice; Kosevic, Dragana; Rajda, Miroslaw; Chrzanowski, Lukasz; Deja, Marek; Lee, Kerry L.; White, Harvey; Oh, Jae K.; Doenst, Torsten; Hill, James A; Rouleau, Jean L.; Menicanti, Lorenzo

    2015-01-01

    Objectives The objectives of this study were to test the hypothesis that end-systolic volume (ESV), as a marker of severity of left ventricular (LV) remodeling, influences the relationship between myocardial viability and survival in patients with coronary artery disease and LV systolic dysfunction. Background Retrospective studies of ischemic LV dysfunction suggest that severity of LV remodeling determines whether myocardial viability predicts improved survival with surgical (CABG) compared to medical (MED) therapy, with CABG only benefitting patients with viable myocardium who have smaller ESV. However, this has not been tested prospectively. Methods Interactions of ESV index (ESVI), myocardial viability and treatment with respect to survival were assessed in patients in the prospective randomized STICH trial of CABG vs MED who underwent viability assessment (n=601, age 61±9 years, ejection fraction ≤35%), median follow-up 5.1 years. Median ESVI was 84 ml/m2. Viability was assessed by SPECT or dobutamine echocardiography using prespecified criteria. Results Mortality was highest among patients with larger ESVI and non-viability (P84 ml/m2 (HR 0.87, 95% CI 0.57,1.31). Other ESVI thresholds yielded similar results, including ESVI ≤60 ml/m2 (HR 0.87, 95% CI 0.44,1.74). ESVI and viability assessed as continuous rather than dichotomous variables yielded similar results (P=0.562). Conclusions Among patients with ischemic cardiomyopathy, those with greater LVESVI and no substantial viability have worse prognosis. However, the effect of CABG relative to MED is not differentially influenced by the combination of these two factors. Lower ESVI does not identify patients in whom myocardial viability predicts better outcome with CABG relative to MED. PMID:26363840

  14. Off-pump total myocardial revascularization in patients with left ventricular dysfunction.

    Science.gov (United States)

    Milani, Rodrigo; Paulo, Brofman; Moutinho, José Augusto; Laura, Barboza; Maximiliano, Guimarães; Alexandre, Barbosa; Lidia, Zitynski; Dalton, Précoma; Alexandre, Varela; Ravanelli, Marcel Rogers; Maia, Francisco

    2007-07-01

    To assess off-pump myocardial revascularization in patients with significant left ventricular dysfunction. Four hundred and five patients with an ejection fraction less than 35% underwent myocardial revascularization without extracorporeal circulation. The procedure was performed with the aid of a suction stabilizer and the LIMA stitch. The distal anastomoses were performed first. A total of 405 patients were evaluated whose mean age was 63.4 +/- 9.78 years. Two hundred and seventy-nine patients were men (68.8%). With regard to risk factors, 347 patients were hypertensive, 194 were smokers, 202 were dyslipidemic, and 134 had diabetes. Two hundred and sixty patients were classified as NYHA functional class III and IV. Twenty patients suffered from chronic renal disease and were under dialysis. Fifty-one underwent emergency surgery, and 33 had been previously operated on. The mean ejection fraction was 27.2 +/- 3.54%. The mean EuroSCORE was 8.46 +/- 4.41. The mean number of anastomoses performed was 3.03 +/- 1.54 per patient. Forty-nine patients (12%) needed an intra-aortic balloon inserted after induction of anesthesia, whereas 73 (18%) needed inotropic support during the perioperative period. As to complications, 2 patients (0.49%) had renal failure, 2 had mediastinitis (0.49%), 7 (1.7%) needed to be reoperated because of bleeding, 5 patients (1.2%) suffered acute myocardial infarction, and 70 patients (17.3%) experienced atrial fibrillation. Eighteen (4.4%) patients died. Based on the data above, we concluded that myocardial revascularization without extracorporeal circulation in patients with left ventricular dysfunction is a safe and effective technique, and an alternative for high-risk patients. Results obtained were better than those predicted by EuroSCORE.

  15. Types of Diastolic Dysfunction of the Left Ventricle in Adolescents with Myocardial Pathology

    Directory of Open Access Journals (Sweden)

    L.F. Bogmat

    2014-07-01

    Full Text Available In adolescents with myocardial pathology during isometric tests we detected three types of diastolic dysfunction of the left ventricle (LV of the heart, depending on E/A ratio. The most pronounced signs of diastolic filling disorders were detected in the third group of patients, as evidenced: by a tendency to increase isovolumic relaxation time, a significant increase of slowing down time of the first phase of left ventricular filling, reduced LV filling rate both in the first phase of the passive filling and the second phase of active LV filling, increasing E/A ratio of more than 2, significant dilation of the left atrium, as well as positive increase in diastolic reserve that confirms deeper diastolic dysfunction in these adolescents compared with other subgroups.

  16. Diastolic dysfunction predicts new-onset atrial fibrillation and cardiovascular events in patients with acute myocardial infarction and depressed left ventricular systolic function: a CARISMA substudy

    DEFF Research Database (Denmark)

    Jons, Christian; Joergensen, Rikke Moerch; Hassager, Christian;

    2010-01-01

    The aim of this study was to investigate the association between diastolic dysfunction and long-term occurrence of new-onset atrial fibrillation (AF) and cardiac events in patients with acute myocardial infarction (AMI) and left ventricular (LV) systolic dysfunction.......The aim of this study was to investigate the association between diastolic dysfunction and long-term occurrence of new-onset atrial fibrillation (AF) and cardiac events in patients with acute myocardial infarction (AMI) and left ventricular (LV) systolic dysfunction....

  17. Involvement of AMPK in alcohol dehydrogenase accentuated myocardial dysfunction following acute ethanol challenge in mice.

    Science.gov (United States)

    Guo, Rui; Scott, Glenda I; Ren, Jun

    2010-06-23

    Binge alcohol drinking often triggers myocardial contractile dysfunction although the underlying mechanism is not fully clear. This study was designed to examine the impact of cardiac-specific overexpression of alcohol dehydrogenase (ADH) on ethanol-induced change in cardiac contractile function, intracellular Ca(2+) homeostasis, insulin and AMP-dependent kinase (AMPK) signaling. ADH transgenic and wild-type FVB mice were acutely challenged with ethanol (3 g/kg/d, i.p.) for 3 days. Oral glucose tolerance test, cardiac AMP/ATP levels, cardiac contractile function, intracellular Ca(2+) handling and AMPK signaling (including ACC and LKB1) were examined. Ethanol exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca(2+) properties, downregulated protein phosphatase PP2A subunit and PPAR-gamma, as well as phosphorylation of AMPK, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene. Interestingly, myocardium from ethanol-treated FVB mice displayed enhanced expression of PP2Calpha and PGC-1alpha, decreased insulin receptor expression as well as unchanged expression of Glut4, the response of which was unaffected by ADH. Cardiac AMP-to-ATP ratio was significantly enhanced by ethanol exposure with a more pronounced increase in ADH mice. In addition, the AMPK inhibitor compound C (10 microM) abrogated acute ethanol exposure-elicited cardiomyocyte mechanical dysfunction. In summary, these data suggest that the ADH transgene exacerbated acute ethanol toxicity-induced myocardial contractile dysfunction, intracellular Ca(2+) mishandling and glucose intolerance, indicating a role of ADH in acute ethanol toxicity-induced cardiac dysfunction possibly related to altered cellular fuel AMPK signaling cascade.

  18. Management of erectile dysfunction post-radical prostatectomy

    Directory of Open Access Journals (Sweden)

    Saleh A

    2015-02-01

    Full Text Available Alan Saleh, Hamid Abboudi, MB Ghazal-Aswad, Erik K Mayer, Justin A Vale Division of Surgery and Cancer, Imperial College Healthcare NHS Trust, St Mary's Hospital, London, UK Abstract: Radical prostatectomy is a commonly performed procedure for the treatment of localized prostate cancer. One of the long-term complications is erectile dysfunction. There is little consensus on the optimal management; however, it is agreed that treatment must be prompt to prevent fibrosis and increase oxygenation of penile tissue. It is vital that patient expectations are discussed, a realistic time frame of treatment provided, and treatment started as close to the prostatectomy as possible. Current treatment regimens rely on phosphodiesterase 5 inhibitors as a first-line therapy, with vacuum erection devices and intraurethral suppositories of alprostadil as possible treatment combination options. With nonresponders to these therapies, intracavernosal injections are resorted to. As a final measure, patients undergo the highly invasive penile prosthesis implantation. There is no uniform, objective treatment program for erectile dysfunction post-radical prostatectomy. Management plans are based on poorly conducted and often underpowered studies in combination with physician and patient preferences. They involve the aforementioned drugs and treatment methods in different sequences and doses. Prospective treatments include dietary supplements and gene therapy, which have shown promise with there proposed mechanisms of improving erectile function but are yet to be applied successfully in human patients. Keywords: erectile dysfunction, phosphodiesterase 5 inhibitors, vacuum erection devices, intraurethral suppositories, intracavernosal injections

  19. Autonomic dysfunction and new-onset atrial fibrillation in patients with left ventricular systolic dysfunction after acute myocardial infarction: a CARISMA substudy

    DEFF Research Database (Denmark)

    Jøns, Christian; Raatikainen, Pekka; Gang, Uffe J;

    2010-01-01

    Atrial fibrillation (AF) increases morbidity and mortality in patients with previous myocardial infarction and left ventricular systolic dysfunction. The purpose of this study was to identify patients with a high risk for new-onset AF in this population using invasive and noninvasive...

  20. Myocardial structural alteration and systolic dysfunction in preclinical hypertrophic cardiomyopathy mutation carriers.

    Directory of Open Access Journals (Sweden)

    Kai Hang Yiu

    Full Text Available BACKGROUND: To evaluate the presence of myocardial structural alterations and subtle myocardial dysfunction during familial screening in asymptomatic mutation carriers without hypertrophic cardiomyopathy (HCM phenotype. METHODS AND FINDINGS: Sixteen HCM families with pathogenic mutation were studied and 46 patients with phenotype expression (Mut+/Phen+ and 47 patients without phenotype expression (Mut+/Phen- were observed. Twenty-five control subjects, matched with the Mut+/Phen- group, were recruited for comparison. Echocardiography was performed to evaluate conventional parameters, myocardial structural alteration by calibrated integrated backscatter (cIBS and global and segmental longitudinal strain by speckle tracking analysis. All 3 groups had similar left ventricular dimensions and ejection fraction. Basal anteroseptal cIBS was the highest in Mut+/Phen+ patients (-14.0±4.6 dB, p-19.0 dB basal anteroseptal cIBS or >-18.0% basal anteroseptal longitudinal strain had a sensitivity of 98% and a specificity of 72% in differentiating Mut+/Phen- group from controls. CONCLUSION: The use of cIBS and segmental longitudinal strain can differentiate HCM Mut+/Phen- patients from controls with important clinical implications for the family screening and follow-up of these patients.

  1. Vascular dysfunction and myocardial contractility in the JCR:LA-corpulent rat.

    Science.gov (United States)

    Brunner, F; Wölkart, G; Pfeiffer, S; Russell, J C; Wascher, T C

    2000-07-01

    The JCR:LA-corpulent rat is a unique animal model of human vascular disease that exhibits a profound insulin resistance, vasculopathy, and cardiovascular dysfunction. We tested the hypothesis that the defects affect endothelial and smooth muscle function of the coronary microvasculature as well as cardiac contractility. Coronary, myocardial and aortic function were assessed in obese (homozygous for the cp gene, cp/cp) and lean (heterozygous or homozygous normal, +/?) littermates aged 7 and 18 weeks. Coronary endothelial relaxation was examined in isolated perfused hearts by determining the effect of bradykinin (0. 1-1000 nmol l(-1)) on coronary perfusion pressure (CPP), myocardial mechanical function was evaluated in terms of left-ventricular developed pressure (LVDevP), and aortic relaxation with the endothelium-dependent agonist, A 23187 (1-1000 nmol l(-1)). In rats aged 7 weeks, bradykinin reduced CPP from 133+/-1 mmHg to 43+/-1 mmHg (-67%) in lean rats, but only to 64+/-3 mmHg (-52%) in corpulent rats (n=6, PJCR:LA-corpulent rat that is not associated with impaired baseline myocardial contractility, and (ii) exogenous tetrahydrobiopterin reversed the relaxation defects that are part of the vascular complications typical for the insulin resistance syndrome.

  2. Comparison of myocardial function between post-menopausal and pre-menopausal women: evaluation by gated myocardial SPECT

    Energy Technology Data Exchange (ETDEWEB)

    Hwang, K. H.; Choa, Won Sick; Yoon, Min Ki [Gachon Medical School, Gil Hospital, Incheon (Korea, Republic of)

    2005-07-01

    In addition to inhibiting coronary atherosclerosis, estrogen is expected to have protective effects on cardiac myocytes. We investigated the difference in myocardial functional parameters evaluated by gated myocardial SPECT after adenosine-stress between post-menopausal and pre-menopausal healthy women. This study included 22 healthy post-menopausal women (mean age: 53.0 yr) and 20 pre-menopausal women (mean age: 43.0 yr) who performed Tc-99m tetrofosmin gated myocardial SPECT after adenosine-stress. Measured hemodynamic parameters, EDV, ESV, stroke volume, EF, cardiac output and cardiac index were compared between the two groups. For comparison, similar-aged two male groups with matched numbers were also studied. There was no significant difference in hemodynamic parameters. EDV, ESV, stroke volume, EF, or cardiac output between the post-menopausal and pre-menopausal women. However, post-menopausal women have a smaller cardiac index (mean: 1.95 L/min/m2 vs 2.20 L/min/m2; p=0.045) and adenosine-induced HR increase (mean : 80.5/min vs 89.7/min ; p=0.03), compared to the pre-menopausal women. On the contrary, the two male groups of the same age range and numbers with the women groups showed no significant difference in any myocardial parameters. These results suggest that menopause may be correlated with reduced increase in cardiac index and HR increase after adenosine-stress.

  3. The Post-Myocardial Infarction Pacing Remodeling Prevention Therapy (PRomPT) Trial

    DEFF Research Database (Denmark)

    Chung, Eugene S; Fischer, Trent M; Kueffer, Fred

    2015-01-01

    BACKGROUND: Despite considerable improvements in the medical management of patients with myocardial infarction (MI), patients with large MI still have substantial risk of developing heart failure. In the early post-MI setting, implantable cardioverter defibrillators have reduced arrhythmic deaths...

  4. Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris.

    Science.gov (United States)

    Bartels, G L; Remme, W J; Pillay, M; Schönfeld, D H; Kruijssen, D A

    1994-07-15

    To identify the effect of L-propionylcarnitine (LPC) on ischemia, 31 fasting, untreated male patients with left coronary artery disease were studied during 2 identical pacing stress tests 45 minutes before (atrial pacing test I [APST I]) and 15 minutes after (APST II) administration of 15 mg/kg of LPC or placebo. Hemodynamic, metabolic, and nuclear angiographic variables were studied before, during, and for 10 minutes after pacing. After LPC administration, arterial total carnitine levels increased from 47 +/- 1.7 mumol/liter (control) to 730 +/- 30 mumol/liter. Hemodynamic and metabolic variables were comparable in LPC and placebo during APSI I, and reproducible in placebo during both tests. Although LPC did not affect myocardial oxygen demand and supply, it diminished myocardial ischemia, indicated by a significant 12% and 50% reduction in ST-segment depression and left ventricular end-diastolic pressure, respectively, during APST II. Moreover, during APST II, left ventricular ejection fraction increased by 18% (p < 0.05 vs APST I). Furthermore, LPC improved recovery of myocardial function after pacing, with a reduction in the time to peak filling and a 21% increase in both peak ejection and filling rates 10 minutes after pacing (all p < 0.05). Thus, LPC prevents ischemia-induced ventricular dysfunction, not by affecting the myocardial oxygen supply-demand ratio but as a result of its intrinsic metabolic actions, increasing pyruvate dehydrogenase activity and flux through the citric acid cycle. Because it is well tolerated, it may be a valuable alternative or addition to available antiischemic therapy.

  5. Altered myocardial substrate metabolism is associated with myocardial dysfunction in early diabetic cardiomyopathy in rats: studies using positron emission tomography

    NARCIS (Netherlands)

    Brom, van den C.E.; Huisman, M.C.; Vlasblom, R.; Boontje, N.; Duijst, S.; Lubberink, J.M.; Molthoff, C.F.M.; Lammertsma, A.A.; Velden, van der J.; Boer, C.; Ouwens, D.M.; Diamant, M.

    2009-01-01

    0.05). CONCLUSION: Using PET and echocardiography, we found increases in myocardial FA oxidation with a concomitant decrease of insulin-mediated myocardial glucose utilisation in early DCM. In addition, the latter was associated with impaired myocardial function. These in vivo data expand previous i

  6. Hereditary vulnerabilities to post-operative cognitive dysfunction and dementia.

    Science.gov (United States)

    Hogan, Kirk J

    2013-12-01

    In view of multiple prospective investigations reporting an incidence of 10% or greater in elderly patients after cardiac and non-cardiac procedures, it is surprising that no families, twins or even individual cases have been reported with persistent post-operative cognitive dysfunction (POCD) or post-operative dementia (POD) that is otherwise unexplained. As POCD and POD research has shifted in recent years from surgical and anesthetic variables to predictors of intrinsic, patient-specific susceptibility, a number of markers based on DNA sequence variation have been investigated. Nevertheless, no heritable, genomic indices of persistent POCD or post-operative dementia lasting 3 months or longer after surgery have been identified to date. The present manuscript surveys challenges confronting the search for markers of heritable vulnerability to POCD and POD, and proposes steps forward to be taken now, including the addition of surgical and anesthetic descriptors to ongoing longitudinal dementia protocols and randomized clinical trials (RCTs) comprising serial psychometric testing, and a fresh focus on phenotypes and genotypes shared between outliers with "extreme" POCD and POD traits.

  7. Relative lack of depressive cognitions in post-myocardial infarction depression

    DEFF Research Database (Denmark)

    Martens, Elisabeth J; Denollet, Johan; Pedersen, Susanne S.;

    2006-01-01

    Depression has been associated with adverse clinical events in myocardial infarction (MI) patients, but many questions about the nature of post-MI depression remain unanswered. We examined whether depressive cognitions characteristic of depression in psychiatric patients are also present in post-......-MI patients with major depression (MD).......Depression has been associated with adverse clinical events in myocardial infarction (MI) patients, but many questions about the nature of post-MI depression remain unanswered. We examined whether depressive cognitions characteristic of depression in psychiatric patients are also present in post...

  8. Takotsubo-Like Myocardial Dysfunction in Ischemic Stroke: A Hospital-Based Registry and Systematic Literature Review.

    Science.gov (United States)

    Jung, Jin-Man; Kim, Jae-Gyum; Kim, Jung Bin; Cho, Kyung-Hee; Yu, Sungwook; Oh, Kyungmi; Kim, Yong-Hyun; Choi, Jeong-Yoon; Seo, Woo-Keun

    2016-11-01

    We investigated clinical and radiological characteristics of ischemic stroke patients with Takotsubo-like myocardial dysfunction. From multicenter stroke registry database, ischemic stroke patients who underwent transthoracic echocardiography were found. Among these, patients were classified if they had specific ventricular regional wall motion abnormalities discording with coronary artery distribution, such as apical (typical pattern) or nonapical ballooning (atypical pattern), considered as echocardiographic findings of Takotsubo cardiomyopathy. Patients with ischemic heart disease history, myocarditis, or pheochromocytoma were excluded. We compared patients with Takotsubo-like myocardial dysfunction with those without and further performed systematic literature review on those with Takotsubo cardiomyopathy. This study included 23 patients (0.42%). The mean age was 70.7±13.9 years, with predominance of women (73.9%) and typical pattern of Takotsubo-like myocardial dysfunction (91.3%). They were associated with short-term poor functional outcomes, including high mortality, neurological deterioration, and functional status at discharge, compared with those without (39.1% versus 2.4%, 47.8% versus 7.4%; and median [interquartile range], 5 [5-6] versus 3 [2-4]; all PTakotsubo cardiomyopath criteria, and was as reported in literature review. Stroke patients with Takotsubo-like myocardial dysfunction may differ from those without in clinical outcomes, laboratory findings, and radiological features. © 2016 American Heart Association, Inc.

  9. Sudden cardiovascular death following myocardial infarction: the importance of left ventricular systolic dysfunction and congestive heart failure

    DEFF Research Database (Denmark)

    Abildstrøm, Steen Zabell; Ottesen, Michael M; Rask-Madsen, Christian;

    2005-01-01

    BACKGROUND: To study the prognostic information of congestive heart failure (CHF) and left ventricular systolic dysfunction regarding sudden and non-sudden cardiovascular death (SCD and non-SCD) in patients with acute myocardial infarction (MI), as this may indicate the potential benefit...

  10. Effect of quinapril or metoprolol on heart rate variability in post-myocardial infarction patients.

    Science.gov (United States)

    Kontopoulos, A G; Athyros, V G; Papageorgiou, A A; Papadopoulos, G V; Avramidis, M J; Boudoulas, H

    1996-02-01

    The effect of quinapril or metoprolol on heart rate variability (HRV) indexes was studied in patients who had recovered from acute myocardial infarction. Patients with stable coronary artery disease and normal volunteers were used as controls. Sixty patients with uncomplicated myocardial infarction (aged 32 to 74 years [mean 56.7]) were randomized to quinapril (n = 25), metoprolol (n = 25), and placebo (n = 10). HRV was assessed 5 days (baseline) and 35 days after the onset of acute myocardial infarction. After the baseline studies, the post-myocardial infarction patients were treated with metoprolol (50 to 100 mg/day), quinapril (5 to 10 mg/day), or placebo. Twenty patients with stable coronary artery disease and 20 healthy volunteers, age- and sex-matched to myocardial infarction patients, were used as controls. Compared with placebo, quinapril and metoprolol increased HRV indexes significantly 35 days after the onset of myocardial infarction. HRV indexes were not statistically different between the 2 treatment groups. At baseline and after therapy, HRV was similar in patients with anterior or inferior wall myocardial infarction. HRV 35 days after the onset of myocardial infarction was not different from HRV in patients with stable coronary artery disease, but was decreased when compared with that in normal volunteers. Data suggest that quinapril has the same beneficial effect on HRV indexes as metoprolol in patients who have recovered from uncomplicated acute myocardial infarction.

  11. Dipyridamole, cold pressor test, and demonstration of endothelial dysfunction: a PET study of myocardial perfusion in diabetes

    DEFF Research Database (Denmark)

    Kjaer, Andreas; Meyer, Christian; Nielsen, Flemming S;

    2003-01-01

    Much evidence suggests endothelial dysfunction to be present in non-insulin-dependent diabetes mellitus (NIDDM) and to be important for the development of myocardial ischemia. Endothelial function in the coronary vessels may be studied in various ways. We compared the effect of cold pressor testing...... coronary disease, endothelial dysfunction is strongly suggested by an impaired increase in CBF both to dipyridamole and to CPT. This dysfunction was reversed by infusion of an ACE inhibitor. Although ACE inhibition during CPT did induce significant increases in CBF in the patients, the changes during ACE...

  12. Sildenafil and diastolic dysfunction after acute myocardial infarction in patients with preserved ejection fraction

    DEFF Research Database (Denmark)

    Andersen, Mads J; Ersbøll, Mads; Axelsson, Anna

    2013-01-01

    BACKGROUND: Diastolic dysfunction is frequently seen after myocardial infarction and is characterized by a disproportionate increase in filling pressure during exercise to maintain stroke volume. We hypothesized that sildenafil would reduce filling pressure during exercise in patients...... weeks of treatment patients underwent simultaneous echocardiography and right heart catheterization at rest and during exercise. Primary end point was pulmonary capillary wedge pressure, and secondary end points comprised cardiac index and pulmonary arterial pressure at rest and during exercise after 9...... weeks. After 9 weeks there were no differences in pulmonary capillary wedge pressure at rest (13±4 versus 13±3 mm Hg, P=0.25) or at peak exercise (35±8 mm Hg versus 31±7 mm Hg, P=0.07). However, with treatment cardiac index increased at rest (P=0.006) and peak exercise (P=0.02) in the sildenafil group...

  13. Sarcoplasmic phospholamban protein is involved in the mechanisms of postresuscitation myocardial dysfunction and the cardioprotective effect of nitrite during resuscitation.

    Directory of Open Access Journals (Sweden)

    Yu Huang

    Full Text Available OBJECTIVES: Sarcoplasmic reticulum (SR Ca(2+-handling proteins play an important role in myocardial dysfunction after acute ischemia/reperfusion injury. We hypothesized that nitrite would improve postresuscitation myocardial dysfunction by increasing nitric oxide (NO generation and that the mechanism of this protection is related to the modulation of SR Ca(2+-handling proteins. METHODS: We conducted a randomized prospective animal study using male Sprague-Dawley rats. Cardiac arrest was induced by intravenous bolus of potassium chloride (40 µg/g. Nitrite (1.2 nmol/g or placebo was administered when chest compression was started. No cardiac arrest was induced in the sham group. Hemodynamic parameters were monitored invasively for 90 minutes after the return of spontaneous circulation (ROSC. Echocardiogram was performed to evaluate cardiac function. Myocardial samples were harvested 5 minutes and 1 hour after ROSC. RESULTS: Myocardial function was significantly impaired in the nitrite and placebo groups after resuscitation, whereas cardiac function (i.e., ejection fraction and fractional shortening was significantly greater in the nitrite group than in the placebo group. Nitrite administration increased the level of nitric oxide in the myocardium 5 min after resuscitation compared to the other two groups. The levels of phosphorylated phospholamban (PLB were decreased after resuscitation, and nitrite increased the phosphorylation of phospholamban compared to the placebo. No significant differences were found in the expression of sarcoplasmic reticulum Ca(2+ ATPase (SERCA2a and ryanodine receptors (RyRs. CONCLUSIONS: postresuscitation myocardial dysfunction is associated with the impairment of PLB phosphorylation. Nitrite administered during resuscitation improves postresuscitation myocardial dysfunction by preserving phosphorylated PLB protein during resuscitation.

  14. Low Intensity Physical Exercise Attenuates Cardiac Remodeling and Myocardial Oxidative Stress and Dysfunction in Diabetic Rats

    Directory of Open Access Journals (Sweden)

    C. Gimenes

    2015-01-01

    Full Text Available We evaluated the effects of a low intensity aerobic exercise protocol on cardiac remodeling and myocardial function in diabetic rats. Wistar rats were assigned into four groups: sedentary control (C-Sed, exercised control (C-Ex, sedentary diabetes (DM-Sed, and exercised diabetes (DM-Ex. Diabetes was induced by intraperitoneal injection of streptozotocin. Rats exercised for 9 weeks in treadmill at 11 m/min, 18 min/day. Myocardial function was evaluated in left ventricular (LV papillary muscles and oxidative stress in LV tissue. Statistical analysis was given by ANOVA or Kruskal-Wallis. Echocardiogram showed diabetic groups with higher LV diastolic diameter-to-body weight ratio and lower posterior wall shortening velocity than controls. Left atrium diameter was lower in DM-Ex than DM-Sed (C-Sed: 5.73±0.49; C-Ex: 5.67±0.53; DM-Sed: 6.41±0.54; DM-Ex: 5.81±0.50 mm; P<0.05 DM-Sed vs C-Sed and DM-Ex. Papillary muscle function was depressed in DM-Sed compared to C-Sed. Exercise attenuated this change in DM-Ex. Lipid hydroperoxide concentration was higher in DM-Sed than C-Sed and DM-Ex. Catalase and superoxide dismutase activities were lower in diabetics than controls and higher in DM-Ex than DM-Sed. Glutathione peroxidase activity was lower in DM-Sed than C-Sed and DM-Ex. Conclusion. Low intensity exercise attenuates left atrium dilation and myocardial oxidative stress and dysfunction in type 1 diabetic rats.

  15. Asymptomatic cardiovascular manifestations in diabetes mellitus: Left ventricular diastolic dysfunction and silent myocardial ischemia

    Directory of Open Access Journals (Sweden)

    Seferović-Mitrović Jelena P.

    2011-01-01

    Full Text Available Introduction. Several cardiovascular manifestations in patients with diabetes may be asymptomatic. Left ventricular diastolic dysfunction (LVDD is considered to be the earliest metabolic myocardial lesion in these patients, and can be diagnosed with tissue Doppler echocardiography. Silent myocardial ischemia (SMI is a characteristic and frequently described form of ischemic heart disease in patients with diabetes. Objective. The aim of the study was to assess the prevalence of LVDD and SMI in patients with type 2 diabetes, as well as to compare demographic, clinical, and metabolic data among defined groups (patients with LVDD, patients with SMI and patients with type 2 diabetes, without LVDD and SMI. Methods. We investigated 104 type 2 diabetic patients (mean age 55.4±9.1 years, 64.4% males with normal blood pressure, prehypertension and arterial hypertension stage I. Study design included basic laboratory assessment and cardiological workup (transthoracic echocardiography and tissue Doppler, as well as the exercise stress echocardiography. Results. LVDD was diagnosed in twelve patients (11.5%, while SMI was revealed in six patients (5.8%. Less patients with LVDD were using metformin, in comparison to other two groups (χ2 =12.152; p=0.002. Values of HDL cholesterol (F=4.515; p=0.013 and apolipoprotein A1 (F=5.128; p= 0.008 were significantly higher in patients with LVDD. Conclusion. The study confirmed asymptomatic cardiovascular complications in 17.3% patients with type 2 diabetes.

  16. Coronary arterial BK channel dysfunction exacerbates ischemia/reperfusion-induced myocardial injury in diabetic mice.

    Science.gov (United States)

    Lu, Tong; Jiang, Bin; Wang, Xiao-Li; Lee, Hon-Chi

    2016-09-01

    The large conductance Ca(2+)-activated K(+) (BK) channels, abundantly expressed in coronary artery smooth muscle cells (SMCs), play a pivotal role in regulating coronary circulation. A large body of evidence indicates that coronary arterial BK channel function is diminished in both type 1 and type 2 diabetes. However, the consequence of coronary BK channel dysfunction in diabetes is not clear. We hypothesized that impaired coronary BK channel function exacerbates myocardial ischemia/reperfusion (I/R) injury in streptozotocin-induced diabetic mice. Combining patch-clamp techniques and cellular biological approaches, we found that diabetes facilitated the colocalization of angiotensin II (Ang II) type 1 receptors and BK channel α-subunits (BK-α), but not BK channel β1-subunits (BK-β1), in the caveolae of coronary SMCs. This caveolar compartmentation in vascular SMCs not only enhanced Ang II-mediated inhibition of BK-α but also produced a physical disassociation between BK-α and BK-β1, leading to increased infarct size in diabetic hearts. Most importantly, genetic ablation of caveolae integrity or pharmacological activation of coronary BK channels protected the cardiac function of diabetic mice from experimental I/R injury in both in vivo and ex vivo preparations. Our results demonstrate a vascular ionic mechanism underlying the poor outcome of myocardial injury in diabetes. Hence, activation of coronary BK channels may serve as a therapeutic target for cardiovascular complications of diabetes.

  17. Myocardial protection during heart surgery in China

    Institute of Scientific and Technical Information of China (English)

    Bingyang Ji; Jinping Liu

    2007-01-01

    @@ Myocardial protection (MP) is the key for cardiopulmonary bypass (CPB) heart surgery. MP during cardiac surgery (CS) aims to preserve myocardial function while providing a bloodless and motionless operating field. Strategies on how to attenuate or prevent post-ischemic myocardial dysfunction that occurs intra-operatively during CS have been discussed for more than half a century. In 1950, Bigelow et al1 first reported to decrease myocardial oxygen demand by means of hypothermia.

  18. Influence of renal dysfunction on clinical outcomes in patients with congestive heart failure complicating acute myocardial infarction.

    Science.gov (United States)

    Kim, Chang Seong; Kim, Min Jee; Kang, Yong Un; Choi, Joon Seok; Bae, Eun Hui; Ma, Seong Kwon; Ahn, Young-Keun; Jeong, Myung Ho; Kim, Young Jo; Cho, Myeong Chan; Kim, Chong Jin; Kim, Soo Wan

    2013-01-01

    The clinical course and medical treatment of patients with congestive heart failure (CHF) complicating acute myocardial infarction (AMI) are not well established, especially in patients with concomitant renal dysfunction. We performed a retrospective analysis of the prospective Korean Acute Myocardial Infarction Registry to assess the medical treatments and clinical outcomes of patients with CHF (Killip classes II or III) complicated by AMI, in the presence or absence of renal dysfunction. Of 13,498 patients with AMI, 2769 (20.5%) had CHF on admission. Compared to CHF patients with preserved renal function, in-hospital mortality and major adverse cardiac events were increased both at 1 month and at 1 year after discharge in patients with renal dysfunction (1154; 41.7%). Postdischarge use of aspirin, betablockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers and statins significantly reduced the 1-year mortality rate for CHF patients with renal dysfunction; such reduction was not observed for those without renal dysfunction, except in the case of aspirin. Patients with CHF complicating AMI, which is accompanied by renal dysfunction, are at higher risk for adverse cardiovascular outcomes than patients without renal dysfunction. However, they receive fewer medications proven to reduce mortality rates.

  19. Sodium hydrosulfide prevents myocardial dysfunction through modulation of extracellular matrix accumulation and vascular density.

    Science.gov (United States)

    Pan, Li-Long; Wang, Xian-Li; Wang, Xi-Ling; Zhu, Yi-Zhun

    2014-12-12

    The aim was to examine the role of exogenous hydrogen sulfide (H2S) on cardiac remodeling in post-myocardial infarction (MI) rats. MI was induced in rats by ligation of coronary artery. After treatment with sodium hydrosulfide (NaHS, an exogenous H2S donor, 56 μM/kg·day) for 42 days, the effects of NaHS on left ventricular morphometric features, echocardiographic parameters, heme oxygenase-1 (HO-1), matrix metalloproteinases-9 (MMP-9), type I and type III collagen, vascular endothelial growth factor (VEGF), CD34, and α-smooth muscle actin (α-SMA) in the border zone of infarct area were analyzed to elucidate the protective mechanisms of exogenous H2S on cardiac function and fibrosis. Forty-two days post MI, NaHS-treatment resulted in a decrease in myocardial fibrotic area in association with decreased levels of type I, type III collagen and MMP-9 and improved cardiac function. Meanwhile, NaHS administration significantly increased cystathionine γ-lyase (CSE), HO-1, α-SMA, and VEGF expression. This effect was accompanied by an increase in vascular density in the border zone of infarcted myocardium. Our results provided the strong evidences that exogenous H2S prevented cardiac remodeling, at least in part, through inhibition of extracellular matrix accumulation and increase in vascular density.

  20. Sodium Hydrosulfide Prevents Myocardial Dysfunction through Modulation of Extracellular Matrix Accumulation and Vascular Density

    Directory of Open Access Journals (Sweden)

    Li-Long Pan

    2014-12-01

    Full Text Available The aim was to examine the role of exogenous hydrogen sulfide (H2S on cardiac remodeling in post-myocardial infarction (MI rats. MI was induced in rats by ligation of coronary artery. After treatment with sodium hydrosulfide (NaHS, an exogenous H2S donor, 56 μM/kg·day for 42 days, the effects of NaHS on left ventricular morphometric features, echocardiographic parameters, heme oxygenase-1 (HO-1, matrix metalloproteinases-9 (MMP-9, type I and type III collagen, vascular endothelial growth factor (VEGF, CD34, and α-smooth muscle actin (α-SMA in the border zone of infarct area were analyzed to elucidate the protective mechanisms of exogenous H2S on cardiac function and fibrosis. Forty-two days post MI, NaHS-treatment resulted in a decrease in myocardial fibrotic area in association with decreased levels of type I, type III collagen and MMP-9 and improved cardiac function. Meanwhile, NaHS administration significantly increased cystathionine γ-lyase (CSE, HO-1, α-SMA, and VEGF expression. This effect was accompanied by an increase in vascular density in the border zone of infarcted myocardium. Our results provided the strong evidences that exogenous H2S prevented cardiac remodeling, at least in part, through inhibition of extracellular matrix accumulation and increase in vascular density.

  1. Occurrence and predictors of left ventricular systolic dysfunction at hospital discharge and in long−term follow−up after acute myocardial infarction treated with primary percutaneous coronary intervention

    OpenAIRE

    Świątkiewicz, Iwona; Magielski, Przemysław; Woźnicki, Marek; Gierach, Joanna; Jabłoński, Mirosław; Fabiszak, Tomasz; Koziński, Marek; Sukiennik, Adam; Bronisz, Agata; Kubica, Jacek

    2011-01-01

    Background: Post-ST-segment elevation myocardial infarction (STEMI) left ventricular systolic dysfunction (LVSD) has been identified as an important marker of poor prognosis. Aim: To assess the prevalence and course of LVSD at hospital discharge and in long-term follow-up in STEMI patients treated with primary percutaneous coronary intervention (pPCI). Methods: We enrolled 205 patients (157 male, 48 female) with a first STEMI. Echocardiography was performed before hospital disc...

  2. Adenoviral short hairpin RNA targeting phosphodiesterase 5 attenuates cardiac remodeling and cardiac dysfunction following myocardial infarction in mice

    Institute of Scientific and Technical Information of China (English)

    张健

    2014-01-01

    Objective To observe the impact of PDE5shRNA on cardiac remodeling and heart function following myocardial infarction in mice.Methods Myocardial infarction(MI)was induced in mice by left coronary artery ligation.Mice were randomly assigned to sham operation group(n=6),PDE5shRNA group(n=12),common adenovirus group(n=15)and DMEM group(n=8).Four weeks post-MI,the survival rate was evaluated.

  3. Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction

    DEFF Research Database (Denmark)

    Pedersen, O D; Bagger, H; Køber, Lars Valeur;

    1999-01-01

    BACKGROUND: Studies have suggested that ACE inhibitors have an antiarrhythmic effect on ventricular arrhythmias. Whether they have an effect on atrial fibrillation is unknown. METHODS AND RESULTS: We investigated the effect of ACE inhibition with trandolapril on the incidence of atrial fibrillation...... of atrial fibrillation in patients with left ventricular dysfunction after acute myocardial infarction....... in patients with reduced left ventricular function secondary to acute myocardial infarction. The patients in this study were those who qualified for inclusion into the TRAndolapril Cardiac Evaluation (TRACE) study, a randomized double-blind placebo-controlled study and who had sinus rhythm on the ECG obtained...

  4. Effect of dofetilide in patients with recent myocardial infarction and left-ventricular dysfunction: a randomised trial

    DEFF Research Database (Denmark)

    Køber, L; Bloch Thomsen, P E; Møller, M;

    2000-01-01

    BACKGROUND: Arrhythmias cause much morbidity and mortality after myocardial infarction, but in previous trials, antiarrhythmic drug therapy has not been convincingly effective. Dofetilide, a new class III agent, was investigated for effects on all-cause mortality and morbidity in patients with left...... vs seven of 56; p=0.002). There were seven cases of torsade de pointes ventricular tachycardia, all in the dofetilide group. INTERPRETATION: In patients with severe left-ventricular dysfunction and recent myocardial infarction, treatment with dofetilide did not affect all-cause mortality, cardiac...

  5. [Interest of post mortem analysis in diagnosis and etiopathogeny of ischemic myocardial infarction].

    Science.gov (United States)

    Guilbeau-Frugier, Céline; Rambaud, Caroline; Dedouit, Fabrice; Telmon, Norbert; Rougé, Daniel; Delisle, Marie Bernadette

    2006-12-01

    The discovery of an ischaemic myocardial infarction during forensic or scientific autopsy is sometimes surprising when found in a young subject. It is therefore important to find out the etiology of vascular lesions to take preventive measures in the family. In post mortem, some complementary analysis can be performed to determine the diagnosis of ischaemic myocardial infarction and its etiopathogeny. Such analyses, routinely made in forensic practice, are rarely used by pathologists during scientific autopsy. Some biological mediums are stable enough to be used for biological, biochemical and even genetical analyses. We will study the different post mortem analyses, and see their interest and reliability.

  6. Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling.

    Directory of Open Access Journals (Sweden)

    Tingqiao Ye

    Full Text Available Calpain is activated following myocardial infarction and ablation of calpastatin (CAST, an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI. The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-infarction myocardial remodeling process.We established transgenic mice (TG ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT littermates.The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01. Overexpression of CAST significantly reduced the infarct size (P < 0.01 and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.Transgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling.

  7. Edema is a sign of early acute myocardial infarction on post-mortem magnetic resonance imaging.

    Science.gov (United States)

    Ruder, Thomas D; Ebert, Lars C; Khattab, Ahmed A; Rieben, Robert; Thali, Michael J; Kamat, Pranitha

    2013-12-01

    The aim of this study was to investigate if acute myocardial infarction can be detected by post-mortem cardiac magnetic resonance (PMMR) at an earlier stage than by traditional autopsy, i.e., within less than 4 h after onset of ischemia; and if so, to determine the characteristics of PMMR findings in early acute infarcts. Twenty-one ex vivo porcine hearts with acute myocardial infarction underwent T2-weighted cardiac PMMR imaging within 3 h of onset of iatrogenic ischemia. PMMR imaging findings were compared to macroscopic findings. Myocardial edema induced by ischemia and reperfusion was visible on PMMR in all cases. Typical findings of early acute ischemic injury on PMMR consist of a central zone of intermediate signal intensity bordered by a rim of increased signal intensity. Myocardial edema can be detected on cardiac PMMR within the first 3 h after the onset of ischemia in porcine hearts. The size of myocardial edema reflects the area of ischemic injury in early acute (per-acute) myocardial infarction. This study provides evidence that cardiac PMMR is able to detect acute myocardial infarcts at an earlier stage than traditional autopsy and routine histology.

  8. Mesenchymal stem cells with overexpression of midkine enhance cell survival and attenuate cardiac dysfunction in a rat model of myocardial infarction

    NARCIS (Netherlands)

    S.-L. Zhao (Shu-Li); Y. Zhang (Yaojun); M.-H. Li (Ming-Hui); X.-L. Zhang (Xin-Lei); S.-L. Chen (Shao-Liang)

    2014-01-01

    textabstractIntroduction. Elevated midkine (MK) expression may contribute to ventricular remodeling and ameliorate cardiac dysfunction after myocardial infarction (MI). Ex vivo modification of signaling mechanisms in mesenchymal stem cells (MSCs) with MK overexpression may improve the efficacy of ce

  9. Alcohol dehydrogenase accentuates ethanol-induced myocardial dysfunction and mitochondrial damage in mice: role of mitochondrial death pathway.

    Science.gov (United States)

    Guo, Rui; Ren, Jun

    2010-01-18

    Binge drinking and alcohol toxicity are often associated with myocardial dysfunction possibly due to accumulation of the ethanol metabolite acetaldehyde although the underlying mechanism is unknown. This study was designed to examine the impact of accelerated ethanol metabolism on myocardial contractility, mitochondrial function and apoptosis using a murine model of cardiac-specific overexpression of alcohol dehydrogenase (ADH). ADH and wild-type FVB mice were acutely challenged with ethanol (3 g/kg/d, i.p.) for 3 days. Myocardial contractility, mitochondrial damage and apoptosis (death receptor and mitochondrial pathways) were examined. Ethanol led to reduced cardiac contractility, enlarged cardiomyocyte, mitochondrial damage and apoptosis, the effects of which were exaggerated by ADH transgene. In particular, ADH exacerbated mitochondrial dysfunction manifested as decreased mitochondrial membrane potential and accumulation of mitochondrial O(2) (*-). Myocardium from ethanol-treated mice displayed enhanced Bax, Caspase-3 and decreased Bcl-2 expression, the effect of which with the exception of Caspase-3 was augmented by ADH. ADH accentuated ethanol-induced increase in the mitochondrial death domain components pro-caspase-9 and cytochrome C in the cytoplasm. Neither ethanol nor ADH affected the expression of ANP, total pro-caspase-9, cytosolic and total pro-caspase-8, TNF-alpha, Fas receptor, Fas L and cytosolic AIF. Taken together, these data suggest that enhanced acetaldehyde production through ADH overexpression following acute ethanol exposure exacerbated ethanol-induced myocardial contractile dysfunction, cardiomyocyte enlargement, mitochondrial damage and apoptosis, indicating a pivotal role of ADH in ethanol-induced cardiac dysfunction possibly through mitochondrial death pathway of apoptosis.

  10. Level of complement activity predicts cardiac dysfunction after acute myocardial infarction treated with primary percutaneous coronary intervention

    DEFF Research Database (Denmark)

    2009-01-01

    BACKGROUND: The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human...... descending coronary artery who were successfully treated with pPCI. Cardiac dysfunction was defined as left ventricular ejection fraction LVEF or = 35%. After adjustment...

  11. Post myocardial infarction of the left ventricle: the course ahead seen by cardiac MRI

    Science.gov (United States)

    Masci, Pier Giorgio

    2012-01-01

    In the last decades, cardiac magnetic resonance imaging (MRI) has gained acceptance in cardiology community as an accurate and reproducible diagnostic imaging modality in patients with ischemic heart disease (IHD). In particular, in patients with acute myocardial infarction (MI) cardiac MRI study allows a comprehensive assessment of the pattern of ischemic injury in term of reversible and irreversible damage, myocardial hemorrhage and microvascular obstruction (MVO). Myocardial salvage index, derived by quantification of myocardium (area) at risk and infarction, has become a promising surrogate end-point increasingly used in clinical trials testing novel or adjunctive reperfusion strategies. Early post-infarction, the accurate and reproducible quantification of myocardial necrosis, along with the characterization of ischemic myocardial damage in its diverse components, provides important information to predict post-infarction left ventricular (LV) remodeling, being useful for patients stratification and management. Considering its non-invasive nature, cardiac MRI suits well for investigating the time course of infarct healing and the changes occurring in peri-infarcted (adjacent) and remote myocardium, which ultimately promote the geometrical, morphological and functional abnormalities of the entire left ventricle (global LV remodeling). The current review will focus on the cardiac MRI utility for a comprehensive evaluation of patients with acute and chronic IHD with particular regard to post-infarction remodeling. PMID:24282705

  12. Depressive disorder and gastrointestinal dysfunction after myocardial infarct are associated with abnormal tryptophan-5-hydroxytryptamine metabolism in rats

    Science.gov (United States)

    Liu, Chunyan; Wang, Yangang

    2017-01-01

    In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the somatic, cognitive

  13. Telmisartan protects against microvascular dysfunction during myocardial ischemia/reperfusion injury by activation of peroxisome proliferator-activated receptor gamma

    Science.gov (United States)

    2013-01-01

    Background We investigated the potential of telmisartan to improve microvascular dysfunction induced by myocardial ischemia/reperfusion (I/R) injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway. Methods Forty-eight male rabbits were randomly allocated into sham-operated, I/R, GW9662, telmisartan, telmisartan–GW9662, or candesartan groups. Rabbits were anesthetized, and the left anterior descending coronary artery (LAD) was ligated for 60 minutes. Following reperfusion for 6 hours, angiotensin II content of the heart was determined using radioimmunoassay. Myocardial neutrophil accumulation and microvessel cross-sectional area were examined histologically. Myocardial capillaries were examined with transmission electron microscopy. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the myocardium were measured using enzyme-linked immunosorbent assay. Western blot was utilized for investigating the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and PPARG. Results Angiotensin II concentration was significantly increased in all treatment groups compared with the sham-operated group (P telmisartan, telmisartan-GW9662, and candesartan groups compared with the I/R group (P telmisartan group compared with the telmisartan–GW9662 and candesartan groups. Telmisartan significantly increased PPARG protein expression compared with all other groups (P telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway. PMID:23738781

  14. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group

    DEFF Research Database (Denmark)

    Køber, L; Torp-Pedersen, C; Carlsen, J E;

    1995-01-01

    BACKGROUND. Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces mortality among survivors of acute myocardial infarction, but whether to use ACE inhibitors in all patients or only in selected patients is uncertain. METHODS. We screened 6676 consecutive patients with 7001...... myocardial infarctions confirmed by enzyme studies. A total of 2606 patients had echocardiographic evidence of left ventricular systolic dysfunction (ejection fraction,

  15. ENDOTHELIAL DYSFUNCTION IN STABLE ANGINA AND MYOCARDIAL INFARCTION COMBINED WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

    Directory of Open Access Journals (Sweden)

    M. A. Popova

    2015-01-01

    Full Text Available The research objective is to determine the state of endothelium-dependent and endothelium-independent vasodilatation in patients with coronary heart disease (CHD associated with chronic obstructive pulmonary disease (COPD.Material and methods. In the cross-sectional study included 122 patients with CHD associated with COPD: 68 people of them are patients with stable angina without acute coronary events in history and 54 patients with acute ST segment elevation myocardial infarction (STEMI. Comparison group comprised 53 patients with stable angina and 51 patients after STEMI without concomitant COPD. Patients were included if they met the following inclusion criteria: male, age <60 years, verified forms of CHD (stable angina, STEMI, documented with COPD without exacerbation and forced expiratory volume in 1 second > 30% in the groups with CHD and COPD. Arterial endothelial function was tested with high-resolution ultrasonography: brachial artery diameter was measured at rest, after flow increase (which causes endothelium-dependent dilatation, and after administration of sublingual nitroglycerin (an endothelium-independent dilator.Results. We found that endothelial dysfunction in patients with acute and chronic forms of CHD in combination with COPD are more pronounced than in isolated CHD.Conclusion. Expressed depression functional vascular reserve in patients with CHD associated with COPD, should be taken into account when conducting individualized therapy of these patients.

  16. The Role of Uncoupling Protein 2 During Myocardial Dysfunction in a Canine Model of Endotoxin Shock.

    Science.gov (United States)

    Wang, Xiaoting; Liu, Dawei; Chai, Wenzhao; Long, Yun; Su, Longxiang; Yang, Rongli

    2015-03-01

    To explore the role of uncoupling protein 2 (UCP2) during myocardial dysfunction in a canine model of endotoxin shock, 26 mongrel canines were randomly divided into the following four groups: A (control group; n = 6), B2 (shock after 2 h; n = 7), B4 (shock after 4 h; n = 7), and B6 (shock after 6 h; n = 6). Escherichia coli endotoxin was injected into the canines via the central vein, and hemodynamics were monitored. Energy metabolism, UCP2 mRNA and protein expression, and UCP2 localization were analyzed, and the correlation between energy metabolism changes, and UCP2 expression was determined. After the canine endotoxin shock model was successfully established, the expression of UCP2 mRNA and protein was found to increase, with later time points showing significant increases (P shock (P shock, and UCP2 may play an important role in this process. The negative correlation between UCP2 expression and energy metabolism requires further study, as the results might contribute to the treatment of sepsis with heart failure.

  17. Factors-related to quality of life in post myocardial infarction patients

    Institute of Scientific and Technical Information of China (English)

    Ali Hassanpour Dehkordi; M. Saeed Heydarnejad

    2009-01-01

    Objective: To identify factors related to quality of life in post myocardial infarction patients. Methods: The subjects were 150 post myocardial infarction patients who were receiving follow up care at Hajar Hospital. SeE-administered questionnaires consisting of physical-and mental health-quality of life (QoL) during a 14-month follow-up were designed. A χ2 test was used to determine relationships between variables. Results: There was significant correlation between demographic variables such as insurance and retirees between the subjects tested. In addition, a significant relationship between the pain intensity, fatigne, reducing or losing job performance and QoL was found. Conclusion: The role of nurses to fulfill all social, psychotically and mental requirements of the patients with myocardial infarction is highly appreciated.

  18. Native T1 value in the remote myocardium is independently associated with left ventricular dysfunction in patients with prior myocardial infarction.

    Science.gov (United States)

    Nakamori, Shiro; Alakbarli, Javid; Bellm, Steven; Motiwala, Shweta R; Addae, Gifty; Manning, Warren J; Nezafat, Reza

    2017-10-01

    To compare remote myocardium native T1 in patients with chronic myocardial infarction (MI) and controls without MI and to elucidate the relationship of infarct size and native T1 in the remote myocardium for the prediction of left ventricular (LV) systolic dysfunction after MI. A total of 41 chronic MI (18 anterior MI) patients and 15 age-matched volunteers with normal LV systolic function and no history of MI underwent cardiac magnetic resonance imaging (MRI) at 1.5T. Native T1 map was performed using a slice interleaved T1 mapping and late gadolinium enhancement (LGE) imaging. Cine MR was acquired to assess LV function and mass. The remote myocardium native T1 time was significantly elevated in patients with prior MI, compared to controls, for both anterior MI and nonanterior MI (anterior MI: 1099 ± 30, nonanterior MI: 1097 ± 39, controls: 1068 ± 25 msec, P infarct size had a moderate correlation with reduced LV ejection fraction (r = -0.33, P infarct size. Native T1 time in the remote myocardium was independently associated with reduced LV ejection fraction, after adjusting for age, gender, infarct size, and comorbidity (β = -0.34, P = 0.03). In chronic MI, the severity of LV systolic dysfunction after MI is independently associated with native T1 in the remote myocardium. Diffuse myocardial fibrosis in the remote myocardium may play an important pathophysiological role of post-MI LV dysfunction. 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2017;46:1073-1081. © 2017 International Society for Magnetic Resonance in Medicine.

  19. Optimal Timing of Surgical Revascularization for Myocardial Infarction and Left Ventricular Dysfunction

    Science.gov (United States)

    Wang, Rong; Cheng, Nan; Xiao, Cang-Song; Wu, Yang; Sai, Xiao-Yong; Gong, Zhi-Yun; Wang, Yao; Gao, Chang-Qing

    2017-01-01

    Background: The optimal timing of surgical revascularization for patients presenting with ST-segment elevation myocardial infarction (STEMI) and impaired left ventricular function is not well established. This study aimed to examine the timing of surgical revascularization after STEMI in patients with ischemic heart disease and left ventricular dysfunction (LVD) by comparing early and late results. Methods: From January 2003 to December 2013, there were 2276 patients undergoing isolated coronary artery bypass grafting (CABG) in our institution. Two hundred and sixty-four (223 male, 41 females) patients with a history of STEMI and LVD were divided into early revascularization (ER, 3 months) groups according to the time interval from STEMI to CABG. Mortality and complication rates were compared among the groups by Fisher's exact test. Cox regression analyses were performed to examine the effect of the time interval of surgery on long-term survival. Results: No significant differences in 30-day mortality, long-term survival, freedom from all-cause death, and rehospitalization for heart failure existed among the groups (P > 0.05). More patients in the ER group (12.90%) had low cardiac output syndrome than those in the MR (2.89%) and LR (3.05%) groups (P = 0.035). The mean follow-up times were 46.72 ± 30.65, 48.70 ± 32.74, and 43.75 ± 32.43 months, respectively (P = 0.716). Cox regression analyses showed a severe preoperative condition (odds ratio = 7.13, 95% confidence interval 2.05–24.74, P = 0.002) rather than the time interval of CABG (P > 0.05) after myocardial infarction was a risk factor of long-term survival. Conclusions: Surgical revascularization for patients with STEMI and LVD can be performed at different times after STEMI with comparable operative mortality and long-term survival. However, ER (cardiac output syndrome. A severe preoperative condition rather than the time interval of CABG after STEMI is a risk factor of long-term survival. PMID:28218210

  20. Problems with balance and binocular visual dysfunction are associated with post-stroke fatigue

    DEFF Research Database (Denmark)

    Schow, Trine; Teasdale, Thomas William; Jensen Quas, Kirsten;

    2016-01-01

    Trine Schow, Thomas William Teasdale, Kirsten Jensen Quas& Morten Arendt Rasmussen (2016): Problems with balance and binocular visual dysfunction are associated with post-stroke fatigue, Topics in Stroke Rehabilitation, DOI: 10.1080/10749357.2016.1188475......Trine Schow, Thomas William Teasdale, Kirsten Jensen Quas& Morten Arendt Rasmussen (2016): Problems with balance and binocular visual dysfunction are associated with post-stroke fatigue, Topics in Stroke Rehabilitation, DOI: 10.1080/10749357.2016.1188475...

  1. Is type D personality an independent risk factor for recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients?

    Science.gov (United States)

    Condén, Emelie; Rosenblad, Andreas; Wagner, Philippe; Leppert, Jerzy; Ekselius, Lisa; Åslund, Cecilia

    2017-03-01

    Background Type D personality refers to a combination of simultaneously high levels of negative affectivity and social inhibition. The present study aimed to examine whether type D personality was independently associated with recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients, using any of the previously proposed methods for measuring type D personality. Design This was a prospective cohort study. Methods Utilising data from the Västmanland Myocardial Infarction Study, 946 post-acute myocardial infarction patients having data on the DS14 instrument used to measure type D personality were followed-up for recurrent myocardial infarction and all-cause mortality until 9 December 2015. Data were analysed using Cox regression, adjusted for established risk factors. Results In total, 133 (14.1%) patients suffered from type D personality. During a mean follow-up time for recurrent myocardial infarction of 5.7 (3.2) years, 166 (17.5%) patients were affected by recurrent myocardial infarction, of which 26 (15.7%) had type D personality, while during a mean follow-up time for all-cause mortality of 6.3 (2.9) years, 321 (33.9%) patients died, of which 42 (13.1%) had type D personality. After adjusting for established risk factors, type D personality was not significantly associated with recurrent myocardial infarction or all-cause mortality using any of the previously proposed methods for measuring type D personality. A weak association was found between the social inhibition part of type D personality and a decreased risk of all-cause mortality, but this association was not significant after taking missing data into account in a multiple imputation analysis. Conclusions No support was found for type D personality being independently associated with recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients, using any of the previously proposed methods for measuring type D personality.

  2. Targeted NGF siRNA delivery attenuates sympathetic nerve sprouting and deteriorates cardiac dysfunction in rats with myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Hesheng Hu

    Full Text Available Nerve growth factor (NGF is involved in nerve sprouting, hyper-innervation, angiogenesis, anti-apoptosis, and preservation of cardiac function after myocardial infarction (MI. Positively modulating NGF expression may represent a novel pharmacological strategy to improve post-infarction prognosis. In this study, lentivirus encoding NGF short interfering RNA (siRNA was prepared, and MI was modeled in the rat using left anterior descending coronary artery ligation. Rats were randomly grouped to receive intramyocardial injection of lentiviral solution containing NGF-siRNA (n = 19, MI-SiNGF group, lentiviral solution containing empty vector (n = 18, MI-GFP group or 0.9% NaCl solution (n = 18, MI-control group, or to receive thoracotomy and pericardiotomy (n = 17, sham-operated group. At 1, 2, 4, and 8 wk after transduction, rats in the MI-control group had higher levels of NGF mRNA and protein than those in the sham-operated group, rats in the MI-GFP group showed similar levels as the MI-control group, and rats in the MI-SiNGF group had lower levels compared to the MI-GFP group, indicating that MI model was successfully established and NGF siRNA effectively inhibited the expression of NGF. At 8 wk, echocardiographic and hemodynamic studies revealed a more severe cardiac dysfunction in the MI-siRNA group compared to the MI-GFP group. Moreover, rats in the MI-siRNA group had lower mRNA and protein expression levels of tyrosine hydroxylase (TH and growth-associated protein 43-positive nerve fibers (GAP-43 at both the infarcted border and within the non-infarcted left ventricles (LV. NGF silencing also reduced the vascular endothelial growth factor (VEGF expression and decreased the arteriolar and capillary densities at the infarcted border compared to the MI-GFP group. Histological analysis indicated a large infarcted size in the MI-SiNGF group. These findings suggested that endogenous NGF silencing attenuated sympathetic nerve sprouting

  3. Respiratory muscle endurance is limited by lower ventilatory efficiency in post-myocardial infarction patients

    Directory of Open Access Journals (Sweden)

    Laura M. T. Neves

    2014-03-01

    Full Text Available Background: Reduced respiratory muscle endurance (RME contributes to increased dyspnea upon exertion in patients with cardiovascular disease. Objective: The objective was to characterize ventilatory and metabolic responses during RME tests in post-myocardial infarction patients without respiratory muscle weakness. Method: Twenty-nine subjects were allocated into three groups: recent myocardial infarction group (RG, n=9, less-recent myocardial infarction group (LRG, n=10, and control group (CG, n=10. They underwent two RME tests (incremental and constant pressure with ventilatory and metabolic analyses. One-way ANOVA and repeated measures one-way ANOVA, both with Tukey post-hoc, were used between groups and within subjects, respectively. Results: Patients from the RG and LRG presented lower metabolic equivalent and ventilatory efficiency than the CG on the second (50± 06, 50± 5 vs. 42± 4 and third part (50± 11, 51± 10 vs. 43± 3 of the constant pressure RME test and lower metabolic equivalent during the incremental pressure RME test. Additionally, at the peak of the incremental RME test, RG patients had lower oxygen uptake than the CG. Conclusions : Post-myocardial infarction patients present lower ventilatory efficiency during respiratory muscle endurance tests, which appears to explain their inferior performance in these tests even in the presence of lower pressure overload and lower metabolic equivalent.

  4. Detection of stunned myocardium in post-reperfusion cases of acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Tanaka, Ryo; Nakamura, Tomoharu; Kumamoto Hideki; Miura, Masatake; Hirabayashi, Kagami; Fujita, Kousuke [Kushiroshi Ishikai Hospital, Hokkaido (Japan); Okamoto, Noriake [Bristol-Myers Squibb Co., Tokyo (Japan); Zaima, Tsuyoshi [Tottori Univ., Yonago (Japan). School of Medicine

    2003-02-01

    This study was designed to evaluate the correlation between improvements in serial images obtained by SPECT imaging with Tc-99m MIBI (MIBI) and I-123 BMIPP (BMIPP) and the recovery of cardiac function in acute myocardial infarction (AMI) patients after reperfusion therapy. Twenty five patients who were admitted to the emergency room within 24 hours after the onset of the first event of AMI were enrolled in this study. The culprit coronary arteries were identified by coronary angiography (CAG) and were treated with direct percutaneous transluminal coronary angiography (PTCA), followed by stent implantation. To determine risk areas, initial image at the onset was acquired by the freeze method, in which MIBI was injected before the treatment and the image was collected after the reperfusion therapy. After the reperfusion treatment was completed, MIBI SPECT images at rest were performed on days 7 and 60. Both early and late images, including gated SPECT images were acquired after 30-60 minutes and 6 hours post injection, respectively. In addition, BMIPP SPECT images at rest were obtained 30 minutes after injection of 148 MBq BMIPP on days 7 and 60 (BMIPP image). The obtained image was divided into 48 segments and percent uptake of each segment was calculated. The number of abnormal areas (NAA) was defined as the segment with a % uptake less than 60% of normal uptake, and the change of NAA over time was evaluated. The NAA on the MIBI-early image significantly improved between the pre image and the day 7 image (p<0.001), but no similar improvement was observed between day 7 and day 60. On the other hand, the NAA of the MIBI-delayed image did not significantly improve up to day 7, but a slight improvement was observed on days 7 and 60 (p<0.05). A significant improvement in the NAA of the BMIPP image was observed between day 7 and day 60, as shown in the delayed image (p<0.05). An excellent correlation on the NAA between the MIBI-delayed image and the BMIPP image was

  5. Regional cardiac dysfunction and outcome in patients with left ventricular dysfunction, heart failure, or both after myocardial infarction

    DEFF Research Database (Denmark)

    Wang, Na; Hung, Chung-Lieh; Shin, Sung Hee

    2016-01-01

    -mode speckle tracking in 12 segments from the apical 4- and 2-chamber views and visually assessed LV wall motion score (WMS). We related these measures of regional myocardial function to each other and to clinical outcomes over 20-month follow-up. Normal reference values for segmental LS were derived from 50...

  6. Prevalence of post-traumatic stress disorder in patients with previous myocardial infarction consulting in general practice

    OpenAIRE

    Jones, Rupert CM; Chung, Man C; Berger, Zoë; Campbell, John L.

    2007-01-01

    Reported prevalence of myocardial infarction-related post-traumatic stress disorder (PTSD) varies from 0 to 25%. PTSD after myocardial infarction may affect quality of life, cardiovascular outcomes, and health service usage. Of 164 patients with previous myocardial infarction, 111 participated in the study and 36 had PTSD, giving a prevalence of 32%; the lowest possible estimate being 22%. PTSD was associated with significantly worse general health than that of individuals without PTSD. Preva...

  7. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both

    DEFF Research Database (Denmark)

    Solomon, Scott D; Zelenkofske, Steve; McMurray, John J V

    2005-01-01

    BACKGROUND: The risk of sudden death from cardiac causes is increased among survivors of acute myocardial infarction with reduced left ventricular systolic function. We assessed the risk and time course of sudden death in high-risk patients after myocardial infarction. METHODS: We studied 14,609 ...

  8. Late post-operative hypoxaemia and organ dysfunction

    DEFF Research Database (Denmark)

    Kehlet, H; Rosenberg, J

    1995-01-01

    an adverse effect of tissue hypoxia on wound healing and on resistance to bacterial wound infections. Finally, mental confusion and surgical delirium may be related to inadequate arterial oxygenation during the late post-operative period. Late post-operative constant and episodic hypoxaemia may therefore...

  9. Cardiac fibroblasts contribute to myocardial dysfunction in mice with sepsis: the role of NLRP3 inflammasome activation.

    Directory of Open Access Journals (Sweden)

    Wenbo Zhang

    Full Text Available Myocardial contractile dysfunction in sepsis is associated with the increased morbidity and mortality. Although the underlying mechanisms of the cardiac depression have not been fully elucidated, an exaggerated inflammatory response is believed to be responsible. Nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3 inflammasome is an intracellular platform that is involved in the maturation and release of interleukin (IL-1β. The aim of the present study is to evaluate whether sepsis activates NLRP3 inflammasome/caspase-1/IL-1β pathway in cardiac fibroblasts (CFs and whether this cytokine can subsequently impact the function of cardiomyocytes (cardiac fibroblast-myocyte cross-talk. We show that treatment of CFs with lipopolysaccharide (LPS induces upregulation of NLRP3, activation of caspase-1, as well as the maturation (activation and release of IL-1β. In addition, the genetic (small interfering ribonucleic acid [siRNA] and pharmacological (glyburide inhibition of the NLRP3 inflammasome in CFs can block this signaling pathway. Furthermore, the inhibition of the NLRP3 inflammasome in cardiac fibroblasts ameliorated the ability of LPS-challenged CFs to impact cardiomyocyte function as assessed by intracellular cyclic adenosine monophosphate (cAMP responses in cardiomyocytes. Salient features of this the NLP3 inflammasome/ caspase-1 pathway were confirmed in in vivo models of endotoxemia/sepsis. We found that inhibition of the NLRP3 inflammasome attenuated myocardial dysfunction in mice with LPS and increased the survival rate in mice with feces-induced peritonitis. Our results indicate that the activation of the NLRP3 inflammasome in cardiac fibroblasts is pivotal in the induction of myocardial dysfunction in sepsis.

  10. Association of poly(ADP-ribose) polymerase activity in circulating mononuclear cells with myocardial dysfunction in patients with septic shock

    Institute of Scientific and Technical Information of China (English)

    Li Li; Hu Bangchuan; Gong Shijin; Yu Yihua; Dai Haiwen; Yan Jing

    2014-01-01

    Background Severe sepsis and septic shock are the leading causes of morbidity and mortality in hospitalized patients.This study aimed to investigate the association of poly(ADP-ribose) polymerase-1 (PARP-1) activity in circulating mononuclear cells with myocardial dysfunction in patients with septic shock.Methods A total of 64 patients with septic shock were divided into the survival group (n=41) and the nonsurvival group (n=23) according to mortality at 28 days after enrollments.PARP-1 activity in circulating mononuclear cells,brain natriuretic peptide,Acute Physiology and Chronic Health Evaluation Ⅱ score,the cardiac index (CI),the cardiac function index (CFI),global ejection fraction (GEF),and the left ventricular contractility index (dp/dt max) were measured after admission to the intensive care unit.Results PARP-1 activity in circulating mononuclear cells of nonsurvival patients with septic shock was significantly higher than that in survival patients.PARP-1 activity in circulating mononuclear cells was strongly,negatively correlated with the CI,the CFI,GEE and dp/dt max.Multiple Logistic regression analysis showed that PARP-1 activity in circulating mononuclear cells was an independent risk factor of myocardial dysfunction.The optimal cutoff point of PARP-1 activity for predicting 28-day mortality was 942 nmol/L with a sensibility of 78.2% and specificity of 65.1%.Conclusion PARP-1 activity in circulating mononuclear cells is significantly associated with myocardial dysfunction and may have prognostic value in patients with septic shock.

  11. Choice reaction time in patients with post-operative cognitive dysfunction

    DEFF Research Database (Denmark)

    Steinmetz, J.; Rasmussen, L.S.

    2008-01-01

    in nine countries. CRT was measured 52 times using the four boxes test. Patients performed the test before surgery (n=1083), at 1 week (n=926) and at 3 months (n=852) post-operatively. CRT for the individual patient was determined as the median time of correct responses. The usefulness of the CRT......BACKGROUND: Post-operative cognitive dysfunction (POCD) is detected by administration of a neuropsychological test battery. Reaction time testing is at present not included as a standard test. Choice reaction time (CRT) data from the first International Study of Post-operative Cognitive Dysfunction...... had a significantly longer CRT. ROC curves revealed that a reaction time of 813 ms was the most appropriate cut-off at 1 week and 762 ms at 3 months but the positive predictive value for POCD was low: 34.4% and 14.7%, respectively. CONCLUSIONS: Post-operative cognitive dysfunction is associated...

  12. Activation of SHH signaling pathway promotes vasculogenesis in post-myocardial ischemic-reperfusion injury

    OpenAIRE

    Guo, Wei; YI, XIN; Ren, Faxin; Liu, Liwen; WU, SUNING; Yang, Jun

    2015-01-01

    This study aimed to investigate the potential roles of sonic Hedgehog (SHH) expression in vasculogenesis in post-myocardial ischemic-reperfusion injury (MIRI) and its underlying mechanism. Cardiac microvascular endothelial cells (CMECs) isolated from the SD rat hearts tissues were used to construct the MIRI model. mRNA level of SHH in control cells and MIRI cells was detected using RT-PCR analysis. Furthermore, effects of SHH expression on CMECs viability and apoptosis were analyzed using MTT...

  13. Impact of post myocardial infarction depression on drug adherence of cardiological medicines

    OpenAIRE

    Hemanta Dutta; Soumitra Ghosh; DJ Dutta

    2015-01-01

    Background: Depressive symptoms are very usual in patients experiencing a history of myocardial infarction (MI). An individual who has developed depression after an episode of MI becomes non compliant with the treatment of cardiology. Aim: To test the impact of post MI depression on drug adherence of cardiological medicines. Settings and design: The study was conducted on patients of acute MI (n=50) attending cardiology outpatient department (OPD) of Assam Medical College and Hospital...

  14. Predictors for development of multiple organ dysfunction syndrome in elderly patients with acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Xiaoying Li; Yusheng Zhao; Qiao Xue; Deshui Wang; Wei Gap

    2008-01-01

    Multiple organ dysfunction syndrome (MODS) is one of the leading causes of death in ICU patients.However,there have been few studies on the role of MODS as a cause of death in patients with acute myocardial infarction (AMI),particularly in those at advanced age.Our study aimed to investigate the incidence and to identify the predicting factors of MODS in elderly patients with AMI.Methods We identified consecutive patients with AMI who were discharged from the Chinese PLA General Hospital between January 1993 to June 2006.Medical records of 800 consecutive patients aged 60 years or over were analyzed retrospectively.Multivariate logistic regression was used to determine factors predicting in-hospital development of MODS.Results Twenty-seven (3.4%) patients developed MODS within 30 days after AMI.Compared with patients without MODS,patients with MODS had higher in-hospital mortality rates (55.6% vs 11.6%,P<0.001 ) and more frequent complications of cardiogenic shock (25.9% vs 6.2%,P<0.001),heart failure (HF) (59.3% vs 18.2%,P<0.001 ),cardiac arrhythmia (44.4% vs 26.4%,P<0.05) and pneumonia (55.6% vs 16.3%,P<0.001).Multivariate logistic regression analysis showed the major predictors for the occurrence of MODS secondary to AMI were advanced age (≥ 75 years,odds ratio 2.64,95% confidence interval [CI] 1.13 to 6.61),heart rate/> 100 bpm on admission (odds ratio 1.74,[CI] 1.14 to 2.64),in-hospital complication of HF (odds ratio 3.03,[CI] 1.26 to 7.26) and pneumonia (odds ratio 2.82,[CI] 1.18 to 6.77).Conclusions MODS is not the uncommon complication in elderly patients with AMI and is associated with poor prognosis.Advanced age,heart failure and pneumonia are predictors of the development of MODS in patients with AMI.(J Geriatr Cardiol 2008;5:199-202)

  15. Pheochromocytoma Is Characterized by Catecholamine-Mediated Myocarditis, Focal and Diffuse Myocardial Fibrosis, and Myocardial Dysfunction.

    Science.gov (United States)

    Ferreira, Vanessa M; Marcelino, Mafalda; Piechnik, Stefan K; Marini, Claudia; Karamitsos, Theodoros D; Ntusi, Ntobeko A B; Francis, Jane M; Robson, Matthew D; Arnold, J Ranjit; Mihai, Radu; Thomas, Julia D J; Herincs, Maria; Hassan-Smith, Zaki K; Greiser, Andreas; Arlt, Wiebke; Korbonits, Márta; Karavitaki, Niki; Grossman, Ashley B; Wass, John A H; Neubauer, Stefan

    2016-05-24

    Pheochromocytoma is associated with catecholamine-induced cardiac toxicity, but the extent and nature of cardiac involvement in clinical cohorts is not well-characterized. This study characterized the cardiac phenotype in patients with pheochromocytoma using cardiac magnetic resonance (CMR). A total of 125 subjects were studied, including patients with newly diagnosed pheochromocytoma (n = 29), patients with previously surgically cured pheochromocytoma (n = 31), healthy control subjects (n = 51), and hypertensive control subjects (HTN) (n = 14), using CMR (1.5-T) cine, strain imaging by myocardial tagging, late gadolinium enhancement, and native T1 mapping (Shortened Modified Look-Locker Inversion recovery [ShMOLLI]). Patients who were newly diagnosed with pheochromocytoma, compared with healthy and HTN control subjects, had impaired left ventricular (LV) ejection fraction (990 ms, as compared with 1% in healthy and 2% in HTN subjects; p pheochromocytoma groups. This first systematic CMR study characterizing the cardiac phenotype in pheochromocytoma showed that cardiac involvement was frequent and, for some variables, persisted after curative surgery. These effects surpass those of hypertensive heart disease alone, supporting a direct role of catecholamine toxicity that may produce subtle but long-lasting myocardial alterations. Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

  16. Post-mortem cardiac diffusion tensor imaging: detection of myocardial infarction and remodeling of myofiber architecture

    Energy Technology Data Exchange (ETDEWEB)

    Winklhofer, Sebastian; Berger, Nicole; Stolzmann, Paul [University Hospital Zurich, Institute of Diagnostic and Interventional Radiology, Zurich (Switzerland); University of Zurich, Department of Forensic Medicine and Radiology, Institute of Forensic Medicine, Zurich (Switzerland); Stoeck, Christian T.; Kozerke, Sebastian [Institute for Biomedical Engineering University and ETH Zurich, Zurich (Switzerland); Thali, Michael [University of Zurich, Department of Forensic Medicine and Radiology, Institute of Forensic Medicine, Zurich (Switzerland); Manka, Robert [University Hospital Zurich, Institute of Diagnostic and Interventional Radiology, Zurich (Switzerland); Institute for Biomedical Engineering University and ETH Zurich, Zurich (Switzerland); University Hospital Zurich, Clinic for Cardiology, Zurich (Switzerland); Alkadhi, Hatem [University Hospital Zurich, Institute of Diagnostic and Interventional Radiology, Zurich (Switzerland)

    2014-11-15

    To investigate the accuracy of post-mortem diffusion tensor imaging (DTI) for the detection of myocardial infarction (MI) and to demonstrate the feasibility of helix angle (HA) calculation to study remodelling of myofibre architecture. Cardiac DTI was performed in 26 deceased subjects prior to autopsy for medicolegal reasons. Fractional anisotropy (FA) and mean diffusivity (MD) were determined. Accuracy was calculated on per-segment (AHA classification), per-territory, and per-patient basis, with pathology as reference standard. HAs were calculated and compared between healthy segments and those with MI. Autopsy demonstrated MI in 61/440 segments (13.9 %) in 12/26 deceased subjects. Healthy myocardial segments had significantly higher FA (p < 0.01) and lower MD (p < 0.001) compared to segments with MI. Multivariate logistic regression demonstrated that FA (p < 0.10) and MD (p = 0.01) with the covariate post-mortem time (p < 0.01) predicted MI with an accuracy of 0.73. Analysis of HA distribution demonstrated remodelling of myofibre architecture, with significant differences between healthy segments and segments with chronic (p < 0.001) but not with acute MI (p > 0.05). Post-mortem cardiac DTI enablesdifferentiation between healthy and infarcted myocardial segments by means of FA and MD. HA assessment allows for the demonstration of remodelling of myofibre architecture following chronic MI. (orig.)

  17. Lin28a protects against postinfarction myocardial remodeling and dysfunction through Sirt1 activation and autophagy enhancement.

    Science.gov (United States)

    Hao, Yuanyuan; Lu, Qun; Yang, Guodong; Ma, Aiqun

    2016-10-28

    Myocardial remodeling and cardiac dysfunction prevention may represent a therapeutic approach to reduce mortality in patients with myocardial infarction (MI). We investigated the effects of Lin28a in experimental MI models, as well as the mechanisms underlying these effects. Left anterior descending (LAD) coronary artery ligation was used to construct an MI-induced injury model. Neonatal cardiomyocytes were isolated and cultured to investigate the mechanisms underlying the protective effects of Lin28a against MI-induced injury. Lin28a significantly inhibited left ventricular remodeling and cardiac dysfunction after MI, as demonstrated via echocardiography and hemodynamic measurements. Lin28a reduced cardiac enzyme and inflammatory marker release in mice subjected to MI-induced injury. The mechanisms underlying the protective effects of Lin28a against MI-induced injury were associated with autophagy enhancements and apoptosis inhibition. Consistent with these findings, Lin28a knockdown aggravated cardiac remodeling and dysfunction after MI-induced injury. Lin28a knockdown also inhibited cardiomyocyte autophagy and increased cardiomyocyte apoptosis in mice subjected to MI-induced injury. Interestingly, Sirt1 knockdown abolished the protective effects of Lin28a against cardiac remodeling and dysfunction after MI, and Lin28a failed to increase the numbers of GFP-LC3-positive punctae and decrease aggresome and p62 accumulation in Sirt1-knockdown neonatal cardiomyocytes subjected to hypoxia-induced injury. Lin28a inhibits cardiac remodeling, improves cardiac function, and reduces cardiac enzyme and inflammatory marker release after MI. Lin28a also up-regulates cardiomyocyte autophagy and inhibits cardiomyocyte apoptosis through Sirt1 activation. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Effective treatment of depression improves post-myocardial infarction survival

    Institute of Scientific and Technical Information of China (English)

    Soudabeh; Khojasteh; Banankhah; Erika; Friedmann; Sue; Thomas

    2015-01-01

    AIM: To examine the contribution of treatment resistant depression(TRD) to mortality in depressed postmyocardial infarction(MI) patients independent of biological and social predictors.METHODS: This secondary analysis study utilizes the Enhancing Recovery in Coronary Heart Disease(ENRICHD) clinical trial data.From 1834 depressed patients in the ENRICHD study,there were 770 depressed post-MI patients who were treated for depression.In this study,TRD is defined as having a less than 50% reduction in Hamilton Depression(HAM-D) score from baseline and a HAM-D score of greater than 10 in 6 mo after depression treatment began.Cox regression analysis was used to examine the independent contributions of TRD to mortality after controlling for the biological and social predictors.RESULTS: TRD occurred in 13.4%(n = 103) of the 770 patients treated for depression.Patients with TRD were significantly younger in age(P = 0.04)(mean = 57.0 years,SD = 11.7) than those without TRD(mean = 59.2 years,SD = 12.0).There was a significantly higher percentage of females with TRD(57.3%) compared to females without TRD(47.4%) [χ2(1) = 4.65,P = 0.031].There were significantly more current smokers with TRD(44.7%) than without TRD(33.0%) [χ2(1) = 7.34,P = 0.007].There were no significant differences in diabetes(P = 0.120),history of heart failure(P = 0.258),prior MI(P = 0.524),and prior stroke(P = 0.180) between patients with TRD and those without TRD.Mortality was 13%(n = 13) in patients with TRD and 7%(n = 49) in patients without TRD,with a mean follow-up of 29 mo(18 mo minimum and maximum of 4.5 years).TRD was a significant independent predictor of mortality(HR =1.995; 95%CI: 1.011-3.938,P = 0.046) after controlling for age(HR = 1.036; 95%CI: 1.011-1.061,P = 0.004),diabetes(HR = 2.912; 95%CI: 1.638-5.180,P < 0.001),heart failure(HR = 2.736; 95%CI: 1.551-4.827,P = 0.001),and smoking(HR = 0.502; 95%CI: 0.228-1.105,P = 0.087).CONCLUSION: The analysis of TRD in the ENRICHD study shows that the

  19. Myocardial dysfunction in patients with type 2 diabetes mellitus: role of endothelial progenitor cells and oxidative stress

    Directory of Open Access Journals (Sweden)

    Zhao Chun

    2012-12-01

    Full Text Available Abstract Background Endothelial progenitor cells (EPCs are responsible for angiogenesis and maintenance of microvascular integrity, the number of EPCs is correlated with oxidative stress. Their relation to myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM is nonetheless unknown. Methods Eighty-seven patients with T2DM and no history of coronary artery disease were recruited. Transthoracic echocardiography and detailed evaluation of left ventricular (LV systolic function by 2-dimensional (2D speckle tracking derived strain analysis in 3 orthogonal directions was performed. Four subpopulations of EPCs, including CD34+, CD133+, CD34+/kinase insert domain-containing receptor (KDR + and CD133+/KDR + EPCs, were measured by flow cytometry. Oxidative stress was assessed by superoxide dismutase (SOD. Results The mean age of the patients was 62 ± 9 years and 39.6% were male. Those with an impaired longitudinal strain had a lower number of CD34+ EPCs (2.82 ± 1.87% vs. 3.74 ± 2.12%, P  Conclusions LV global circumferential strain was independently associated with number of CD34+ EPCs and SOD. These findings suggest that myocardial dysfunction in patients with T2DM is related to depletion of EPCs and increased oxidative stress.

  20. Soluble TNF receptors are associated with infarct size and ventricular dysfunction in ST-elevation myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Lennart Nilsson

    Full Text Available OBJECTIVES: The aim of the study was to investigate circulating markers of apoptosis in relation to infarct size, left ventricular dysfunction and remodeling in an ST-elevation myocardial infarction (STEMI population undergoing primary percutaneous coronary intervention (PCI. BACKGROUND: Immediate re-opening of the acutely occluded infarct-related artery via primary PCI is the treatment of choice in STEMI to limit ischemia injury. However, the sudden re-initiation of blood flow can lead to a local acute inflammatory response with further endothelial and myocardial damage, so-called reperfusion injury. Apoptosis is suggested to be a key event in ischemia-reperfusion injury, resulting in LV-dysfunction, remodeling and heart failure. METHODS: The present study is a prespecified substudy of the F.I.R.E. trial. We included 48 patients with STEMI undergoing primary PCI. Blood samples were collected prior to PCI and after 24 hours. Plasma was separated for later analysis of soluble tumor necrosis factor receptor (sTNFR 1, sTNFR2, sFas and sFas ligand (sFasL by ELISA. Infarct size, left ventricular (LV dysfunction and remodeling were assessed by cardiac magnetic resonance imaging at five days and four months after STEMI. RESULTS: The levels of sTNFR1 at 24 h as well as the relative increases in sTNFR1 and sTNFR2 over 24 h showed consistent and significant correlations with infarct size and LV-dysfunction at four months. Moreover, both sTNFRs correlated strongly with Troponin I and matrix metalloproteinase (MMP-2 measurements. Soluble Fas and sFasL did not overall correlate with measures of infarct size or LV-dysfunction. None of the apoptosis markers correlated significantly with measures of remodeling. CONCLUSIONS: In STEMI patients, circulating levels of sTNFR1 and sTNFR2 are associated with infarct size and LV dysfunction. This provides further evidence for the role of apoptosis in ischemia-reperfusion injury.

  1. Toll-like receptor 4 ablation rescues against paraquat-triggered myocardial dysfunction: Role of ER stress and apoptosis.

    Science.gov (United States)

    Lei, Yonghong; Li, Xue; Yuan, Fang; Liu, Lu; Zhang, Juan; Yang, Yanping; Zhao, Jieqiong; Han, Yan; Ren, Jun; Fu, Xiaobing

    2017-02-01

    Paraquat is a nitrogen herbicide imposing severe organ toxicity in human leading to acute lung injury and heart failure. The present study was designed to examine the impact of ablation of the innate proinflammatory mediator toll-like receptor 4 (TLR4) in paraquat-induced cardiac contractile dysfunction and the underlying mechanisms involved with a focus on endoplasmic reticulum (ER) stress and apoptosis. Adult male wild-type (WT) and TLR4 knockout (TLR4(-/-) ) mice were challenged with paraquat (45 mg/kg, i.p.) for 48 h prior to the assessment of myocardial and cardiomyocyte sarcomere function, ER stress, apoptosis and inflammation. Acute paraquat challenge exerted myocardial functional and geometric alterations including enlarged left ventricular end systolic diameter (LVESD), reduced fractional shortening, decreased sarcomere shortening, maximal velocities of sarcomere shortening and relengthening associated with unchanged LV posterior wall thickness, septal thickness, LV end diastolic diameter (LVEDD), heart rate, sarcomere length, time-to-peak shortening and time-to-90% relengthening. Although TLR4 ablation did not affect mechanical properties in the heart, it significantly attenuated or ablated paraquat-induced cardiac contractile anomalies. Moreover, paraquat imposed overt ER stress, apoptosis and inflammation as evidenced by upregulation of Bip, CHOP, Caspase-3, -9, Bax, Bad, and IL-1β, phosphorylation of PERK, eIF2α and IΚB, as well as activation of the stress molecules ERK and p38, with unchanged Caspase-8, Bcl2, TNF-α, p53, HMGB1, MyD88 and phosphorylation of Akt, GSK3β and JNK, the effects of which were attenuated or negated by TLR4 knockout. Taken together, our results suggested that TLR4 ablation alleviated paraquat-induced myocardial contractile dysfunction possibly through attenuation of ER stress, apoptosis and inflammation. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 656-668, 2017.

  2. Myocardial perfusion/metabolism mismatch and ventricular arrhythmias in the chronic post infarction state

    Energy Technology Data Exchange (ETDEWEB)

    Krause, B.J.; Poeppel, T.D.; Vosberg, H.; Mueller, H.W. [Dept. of Nuclear Medicine, Heinrich Heine Univ., Duesseldorf (Germany); Reinhardt, M. [Praxis fuer Radiologie und Nuklearmedizin, Dorsten (Germany); Vester, E.G. [Dept. of Cardiology, Evangelisches Krankenhaus, Duesseldorf (Germany); Yong, M.; Mau, J. [Dept. of Statistics in Medicine, Heinrich Heine Univ., Duesseldorf (Germany); Strauer, B.E. [Dept. of Medicine, Div. of Cardiology, Angiology and Pulmonary Disease, Heinrich Heine Univ., Duesseldorf (Germany)

    2005-07-01

    Aim: Ventricular arrhythmias have been shown to originate in the myocardial peri-infarct region due to irregular heterotopic conduction. Hypoperfused but viable myocardium is often localised in those areas and may be involved in the pathogenesis of arrhythmias. We tested the hypothesis that these myocardial perfusion/metabolism mismatches (MM) are significantly associated with ventricular arrhythmias in the chronic post infarction state. Patients, methods: 47 post infarction patients were included in the study. 33 suffered from ventricular arrhythmia whereas 14 did not. All patients underwent {sup 99m}Tc tetrofosmin SPECT and {sup 18}F-FDG PET. A region-of-interest(ROI)-analysis was used to assess viable myocardium based on predefined MM-criteria. Univariate analyses as well as a logistic regression model for the multivariate analysis were carried out. Results: 94% of the arrhythmic patients displayed at least one MM-segment as compared to 64% of the non-arrhythmic patients. MM-segments and arrhythmia showed a statistically significant relation (p=0.018). The logistic regression model predicted the occurrence or absence of arrhythmia in 85% of all cases. Multivariate analysis gave consistent results, after adjusting for symptomatic chronic heart failure (CHF), aneurysms and age. Conclusion: Our results support the hypothesis that hypoperfused but viable myocardium represents an arrhyhmogenic substrate and is a relevant risk factor for developing ventricular arrhythmias following myocardial infarction. Therefore, the detection of MM-segments allows the identification of patients with a higher risk for future cardiac events. (orig.)

  3. Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both

    DEFF Research Database (Denmark)

    Pouleur, Anne-Catherine; Barkoudah, Ebrahim; Uno, Hajime;

    2010-01-01

    The frequency of sudden unexpected death is highest in the early post-myocardial infarction (MI) period; nevertheless, 2 recent trials showed no improvement in mortality with early placement of an implantable cardioverter-defibrillator after MI....

  4. Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both

    DEFF Research Database (Denmark)

    Pouleur, Anne-Catherine; Barkoudah, Ebrahim; Uno, Hajime

    2010-01-01

    The frequency of sudden unexpected death is highest in the early post-myocardial infarction (MI) period; nevertheless, 2 recent trials showed no improvement in mortality with early placement of an implantable cardioverter-defibrillator after MI....

  5. An anthelmintic drug, pyrvinium pamoate, thwarts fibrosis and ameliorates myocardial contractile dysfunction in a mouse model of myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Motoaki Murakoshi

    Full Text Available Metabolic adaptation to limited supplies of oxygen and nutrients plays a pivotal role in health and disease. Heart attack results from insufficient delivery of oxygen and nutrients to the heart, where cardiomyocytes die and cardiac fibroblasts proliferate--the latter causing scar formation, which impedes regeneration and impairs contractility of the heart. We postulated that cardiac fibroblasts survive metabolic stress by adapting their intracellular metabolism to low oxygen and nutrients, and impeding this metabolic adaptation would thwart their survival and facilitate the repair of scarred heart. Herein, we show that an anthelmintic drug, Pyrvinium pamoate, which has been previously shown to compromise cancer cell survival under glucose starvation condition, also disables cardiac fibroblast survival specifically under glucose deficient condition. Furthermore, Pyrvinium pamoate reduces scar formation and improves cardiac contractility in a mouse model of myocardial infarction. As Pyrvinium pamoate is an FDA-approved drug, our results suggest a therapeutic use of this or other related drugs to repair scarred heart and possibly other organs.

  6. Vision Therapy for Binocular Dysfunction Post Brain Injury.

    Science.gov (United States)

    Conrad, Joseph Samuel; Mitchell, G Lynn; Kulp, Marjean Taylor

    2017-01-01

    To prospectively evaluate the effectiveness of home-based computer vergence therapy for the treatment of binocular vision disorders in adults at least 3 months after an acquired brain injury. Eligibility criteria included presence of binocular dysfunction characterized by receded near point of convergence (≥6 cm break), insufficient positive fusional vergence at near (failing Sheard's criterion or computer vergence therapy. Phoria (cover test), negative fusional vergence, positive fusional vergence, near point of convergence, vergence facility, and symptoms (convergence insufficiency symptom survey [CISS]) were assessed at baseline and after 4, 8, and 12 weeks of prescribed therapy. ANOVA was used to evaluate change in each measure. Percentage successful was also determined. Nineteen participants were enrolled (mean age 45.4 ± 12.9 years); six participants were lost to follow-up. Baseline findings were orthophoria at distance, 7.2△ exophoria at near, near point of convergence break = 17.5 cm, near point of convergence recovery = 21.8 cm, negative fusional vergence = 12.3△, positive fusional vergence blur = 8.4△, vergence facility = 3.9 cycles per minute, and CISS = 32.1. ANOVA showed a statistically significant improvement for near point of convergence break (p = 0.002) and recovery (p 15△ and passing Sheard's criterion or increase of ≥10△), 77% for negative fusional vergence (≥12△ or increase of ≥6△), 62% for positive fusional vergence and near point of convergence composite, and 92% for vergence facility (15 cycles per minute or increase of 3 cycles per minute). The majority of participants who completed the study experienced meaningful improvements in signs and symptoms.

  7. EFFECT OF LEFT VENTRICULAR SYSTOLIC DYSFUNCTION ON CEREBRAL HEMODYNAMICS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION (THE RESULTS OF OBSERVATIONAL STUDIES

    Directory of Open Access Journals (Sweden)

    V. E. Kulikov

    2015-12-01

    Full Text Available Aim. To study the effect of left ventricular (LV systolic dysfunction on cerebral hemodynamic in patients with ST segment elevation myocardial infarction (STEMI during acute period. Material and methods. Cerebral hemodynamics ultrasound assessment was performed in the extra-and intracranial vessels in 118 patients with STEMI. Results. Significant changes in cerebral hemodynamics were found in LV systolic dysfunction with ejection fraction (LVEF ≤40% due to hemispheric blood flow asymmetry in the middle cerebral artery (MCA as large as 45.1±6.7% with correlation coefficient r=-0.87. Compensation of cerebral blood flow was manifested in vasoconstriction or vasodilation (resistive index 0.63-0.76 and 0.49-0.43 c.u., respectively. Conclusion. A strong relationship between LV systolic dysfunction and cerebral hemodynamic was found in patients with STEMI. It was manifested in significant contralateral hemispheric blood flow asymmetry in MCA in patients with LVEF ≤40%. Reduction in cerebral blood flow velocity activated autoregulation mechanism in the form of vasoconstriction or vasodilation.

  8. Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.

    Science.gov (United States)

    Lindsey, Merry L; Iyer, Rugmani Padmanabhan; Jung, Mira; DeLeon-Pennell, Kristine Y; Ma, Yonggang

    2016-02-01

    Despite current optimal therapeutic regimens, approximately one in four patients diagnosed with myocardial infarction (MI) will go on to develop congestive heart failure, and heart failure has a high five-year mortality rate of 50%. Elucidating mechanisms whereby heart failure develops post-MI, therefore, is highly needed. Matrix metalloproteinases (MMPs) are key enzymes involved in post-MI remodeling of the left ventricle (LV). While MMPs process cytokine and extracellular matrix (ECM) substrates to regulate the inflammatory and fibrotic components of the wound healing response to MI, MMPs also serve as upstream signaling initiators with direct actions on cell signaling cascades. In this review, we summarize the current literature regarding MMP roles in post-MI LV remodeling. We also identify the current knowledge gaps and provide templates for experiments to fill these gaps. A more complete understanding of MMP roles, particularly with regards to upstream signaling roles, may provide new strategies to limit adverse LV remodeling.

  9. Post-void residual urine under 150 ml does not exclude voiding dysfunction in women

    DEFF Research Database (Denmark)

    Khayyami, Yasmine; Klarskov, Niels; Lose, Gunnar

    2016-01-01

    INTRODUCTION AND HYPOTHESIS: It has been claimed that post-void residual urine (PVR) below 150 ml rules out voiding dysfunction in women with stress urinary incontinence (SUI) and provides license to perform sling surgery. The cut-off of 150 ml seems arbitrary, not evidence-based, and so we sough...

  10. Extrapyramidal Motor Dysfunction and Resultant Orofacial Dystonia Post-Cocaine Abuse: A Clinical Case Study

    Science.gov (United States)

    McMicken, Betty L.; Ostergren, Jennifer A.; Vento-Wilson, Margaret

    2010-01-01

    This case study investigated the consequences of cocaine use and resultant extrapyramidal motor dysfunction. The study focused on a female client, post-long-term drug abuse with concomitant untreated head trauma, experiencing extraneous motor movements of the lips, tongue, jaw, and upper and lower extremities. The goals of this study were to (a)…

  11. Extrapyramidal Motor Dysfunction and Resultant Orofacial Dystonia Post-Cocaine Abuse: A Clinical Case Study

    Science.gov (United States)

    McMicken, Betty L.; Ostergren, Jennifer A.; Vento-Wilson, Margaret

    2010-01-01

    This case study investigated the consequences of cocaine use and resultant extrapyramidal motor dysfunction. The study focused on a female client, post-long-term drug abuse with concomitant untreated head trauma, experiencing extraneous motor movements of the lips, tongue, jaw, and upper and lower extremities. The goals of this study were to (a)…

  12. Effect of therapeutic hypothermia vs δ-opioid receptor agonist on post resuscitation myocardial function in a rat model of CPR.

    Science.gov (United States)

    Chung, Sung Phil; Song, Feng-Qing; Yu, Tao; Weng, Yinlun; Sun, Shijie; Weil, Max Harry; Tang, Wanchun

    2011-03-01

    This study is to compare the effect of the δ-opioid receptor agonist, D-Ala(2)-D-Leu(5) enkephalin (DADLE) with normothermic control and therapeutic hypothermia on post resuscitation myocardial function and 72-h survival in a rat model of cardiac arrest and resuscitation. Ventricular fibrillation (VF) was induced in 15 male Sprague-Dawley rats. After 8 min of untreated VF, cardiopulmonary resuscitation was performed for 8 min before defibrillation. Animals were randomized to three groups of five: (a) normothermia; (b) hypothermia (32 °C); and (c) normothermia with DADLE intravenous infusion (1 mg/kg h(-1)). Hypothermia and drug infusion were started after successful defibrillation. Myocardial functions, including cardiac output (CO), left ventricular ejection fraction (LVEF), and myocardial performance index (MPI) were measured echocardiographically together with duration of survival. The 72-h survival was significantly greater in the hypothermic group than in both DADLE and normothermic group (p = 0.02). However, the survival time of the DADLE treated animals was significantly longer than that of the normothermia group (51.8 ± 18.9 vs 18.8 ± 10.1h, p PR 60 min, p = 0.049), better LVEF (PR 60 min, p = 0.044; PR 240 min, p PR 60 min, p = 0.043; PR 240 min, p = 0.045) than normothermic group. Hypothermia group also showed significantly better CO (PR 60m in, p = 0.044; PR 240 min, p = 0.007), better LVEF (PR 60 min, p = 0.001; PR 240 min, p PR 60 min, p = 0.003; PR 240 min, p = 0.012) than the normothermic group. DADLE attenuated post resuscitation myocardial dysfunction and increased short term survival time. However, the 72-h survival in the DADLE group was less than that in the hypothermia group. Copyright © 2010. Published by Elsevier Ireland Ltd.

  13. Microvascular dysfunction is associated with plasma osteoprotegerin levels in patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Løgstrup, Brian B; Høfsten, Dan E; Christophersen, Thomas B

    2013-01-01

    Osteoprotegerin (OPG) is a glycoprotein that inhibits nuclear factor-κB's regulatory effects on inflammation, skeletal, and vascular systems, and is a potential biomarker of atherosclerosis and seems to be involved in vascular calcifications. The objective of this study was to assess the relation...... the relationship between OPG, left ventricular function, and microvascular function in patients with acute myocardial infarction (AMI)....

  14. Attenuation of post-infarction remodeling in rats by sustained myocardial growth hormone administration.

    Science.gov (United States)

    Daskalopoulos, Evangelos P; Vilaeti, Agapi D; Barka, Eleonora; Mantzouratou, Polixeni; Kouroupis, Dimitrios; Kontonika, Marianthi; Tourmousoglou, Christos; Papalois, Apostolos; Pantos, Constantinos; Blankesteijn, W Matthijs; Agathopoulos, Simeon; Kolettis, Theofilos M

    2015-01-01

    Prevention of left ventricular remodeling is an important therapeutic target post-myocardial infarction. Experimentally, treatment with growth hormone (GH) is beneficial, but sustained local administration has not been thoroughly investigated. We studied 58 rats (322 ± 4 g). GH was administered via a biomaterial-scaffold, following in vitro and in vivo evaluation of degradation and drug-release curves. Treatment consisted of intra-myocardial injection of saline or alginate-hydrogel, with or without GH, 10 min after permanent coronary artery ligation. Echocardiographic and histologic remodeling-indices were examined 3 weeks post-ligation, followed by immunohistochemical evaluation of angiogenesis, collagen, macrophages and myofibroblasts. GH-release completed at 3 days and alginate-degradation at ∼7 days. Alginate + GH consistently improved left ventricular end-diastolic and end-systolic diameters, ventricular sphericity, wall tension index and infarct-thickness. Microvascular-density and myofibroblast-count in the infarct and peri-infarct areas were higher after alginate + GH. Macrophage-count and collagen-content did not differ between groups. Early, sustained GH-administration enhances angiogenesis and myofibroblast-activation and ameliorates post-infarction remodeling.

  15. Quality of life one year post myocardial revascularization and aortic valve replacement in patients aged 70 year or older

    NARCIS (Netherlands)

    Markou, A L; Selten, K; Krabbe, P F; Noyez, L

    AIM: The aim of this study was to investigate changes of health-related quality of life (HRQOL) at one year post myocardial revascularization (CABG) and post aortic valve replacement (AVR) in patients aged 70 years or older. METHODS: Of 102 CABG patients and 69 AVR patients preoperative and

  16. Quality of life one year post myocardial revascularization and aortic valve replacement in patients aged 70 year or older

    NARCIS (Netherlands)

    Markou, A.L.; Selten, K.; Krabbe, P.F.M.; Noyez, L.

    2011-01-01

    AIM: The aim of this study was to investigate changes of health-related quality of life (HRQOL) at one year post myocardial revascularization (CABG) and post aortic valve replacement (AVR) in patients aged 70 years or older. METHODS: Of 102 CABG patients and 69 AVR patients preoperative and

  17. Quality of life one year post myocardial revascularization and aortic valve replacement in patients aged 70 year or older

    NARCIS (Netherlands)

    Markou, A L; Selten, K; Krabbe, P F; Noyez, L

    2011-01-01

    AIM: The aim of this study was to investigate changes of health-related quality of life (HRQOL) at one year post myocardial revascularization (CABG) and post aortic valve replacement (AVR) in patients aged 70 years or older. METHODS: Of 102 CABG patients and 69 AVR patients preoperative and follow-u

  18. Incidence of atrial fibrillation in patients with either heart failure or acute myocardial infarction and left ventricular dysfunction: a cohort study

    DEFF Research Database (Denmark)

    Schmiegelow, Michelle D; Pedersen, Ole D; Køber, Lars;

    2011-01-01

    We examined the incidence of new-onset atrial fibrillation in patients with left ventricular dysfunction. Patients either had a recent myocardial infarction (with or without clinical heart failure) or symptomatic heart failure (without a recent MI). Patients were with and without treatment...

  19. Incidence of atrial fibrillation in patients with either heart failure or acute myocardial infarction and left ventricular dysfunction: a cohort study

    DEFF Research Database (Denmark)

    Schmiegelow, Michelle D; Pedersen, Ole D; Køber, Lars;

    2011-01-01

    We examined the incidence of new-onset atrial fibrillation in patients with left ventricular dysfunction. Patients either had a recent myocardial infarction (with or without clinical heart failure) or symptomatic heart failure (without a recent MI). Patients were with and without treatment with t...... with the class III antiarrhythmic drug dofetilide over 36 months....

  20. Previously known and newly diagnosed atrial fibrillation: a major risk indicator after a myocardial infarction complicated by heart failure or left ventricular dysfunction

    DEFF Research Database (Denmark)

    Køber, Lars; Swedberg, Karl; McMurray, John J V

    2006-01-01

    AIMS: To characterize the relationship between known and newly diagnosed atrial fibrillation (AF) and the risk of death and major cardiovascular (CV) events in patients with acute myocardial infarction (MI) complicated by heart failure (HF) and/or left ventricular systolic dysfunction (LVSD). MET...

  1. Erythropoietin responsive cardiomyogenic cells contribute to heart repair post myocardial infarction.

    Science.gov (United States)

    Zafiriou, Maria Patapia; Noack, Claudia; Unsöld, Bernhard; Didie, Michael; Pavlova, Elena; Fischer, Henrike J; Reichardt, Holger M; Bergmann, Martin W; El-Armouche, Ali; Zimmermann, Wolfram-Hubertus; Zelarayan, Laura Cecilia

    2014-09-01

    The role of erythropoietin (Epo) in myocardial repair after infarction remains inconclusive. We observed high Epo receptor (EPOR) expression in cardiac progenitor cells (CPCs). Therefore, we aimed to characterize these cells and elucidate their contribution to myocardial regeneration on Epo stimulation. High EPOR expression was detected during murine embryonic heart development followed by a marked decrease until adulthood. EPOR-positive cells in the adult heart were identified in a CPC-enriched cell population and showed coexpression of stem, mesenchymal, endothelial, and cardiomyogenic cell markers. We focused on the population coexpressing early (TBX5, NKX2.5) and definitive (myosin heavy chain [MHC], cardiac Troponin T [cTNT]) cardiomyocyte markers. Epo increased their proliferation and thus were designated as Epo-responsive MHC expressing cells (EMCs). In vitro, EMCs proliferated and partially differentiated toward cardiomyocyte-like cells. Repetitive Epo administration in mice with myocardial infarction (cumulative dose 4 IU/g) resulted in an increase in cardiac EMCs and cTNT-positive cells in the infarcted area. This was further accompanied by a significant preservation of cardiac function when compared with control mice. Our study characterized an EPO-responsive MHC-expressing cell population in the adult heart. Repetitive, moderate-dose Epo treatment enhanced the proliferation of EMCs resulting in preservation of post-ischemic cardiac function.

  2. Digoxin:A systematic review in atrial fibrillation,congestive heart failure and post myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Sebastiano; Virgadamo; Richard; Charnigo; Yousef; Darrat; Gustavo; Morales; Claude; S; Elayi

    2015-01-01

    AIM: To review digoxin use in systolic congestive heart failure, atrial fibrillation, and after myocardial infarction. METHODS: A comprehensive Pub Med search was performed using the key words "digoxin and congestive heart failure", "digoxin and atrial fibrillation", "digoxin, atrial fibrillation and systolic congestive heart failure", and "digoxin and myocardial infarction". Only articles written in English were included in this study. We retained studies originating from randomized controlled trials, registries and included at least 500 patients. The studies included patients with atrial fibrillation or heart failure or myocardial infarction and had a significant proportion of patients(at least 5%) on digoxin. A table reviewing the different hazard ratios was developed based on the articles selected. Our primary endpoint was the overall mortality in the patients on digoxin vs those without digoxin, among patients with atrial fibrillation and also among patients with atrial fibrillation and systolic heart failure. We reviewed the most recent international guidelines to discuss current recommendations.RESULTS: A total of 18 studies were found that evaluated digoxin and overall mortality in different clinical settings including systolic congestive heart failure and normal sinus rhythm(n = 5), atrial fibrillation with and without systolic congestive heart failure(n = 9), and myocardial infarction(n = 4). Overall, patients with systolic congestive heart failure with normal sinus rhythm, digoxin appears to have a neutral effect on mortality especially if close digoxin level monitoring is employed. However, most of the observational studies evaluating digoxin use in atrial fibrillation without systolic congestive heart failure showed an increase in overall mortality when taking digoxin. In the studies evaluated in this systematic review, the data among patients with atrial fibrillation and systolic congestive heart failure, as well as post myocardial infarction were

  3. Targeted P2X7 R shRNA delivery attenuates sympathetic nerve sprouting and ameliorates cardiac dysfunction in rats with myocardial infarction.

    Science.gov (United States)

    Gao, Hongmei; Yin, Jie; Shi, Yugen; Hu, Hesheng; Li, Xiaolu; Xue, Mei; Cheng, Wenjuan; Wang, Ye; Li, Xinran; Li, Yongkang; Wang, Yu; Yan, Suhua

    2017-04-01

    Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in the etiology of arrhythmias resulting in sudden cardiac death; however, the mechanisms responsible remain to be elucidated. Although P2X7 R is a key immune mediator, its role has yet to be explored. We investigated whether P2X7 R regulates NF-κB and affects cardiac sympathetic reinnervation in rats undergoing MI. An adenoviral vector with a short hairpin RNA (shRNA) sequence inserted was adopted for the inhibition of P2X7 R in vivo. Myocardial infarction was induced by left coronary artery ligation, and immediately after that, recombinant P2X7 R-shRNA adenovirus, negative adenovirus (control), or normal saline solution (vehicle) was injected intramyocardially around the MI region and border areas. A high level of P2X7 R was activated in the infarcted tissue at an early stage. The administration of P2X7 R RNAi resulted in the inhibition of Akt and Erk1/2 phosphorylation and decreased the activation of NF-κB and macrophage infiltration, as well as attenuated the expression of nerve growth factor (NGF). Eventually, the NGF-induced sympathetic hyperinnervation was blunted, as assessed by the immunofluorescence of tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP 43). At 7 days post-MI, the arrhythmia score of programmed electrical stimulation in the vehicle-treated infarcted rats was higher than the MI-shRNA group. Further amelioration of cardiac dysfunction was also detected. The administration of P2X7 R RNAi during the acute inflammatory response phase prevented the process of sympathetic hyperinnervation after MI, which was associated in part with inhibiting the Akt and ERK1/2 pathways and NF-κB activation. © 2016 John Wiley & Sons Ltd.

  4. Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats

    Energy Technology Data Exchange (ETDEWEB)

    El-Mas, Mahmoud M., E-mail: mahelm@hotmail.com; Abdel-Rahman, Abdel A., E-mail: abdelrahmana@ecu.edu

    2015-09-15

    Evidence suggests that male rats are protected against the hypotensive and myocardial depressant effects of ethanol compared with females. We investigated whether E{sub 2} modifies the myocardial and oxidative effects of ethanol in male rats. Conscious male rats received ethanol (0.5, 1 or 1.5 g/kg i.v.) 30-min after E{sub 2} (1 μg/kg i.v.) or its vehicle (saline), and hearts were collected at the conclusion of hemodynamic measurements for ex vivo molecular studies. Ethanol had no effect in vehicle-treated rats, but it caused dose-related reductions in LV developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of rise in LV pressure (dP/dt{sub max}) and systolic (SBP) and diastolic (DBP) blood pressures in E{sub 2}-pretreated rats. These effects were associated with elevated (i) indices of reactive oxygen species (ROS), (ii) malondialdehyde (MDA) protein adducts, and (iii) phosphorylated death-associated protein kinase-3 (DAPK3), Akt, and extracellular signal-regulated kinases (ERK1/2). Enhanced myocardial anti-oxidant enzymes (heme oxygenase-1, catalase and aldehyde dehydrogenase 2) activities were also demonstrated. In conclusion, E{sub 2} promotes ethanol-evoked myocardial oxidative stress and dysfunction in male rats. The present findings highlight the risk of developing myocardial dysfunction in men who consume alcohol while receiving E{sub 2} for specific medical conditions. - Highlights: • Ethanol lowers blood pressure and causes LV dysfunction in E{sub 2}-treated rats. • E{sub 2}/ethanol aggravates cardiac oxidative state via of DAPK3/Akt/ERK activation. • E{sub 2}/ethanol causes a feedback increase in cardiac HO-1, catalase and ALDH2. • Alcohol might increase risk of myocardial dysfunction in men treated with E{sub 2}.

  5. Mechanical ventilation with high tidal volumes attenuates myocardial dysfunction by decreasing cardiac edema in a rat model of LPS-induced peritonitis

    Directory of Open Access Journals (Sweden)

    Smeding Lonneke

    2012-03-01

    Full Text Available Abstract Background Injurious mechanical ventilation (MV may augment organ injury remote from the lungs. During sepsis, myocardial dysfunction is common and increased endothelial activation and permeability can cause myocardial edema, which may, among other factors, hamper myocardial function. We investigated the effects of MV with injuriously high tidal volumes on the myocardium in an animal model of sepsis. Methods Normal rats and intraperitoneal (i.p. lipopolysaccharide (LPS-treated rats were ventilated with low (6 ml/kg and high (19 ml/kg tidal volumes (Vt under general anesthesia. Non-ventilated animals served as controls. Mean arterial pressure (MAP, central venous pressure (CVP, cardiac output (CO and pulmonary plateau pressure (Pplat were measured. Ex vivo myocardial function was measured in isolated Langendorff-perfused hearts. Cardiac expression of endothelial vascular cell adhesion molecule (VCAM-1 and edema were measured to evaluate endothelial inflammation and leakage. Results MAP decreased after LPS-treatment and Vt-dependently, both independent of each other and with interaction. MV Vt-dependently increased CVP and Pplat and decreased CO. LPS-induced peritonitis decreased myocardial function ex vivo but MV attenuated systolic dysfunction Vt-dependently. Cardiac endothelial VCAM-1 expression was increased by LPS treatment independent of MV. Cardiac edema was lowered Vt-dependently by MV, particularly after LPS, and correlated inversely with systolic myocardial function parameters ex vivo. Conclusion MV attenuated LPS-induced systolic myocardial dysfunction in a Vt-dependent manner. This was associated with a reduction in cardiac edema following a lower transmural coronary venous outflow pressure during LPS-induced coronary inflammation.

  6. Adenosine A2A receptor agonist prevents cardiac remodeling and dysfunction in spontaneously hypertensive male rats after myocardial infarction

    Science.gov (United States)

    da Silva, Jaqueline S; Gabriel-Costa, Daniele; Sudo, Roberto T; Wang, Hao; Groban, Leanne; Ferraz, Emanuele B; Nascimento, José Hamilton M; Fraga, Carlos Alberto M; Barreiro, Eliezer J; Zapata-Sudo, Gisele

    2017-01-01

    Background This work evaluated the hypothesis that 3,4-methylenedioxybenzoyl-2-thienylhydrazone (LASSBio-294), an agonist of adenosine A2A receptor, could be beneficial for preventing cardiac dysfunction due to hypertension associated with myocardial infarction (MI). Methods Male spontaneously hypertensive rats (SHR) were randomly divided into four groups (six animals per group): sham-operation (SHR-Sham), and myocardial infarction rats (SHR-MI) were treated orally either with vehicle or LASSBio-294 (10 and 20 mg.kg−1.d−1) for 4 weeks. Echocardiography and in vivo hemodynamic parameters measured left ventricle (LV) structure and function. Exercise tolerance was evaluated using a treadmill test. Cardiac remodeling was accessed by LV collagen deposition and tumor necrosis factor α expression. Results Early mitral inflow velocity was significantly reduced in the SHR-MI group, and there was significant recovery in a dose-dependent manner after treatment with LASSBio-294. Exercise intolerance observed in the SHR-MI group was prevented by 10 mg.kg−1.d−1 of LASS-Bio-294, and exercise tolerance exceeded that of the SHR-Sham group at 20 mg.kg−1.d−1. LV end-diastolic pressure increased after MI, and this was prevented by 10 and 20 mg.kg−1.d−1 of LASSBio-294. Sarcoplasmic reticulum Ca2+ ATPase levels were restored in a dose-dependent manner after treatment with LASSBio-294. Fibrosis and inflammatory processes were also counteracted by LASSBio-294, with reductions in LV collagen deposition and tumor necrosis factor α expression. Conclusion In summary, oral administration of LASSBio-294 after MI in a dose-dependent manner prevented the development of cardiac dysfunction, demonstrating this compound’s potential as an alternative treatment for heart failure in the setting of ischemic heart disease with superimposed chronic hypertension.

  7. Assessing left ventricular systolic dysfunction after myocardial infarction: are ejection fraction and dP/dt(max) complementary or redundant?

    Science.gov (United States)

    Ishikawa, Kiyotake; Chemaly, Elie R; Tilemann, Lisa; Fish, Kenneth; Ladage, Dennis; Aguero, Jaime; Vahl, Torsten; Santos-Gallego, Carlos; Kawase, Yoshiaki; Hajjar, Roger J

    2012-04-01

    Among the various cardiac contractility parameters, left ventricular (LV) ejection fraction (EF) and maximum dP/dt (dP/dt(max)) are the simplest and most used. However, these parameters are often reported together, and it is not clear if they are complementary or redundant. We sought to compare the discriminative value of EF and dP/dt(max) in assessing systolic dysfunction after myocardial infarction (MI) in swine. A total of 220 measurements were obtained. All measurements included LV volumes and EF analysis by left ventriculography, invasive ventricular pressure tracings, and echocardiography. Baseline measurements were performed in 132 pigs, and 88 measurements were obtained at different time points after MI creation. Receiver operator characteristic (ROC) curves to distinguish the presence or absence of an MI revealed a good predictive value for EF [area under the curve (AUC): 0.998] but not by dP/dt(max) (AUC: 0.69, P EF). Dividing dP/dt(max) by LV end-diastolic pressure and heart rate (HR) significantly increased the AUC to 0.87 (P EF). In naïve pigs, the coefficient of variation of dP/dt(max) was twice than that of EF (22.5% vs. 9.5%, respectively). Furthermore, in n = 19 pigs, dP/dt(max) increased after MI. However, echocardiographic strain analysis of 23 pigs with EF ranging only from 36% to 40% after MI revealed significant correlations between dP/dt(max) and strain parameters in the noninfarcted area (circumferential strain: r = 0.42, P = 0.05; radial strain: r = 0.71, P EF is a more accurate measure of systolic dysfunction than dP/dt(max) in a swine model of MI. Despite the variability of dP/dt(max) both in naïve pigs and after MI, it may sensitively reflect the small changes of myocardial contractility.

  8. DISFUNCIÓN DIASTÓLICA EN EL INFARTO AGUDO DE MIOCARDIO / Diastolic dysfunction in acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Norge Ramón Lara Pérez

    2010-03-01

    Full Text Available Introduction and objectives: Ischemic heart disease is among the first causes of disability and death in the world. The acute myocardial infarction alters considerably the myocardial relaxation. The echocardiogram is a useful, economic and harmless method to assess diastolic function in these patients; that is why the aim of the study was to characterize the behavior of this left ventricular function by means of an echocardiography. Methods: an observational descriptive study was carried out with 91 patients with myocardial infarction who were hospitalized at the Cardiology Ward of the Arnaldo Milian Castro Provincial University Hospital in Santa Clara during 2008. An echocardiogram was performed between the fifth and the seventh day of evolution, and the patterns of diastolic function were compared with other variables. Results: There was a prevalence of the male sex (74,7 %, the infarctions without ST segment elevation were more frequent (83,1 % – which showed a bigger alteration of the relaxation, much more when the anterior and lateral walls of the left ventricle were involved. The presence of complications was linked to a bigger alteration of the relaxation, and the most associate ones were the contractile dysfunction and malignant arrhythmias. The decrease of the ejection fraction was linked to (p = 0,000 the prolongation of the relaxation. Conclusions: There was a prevalence of the infarction without ST segment elevation. It was more frequent in the male sex and it was associated with a higher level of alteration of the relaxation. The infarctions with anterior or lateral location, and those which caused complications, presented a higher level of this alteration. All patients with a reduced ejection fraction had relaxation disorders.

  9. Oxidative stress and myocardial dysfunction in young rabbits after short term anabolic steroids administration.

    Science.gov (United States)

    Germanakis, Ioannis; Tsarouhas, Konstantinos; Fragkiadaki, Persefoni; Tsitsimpikou, Christina; Goutzourelas, Nikolaos; Champsas, Maria Christakis; Stagos, Demetrios; Rentoukas, Elias; Tsatsakis, Aristidis M

    2013-11-01

    The present study focuses on the short term effects of repeated low level administration of turinabol and methanabol on cardiac function in young rabbits (4 months-old). The experimental scheme consisted of two oral administration periods, lasting 1 month each, interrupted by 1-month wash-out period. Serial echocardiographic evaluation at the end of all three experimental periods was performed in all animals. Oxidative stress markers have also been monitored at the end of each administration period. Treated animals originally showed significantly increased myocardial mass and systolic cardiac output, which normalized at the end of the wash out period. Re-administration led to increased cardiac output, at the cost though of a progressive myocardial mass reduction. A dose-dependent trend towards impaired longitudinal systolic, diastolic and global myocardial function was also observed. The adverse effects were more pronounced in the methanabol group. For both anabolic steroids studied, the low dose had no significant effects on oxidative stress markers monitored, while the high dose created a hostile oxidative environment. In conclusion, anabolic administration has been found to create a possible deleterious long term effect on the growth of the immature heart and should be strongly discouraged especially in young human subjects. Copyright © 2013 Elsevier Ltd. All rights reserved.

  10. Depletion of circulating blood NOS3 increases severity of myocardial infarction and left ventricular dysfunction.

    Science.gov (United States)

    Merx, Marc W; Gorressen, Simone; van de Sandt, Annette M; Cortese-Krott, Miriam M; Ohlig, Jan; Stern, Manuel; Rassaf, Tienush; Gödecke, Axel; Gladwin, Mark T; Kelm, Malte

    2014-01-01

    Nitric oxide (NO) derived from endothelial NO synthase (NOS3) plays a central role in myocardial ischemia/reperfusion (I/R)-injury. Subsets of circulating blood cells, including red blood cells (RBCs), carry a NOS3 and contribute to blood pressure regulation and RBC nitrite/nitrate formation. We hypothesized that the circulating blood born NOS3 also modulates the severity of myocardial infarction in disease models. We cross-transplanted bone marrow in wild-type and NOS3(-/-) mice with wild-type mice, producing chimeras expressing NOS3 only in vascular endothelium (BC-/EC+) or in both blood cells and vascular endothelium (BC+/EC+). After 60-min closed-chest coronary occlusion followed by 24 h reperfusion, cardiac function, infarct size (IS), NOx levels, RBCs NO formation, RBC deformability, and vascular reactivity were assessed. At baseline, BC-/EC+ chimera had lower nitrite levels in blood plasma (BC-/EC+: 2.13 ± 0.27 μM vs. BC+/EC+ 3.17 ± 0.29 μM; *p NOS3 in an acute model of myocardial I/R in chimeric mice.

  11. TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice

    Directory of Open Access Journals (Sweden)

    Kai-Uwe Jarr

    2014-01-01

    Full Text Available Background. TNF-like weak inducer of apoptosis (TWEAK has recently been shown to be potentially involved in adverse cardiac remodeling. However, neither the exact role of TWEAK itself nor of its receptor Fn14 in this setting is known. Aim of the Study. To analyze the effects of sTWEAK on myocardial function and gene expression in response to experimental myocardial infarction in mice. Results. TWEAK directly suppressed the expression of PGC-1α and genes of oxidative phosphorylation (OXPHOS in cardiomyocytes. Systemic sTWEAK application after MI resulted in reduced left ventricular function and increased mortality without changes in interstitial fibrosis or infarct size. Molecular analysis revealed decreased phosphorylation of PI3K/Akt and ERK1/2 pathways associated with reduced expression of PGC-1α and PPARα. Likewise, expression of OXPHOS genes such as atp5O, cycs, cox5b, and ndufb5 was also reduced. Fn14 -/- mice showed significantly improved left ventricular function and PGC-1α levels after MI compared to their respective WT littermates (Fn14 +/+. Finally, inhibition of intrinsic TWEAK with anti-TWEAK antibodies resulted in improved left ventricular function and survival. Conclusions. TWEAK exerted maladaptive effects in mice after myocardial infarction most likely via direct effects on cardiomyocytes. Analysis of the potential mechanisms revealed that TWEAK reduced metabolic adaptations to increased cardiac workload by inhibition of PGC-1α.

  12. Multimodality cardiac imaging of a ventricular septal rupture post myocardial infarction: a case report

    Directory of Open Access Journals (Sweden)

    Dhaliwal Surinder

    2012-10-01

    Full Text Available Abstract Background Ventricular septal rupture (VSR, a mechanical complication following an acute myocardial infarction (MI, is thought to result from coagulation necrosis due to lack of collateral reperfusion. Although the gold standard test to confirm left-to-right shunting between ventricular cavities remains invasive ventriculography, two-dimensional transthoracic echocardiography (TTE with color flow Doppler and cardiac MRI (CMR are reliable tests for the non-invasive diagnosis of VSR. Case presentation A 62-year-old Caucasian female presented with a late case of a VSR post inferior MI diagnosed by multimodality cardiac imaging including TTE, CMR and ventriculography. Conclusion We review the presentation, diagnosis and management of VSR post MI.

  13. Off-Pump Repair of a Post Myocardial Infarction Ventricular Septal Defect

    Directory of Open Access Journals (Sweden)

    Feridoun Sabzi

    2014-01-01

    Full Text Available Refractory cardiogenic shock meant that traditional patch repairs requiring cardiopulmonary bypass would be poorly tolerated and external sandwich closure of post myocardial ventricular septal defect (VSD appears to be simple and effective after initial myocardial infarction (MI. The three cases presented with a VSD after of acute MI with or without thrombolysed with streptokinase during patient admission. The general condition of the three patients was poor with pulmonary edema, low cardiac output and renal failure. The heart was approached through a median sternotomy. Off-pump coronary artery bypass grafting of the coronary artery lesion was done first using octopus and beating heart surgery method and latero - lateral septal plication was performed using sandwich technique. Low cardiac output managed with intra-aortic balloon pump in these patients accompanied with inotropic drugs. Post-operative transesophageal echocardiography revealed that VSD was closed completely in one patient and in two patients small residual VSD remained. More experience is required to ascertain whether this technique will become an accepted alternative to patch repairs.

  14. Effects of interleukin-1 on cardiac fibroblast function: relevance to post-myocardial infarction remodelling.

    Science.gov (United States)

    Turner, Neil A

    2014-01-01

    The cardiac fibroblast (CF) is a multifunctional and heterogeneous cell type that plays an essential role in regulating cardiac development, structure and function. Following myocardial infarction (MI), the myocardium undergoes complex structural remodelling in an attempt to repair the damaged tissue and overcome the loss of function induced by ischemia/reperfusion injury. Evidence is emerging that CF play critical roles in all stages of post-MI remodelling, including the initial inflammatory phase that is triggered in response to myocardial damage. CF are particularly responsive to the proinflammatory cytokine interleukin-1 (IL-1) whose levels are rapidly induced in the myocardium after MI. Studies from our laboratory in recent years have sought to evaluate the functional effects of IL-1 on human CF function and to determine the underlying molecular mechanisms. This review summarises these data and sets it in the context of post-MI cardiac remodelling, identifying the fibroblast as a potential therapeutic target for reducing adverse cardiac remodelling and its devastating consequences. Copyright © 2013 Elsevier Inc. All rights reserved.

  15. Pitavastatin-attenuated cardiac dysfunction in mice with dilated cardiomyopathy via regulation of myocardial calcium handling proteins

    Directory of Open Access Journals (Sweden)

    Hu Wei

    2014-03-01

    Full Text Available C57BL/6 mice with dilated cardiomyopathy (DCM were randomly divided to receive placebo or pitavastatin at a dose of 1 or 3 mg kg-1d-1. After 8 weeks treatment, mice with dilated cardiomyopathy developed serious cardiac dysfunction characterized by significantly enhanced left ventricular end-diastolic diameter (LVIDd, decreased left ventricular ejection fraction (LVEF as well as left ventricular short axis fractional shortening (LVFS, accompanied with enlarged cardiomyocytes, and increased plasma levels of N-terminal pro-B type natriuretic peptide (NT-proBNP and plasma angiotensin II (AngII concentration. Moreover, myocardium sarcoplasmic reticulum Ca2+ pump (SERCA-2 activity was decreased. The ratio of phosphorylated phospholamban (PLB to total PLB decreased significantly with the down-regulation of SERCA- -2a and ryanodine receptor (RyR2 expression. Pitavastatin was found to ameliorate the cardiac dysfunction in mice with dilated cardiomyopathy by reversing the changes in the ratios of phosphorylated PLB to total PLB, SERCA-2a and RyR2 via reducing the plasma AngII concentration and the expressions of myocardium angiotensin II type 1 receptor (AT1R and protein kinase C (PKCb2. The possible underlying mechanism might be the regulation of myocardial AT1R-PKCb2-Ca2+ handling proteins.

  16. Degradation of cardiac myosin light chain kinase by matrix metalloproteinase-2 contributes to myocardial contractile dysfunction during ischemia/reperfusion.

    Science.gov (United States)

    Gao, Ling; Zheng, Yan-Jun; Gu, Shan-Shan; Tan, Ji-Liang; Paul, Christian; Wang, Yi-Gang; Yang, Huang-Tian

    2014-12-01

    Although ischemia/reperfusion (I/R)-induced myocardial contractile dysfunction is associated with a prominent decrease in myofilament Ca(2+) sensitivity, the underlying mechanisms have not yet been fully clarified. Phosphorylation of ventricular myosin light chain 2 (MLC-2v) facilitates actin-myosin interactions and enhances contractility, however, its level and regulation by cardiac MLC kinase (cMLCK) and cMLC phosphatase (cMLCP) in I/R hearts are debatable. In this study, the levels and/or effects of MLC-2v phosphorylation, cMLCK, cMLCP, and proteases during I/R were determined. Global myocardial I/R-suppressed cardiac performance in isolated rat hearts was concomitant with decreases of MLC-2v phosphorylation, myofibrillar Ca(2+)-stimulated ATPase activity, and cMLCK content, but not cMLCP proteins. Consistently, simulated I/R in isolated cardiomyocytes inhibited cell shortening, Ca(2+) transients, MLC-2v phosphorylation, and myofilament sensitivity to Ca(2+). These observations were reversed by cMLCK overexpression, while the specific cMLCK knockdown by short hairpin RNA (shRNA) had the opposite effect. Moreover, the inhibition of matrix metalloproteinase-2 (MMP-2, a zinc-dependent endopeptidase) reversed IR-decreased cMLCK, MLC-2v phosphorylation, myofibrillar Ca(2+)-stimulated ATPase activity, myocardial contractile function, and myofilament sensitivity to Ca(2+), while the inhibition or knockdown of cMLCK by ML-9 or specific shRNA abolished MMP-2 inhibition-induced cardioprotection. Finally, the co-localization in cardiomyocytes and interaction in vivo of MMP-2 and cMLCK were observed. Purified recombinant rat cMLCK was concentration- and time-dependently degraded by rat MMP-2 in vitro, and this was prevented by the inhibition of MMP-2. These findings reveal that the I/R-activated MMP-2 leads to the degradation of cMLCK, resulting in a reduction of MLC-2v phosphorylation, and myofibrillar Ca(2+)-stimulated ATPase activity, which subsequently suppresses

  17. Superiority of zinc complex of acetylsalicylic acid to acetylsalicylic acid in preventing postischemic myocardial dysfunction.

    Science.gov (United States)

    Korkmaz, Sevil; Atmanli, Ayhan; Li, Shiliang; Radovits, Tamás; Hegedűs, Peter; Barnucz, Enikő; Hirschberg, Kristóf; Loganathan, Sivakkanan; Yoshikawa, Yutaka; Yasui, Hiroyuki; Karck, Matthias; Szabó, Gábor

    2015-09-01

    The pathophysiology of ischemic myocardial injury involves cellular events, reactive oxygen species, and an inflammatory reaction cascade. The zinc complex of acetylsalicylic acid (Zn(ASA)2) has been found to possess higher anti-inflammatory and lower ulcerogenic activities than acetylsalicylic acid (ASA). Herein, we studied the effects of both ASA and Zn(ASA)2 against acute myocardial ischemia. Rats were pretreated with ASA (75 mg/kg) or Zn(ASA)2 (100 mg/kg) orally for five consecutive days. Isoproterenol (85 mg/kg, subcutaneously [s.c.]) was applied to produce myocardial infarction. After 17-22 h, animals were anesthetized with sodium pentobarbital (60 mg/kg, intraperitoneally [i.p.]) and both electrical and mechanical parameters of cardiac function were evaluated in vivo. Myocardial histological and gene expression analyses were performed. In isoproterenol-treated rats, Zn(ASA)2 treatment normalized significantly impaired left-ventricular contractility index (Emax 2.6 ± 0.7 mmHg/µL vs. 4.6 ± 0.5 mmHg/µL, P < 0.05), increased stroke volume (30 ± 3 µL vs. 50 ± 6 µL, P < 0.05), decreased systemic vascular resistance (7.2 ± 0.7 mmHg/min/mL vs. 4.2 ± 0.5 mmHg/min/mL, P < 0.05) and reduced inflammatory infiltrate into the myocardial tissues. ECG revealed a restoration of elevated ST-segment (0.21 ± 0.03 mV vs. 0.09 ± 0.02 mV, P < 0.05) and prolonged QT-interval (79.2 ± 3.2 ms vs. 69.5 ± 2.5 ms, P < 0.05) by Zn(ASA)2. ASA treatment did not result in an improvement of these parameters. Additionally, Zn(ASA)2 significantly increased the mRNA-expression of superoxide dismutase 1 (+73 ± 15%), glutathione peroxidase 4 (+44 ± 12%), and transforming growth factor (TGF)-β1 (+102 ± 22%). In conclusion, our data demonstrate that oral administration of zinc and ASA in the form of bis(aspirinato)zinc(II) complex is superior to ASA in preventing electrical

  18. Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats

    Science.gov (United States)

    El-Mas, Mahmoud M.; Abdel-Rahman, Abdel A.

    2015-01-01

    Evidence suggests that male rats are protected against the hypotensive and myocardial depressant effects of ethanol compared with females. We investigated whether E2 modifies the myocardial and oxidative effects of ethanol in male rats. Conscious male rats received ethanol (0.5, 1 or 1.5 g/kg i.v.) 30-min after E2 (1 μg/kg i.v.) or its vehicle (saline), and hearts were collected at the conclusion of hemodynamic measurements for ex vivo molecular studies. Ethanol had no effect in vehicle-treated rats, but it caused dose-related reductions in LV developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of rise in LV pressure (dP/dtmax) and systolic (SBP) and diastolic (DBP) blood pressures in E2-pretreated rats. These effects were associated with elevated (i) indices of reactive oxygen species (ROS), (ii) malondialdehyde (MDA) protein adducts, and (iii) phosphorylated death-associated protein kinase-3 (DAPK3), Akt, and extracellular signal-regulated kinases (ERK1/2). Enhanced myocardial antioxidant enzymes (heme oxygenase-1, catalase and aldehyde dehydrogenase 2) activities were also demonstrated. In conclusion, E2 promotes ethanol-evoked myocardial oxidative stress and dysfunction in male rats. The present findings highlight the risk of developing myocardial dysfunction in men who consume alcohol while receiving E2 for specific medical conditions. PMID:26111663

  19. Remote ischemic preconditioning mitigates myocardial and neurological dysfunction via K(ATP) channel activation in a rat model of hemorrhagic shock.

    Science.gov (United States)

    Hu, Xianwen; Yang, Zhengfei; Yang, Min; Qian, Jie; Cahoon, Jena; Xu, Jiefeng; Sun, Shijie; Tang, Wanchun

    2014-09-01

    Severe hemorrhagic shock and resuscitation is a state of global body ischemia and reperfusion that causes myocardial and cerebral dysfunction. We investigated whether remote ischemic preconditioning (RIPC) would reduce myocardial and cerebral ischemia and reperfusion injuries after hemorrhagic shock as the result of the K(ATP) channel activation. Twenty-one male rats were randomized into three groups: RIPC, RIPC with K(ATP) channel blocker, and control. Remote ischemic preconditioning was induced by four cycles of 5 min of limb ischemia followed by reperfusion for 5 min. Hemorrhagic shock was induced by removing 50% of the estimated total blood volume during an interval of 1 h. Thirty minutes after the completion of bleeding, the animals were reinfused with shed blood during the ensuing 30 min. The animals were monitored for 2 h and observed for an additional 72 h. Myocardial function was measured by echocardiography, and sublingual microcirculation was measured by a sidestream dark-field imaging device at baseline, 1 h after bleeding, 30 min after the completion of bleeding, 30 min after reinfusion, and hourly intervals thereafter. The survival and neurological function were evaluated at 12, 24, 48, and 72 h after reinfusion. At 2 h after reinfusion, ejection fraction and myocardial performance index were significantly better in the RIPC group than in the control group (P shock and resuscitation, RIPC mitigated myocardial and neurological dysfunction with improved survival by activation of the K(ATP) channel.

  20. The impact of dose of the angiotensin-receptor blocker valsartan on the post-myocardial infarction ventricular remodeling: study protocol for a randomized controlled trial

    Directory of Open Access Journals (Sweden)

    Cho Young-Rak

    2011-11-01

    Full Text Available Abstract Background Angiotensin-converting enzyme inhibitors and the angiotensin-receptor blocker valsartan ameliorate ventricular remodeling after myocardial infarction (MI. Based on previous clinical trials, a maximum clinical dose is recommended in practical guidelines. Yet, has not been clearly demonstrated whether the recommended dose is more efficacious compared to the lower dose that is commonly used in clinical practice. Method/Design Valsartan in post-MI remodeling (VALID is a randomized, open-label, single-blinded multicenter study designed to compare the efficacy of different clinical dose of valsartan on the post-MI ventricular remodeling. This study also aims to assess neurohormone change and clinical parameters of patients during the post-infarct period. A total of 1116 patients with left ventricular dysfunction following the first episode of acute ST-elevation MI are to be enrolled and randomized to a maximal tolerable dose (up to 320 mg/day or usual dose (80 mg/day of valsartan for 12 months in 2:1 ratio. Echocardiographic analysis for quantifying post-MI ventricular remodeling is to be conducted in central core laboratory. Clinical assessment and laboratory test are performed at fixed times. Discussion VALID is a multicenter collaborative study to evaluate the impact of dose of valsartan on the post-MI ventricular remodeling. The results of the study provide information about optimal dosing of the drug in the management of patients after MI. The results will be available by 2012. Trial registration NCT01340326

  1. Advanced glycation end products receptor RAGE controls myocardial dysfunction and oxidative stress in high-fat fed mice by sustaining mitochondrial dynamics and autophagy-lysosome pathway.

    Science.gov (United States)

    Yu, Yichi; Wang, Lei; Delguste, Florian; Durand, Arthur; Guilbaud, Axel; Rousselin, Clementine; Schmidt, Ann Marie; Tessier, Frédéric; Boulanger, Eric; Neviere, Remi

    2017-08-19

    Oxidative stress and mitochondrial dysfunction are recognized as major contributors of cardiovascular damage in diabetes and high fat diet (HFD) fed mice. Blockade of receptor for advanced glycation end products (RAGE) attenuates vascular oxidative stress and development of atherosclerosis. We tested whether HFD-induced myocardial dysfunction would be reversed in RAGE deficiency mice, in association with changes in oxidative stress damage, mitochondrial respiration, mitochondrial fission and autophagy-lysosomal pathway. Cardiac antioxidant capacity was upregulated in RAGE(-)/(-) mice under normal diet as evidenced by increased superoxide dismutase and sirtuin mRNA expressions. Mitochondrial fragmentation and mitochondrial fission protein Drp1 and Fis1 expressions were increased in RAGE(-)/(-) mice. Autophagy-related protein expressions and cathepsin-L activity were increased in RAGE(-)/(-) mice suggesting sustained autophagy-lysosomal flux. HFD induced mitochondrial respiration defects, cardiac contractile dysfunction, disrupted mitochondrial dynamics and autophagy inhibition, which were partially prevented in RAGE(-)/(-) mice. Our results suggest that cardioprotection against HFD in RAGE(-)/(-) mice include reactivation of autophagy, as inhibition of autophagic flux by chloroquine fully abrogated beneficial myocardial effects and its stimulation by rapamycin improved myocardial function in HFD wild type mice. As mitochondrial fission is necessary to mitophagy, increased fragmentation of mitochondrial network in HFD RAGE(-)/(-) mice may have facilitated removal of damaged mitochondria leading to better mitochondrial quality control. In conclusion, modulation of RAGE pathway may improve mitochondrial damage and myocardial dysfunction in HFD mice. Attenuation of cardiac oxidative stress and maintenance of healthy mitochondria population ensuring adequate energy supply may be involved in myocardial protection against HFD. Copyright © 2017. Published by Elsevier Inc.

  2. Dobutamine stress radionuclide ventriculography reveals silent myocardial dysfunction in Kawasaki disease

    Energy Technology Data Exchange (ETDEWEB)

    Hamamichi, Yuji; Ichida, Fukiko; Tsubata, Shinichi [Toyama Medical and Pharmaceutical Univ., Sugitani (Japan). Faculty of Medicine] (and others)

    2002-01-01

    Dobutamine (DOB) stress radionuclide ventriculography (RVG) is proposed for evaluating left ventricular performance in patients with Kawasaki disease (KD). Dobutamine stress RVG, up to 15{mu}g{center_dot}kg{sup -1}{center_dot}min{sup -1}, was performed in 40 patients with a history of KD, some of whom had a perfusion defect (PD group) on dipyridamole stress thallium-201 myocardial imaging, some of whom had no perfusion defects (NPD group), and some of whom had no coronary artery lesions (C group). No significant differences in either systolic or diastolic indices of the left ventricle at rest were observed between the 3 groups. Although hemodynamic responses were similar in all patients after DOB stress, early diastolic index of the first third filling fraction decreased only in the PD group and was significantly lower in this group compared with the C group (p<0.01). The asynchrony index increased significantly in those patients with coronary stenosis after DOB stress (p<0.05). No serious side-effects were observed during the study. Even late after onset, patients with myocardial ischemia as a result of KD still had impaired early diastolic filling and asynchronous relaxation of the left ventricle. As an alternative to exercise testing, DOB stress RVG is a safe and promising means for serially evaluating left ventricular performance in patients with KD. (author)

  3. Quantitative analysis of myocardial glucose utilization in patients with left ventricular dysfunction by means of {sup 18}F-FDG dynamic positron tomography and three-compartment analysis

    Energy Technology Data Exchange (ETDEWEB)

    Morita, Koichi; Yoshinaga, Keiichiro; Mabuchi, Megumi; Kageyama, Hiroyuki; Shiga, Tohru; Tamaki, Nagara [Hokkaido University Graduate School of Medicine, Department of Nuclear Medicine, Kita-ku, Sapporo (Japan); Katoh, Chietsugu; Kuge, Yuji [Hokkaido University Graduate School of Medicine, Department of Tracer Kinetics, Kita-ku, Sapporo (Japan); Noriyasu, Kazuyuki; Tsukamoto, Takahiro [Hokkaido University Graduate School of Medicine, Department of Cardiovascular Medicine, Kita-Ku, Sapporo (Japan)

    2005-07-01

    Myocardial glucose utilization (MGU) is altered in various heart diseases. The aim of this study was to quantitatively assess regional myocardial glucose utilization in patients with left ventricular (LV) dysfunction by dynamic{sup 18}F-fluorodeoxyglucose positron emission tomography (FDG PET). A total of 18 subjects were studied, including ten with LV dysfunction (seven with idiopathic dilated cardiomyopathy and three with aortic regurgitation; NYHA II in 8 and III in 2) and eight healthy normal volunteers. Patients with diabetes mellitus were excluded. A dynamic PET study was performed for 40 min following the injection of 370 MBq of FDG after 50-g glucose loading. On the basis of a three-compartment model, MGU, K{sub 1}, k{sub 2}, and k{sub 3} were computed on a pixel by pixel basis to generate LV myocardial parametric maps. FDG standardized uptake value (SUV) was also calculated using static images obtained 40 min after FDG injection. These metabolic values were compared with myocardial flow distribution (%Flow), LVEF, LV volumes, and LV wall thickening (WT) determined by gated myocardial single-photon emission computed tomography using QGS software in eight myocardial segments. MGU correlated positively with LV volumes and negatively with LVEF. K{sub 1} was significantly higher in the segments of the patients than in those of the normal volunteers (0.082{+-}0.055 vs 0.041{+-}0.017 ml min{sup -1} g{sup -1}, p<0.05), although there was no difference in MGU between the groups. On the other hand, SUV, k{sub 2}, and k{sub 3} did not differ significantly between the groups. Among the patients, the K{sub 1} values were significantly higher in the areas with impaired WT (%WT<17%) (0.109{+-}0.063 vs 0.069{+-}0.062 ml min{sup -1} g{sup -1}, p<0.05) and in the areas with flow reduction (%Flow<71%) (0.112{+-}0.076 vs 0.071{+-}0.046 ml min{sup -1} g{sup -1}, p<0.05). These results indicate that glucose utilization was preserved in the patients with LV dysfunction, mainly

  4. Eplerenone survival benefits in heart failure patients post-myocardial infarction are independent from its diuretic and potassium-sparing effects. Insights from an EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) substudy

    DEFF Research Database (Denmark)

    Rossignol, Patrick; Ménard, Joël; Fay, Renaud

    2011-01-01

    The purpose of this study was to determine whether a diuretic effect may be detectable in patients treated with eplerenone, a mineralocorticoid receptor antagonist, as compared with placebo during the first month of EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and S...

  5. Eplerenone survival benefits in heart failure patients post-myocardial infarction are independent from its diuretic and potassium-sparing effects. Insights from an EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) substudy

    DEFF Research Database (Denmark)

    Rossignol, Patrick; Ménard, Joël; Fay, Renaud;

    2011-01-01

    The purpose of this study was to determine whether a diuretic effect may be detectable in patients treated with eplerenone, a mineralocorticoid receptor antagonist, as compared with placebo during the first month of EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy...

  6. Device closure of post-myocardial infarction ventricular septal defect three weeks after coronary angioplasty

    Science.gov (United States)

    Patnaik, A. N.; Barik, Ramachandra; Kumari, N. Rama; Gulati, A. S.

    2012-01-01

    Percutaneus device closure appears to be safe and effective in patients treated for a residual shunt after initial surgical closure, as well as after two to three weeks of index myocardial infarction. The index case presented with a ventricular septal defect on second of acute myocardial infarction thrombolysed with streptokinase. The general condition of the patient was fairly stable. Cardiac catheterization and coronary angiography showed significant left to right shunt and there was 90 % proximal stenosis of left anterior descending coronary artery. Other coronary arteries were normal. Angioplasty and stenting to the coronary artery lesion was done using drug eluting stent (DES) with very good angiographic result. Patient was discharged after four days in stable condtion. After 3 weeks his ventricular septal defect was closed percutaneusly using cardio -O-fix device with tiny residual shunt. The procedure was uneventful and of brief duration. He was discharged after 5 days of the post procedure in very stable condition with minimal residual shunt. A staged procedure is a better option if the condition of the patient allows strengthening ventricular septal defect border. PMID:22629038

  7. Noninvasive Evaluation of Myocardial Systolic Dysfunction in the Early Stage of Kawasaki Disease: A Speckle-Tracking Echocardiography Study.

    Science.gov (United States)

    Hematian, Mohammad-Nasir; Torabi, Shirin; MalaKan-Rad, Elaheh; Sayadpour-Zanjani, Keyhan; Ziaee, Vahid; Lotfi-Tolkaldany, Masoumeh

    2015-06-01

    Evaluation of myocardial function by speckle-tracking echocardiography is a new method for the early diagnosis of systolic dysfunction. We aimed to determine myocardial speckle-tracking echocardiography indices in Kawasaki Disease (KD) patients and compare them with the same indices in control subjects. Thirty-two patients (65.5% males) with KD and 19 control subjects with normal echocardiography participated in this study. After their demographic characteristics and clinical findings were recorded, all the participants underwent transthoracic echocardiography. Strain (S), Strain Rate (SR), Time to Peak Strain (TPS), and Strain Rate (TPSR), longitudinal velocity and view point velocity images in the two, three, and four-chamber views were semi-automatically obtained via speckle-tracking echocardiography. Among the patients, Twenty-four cases (75%) were younger than 4 years. Mean global S and SR was significantly reduced in the KD patients compared to controls (17.03 ± 1.28 vs. 20.22 ± 2.14% and 1.66 ± 0.16 vs. 1.97 ± 0.25 1/second, respectively), while there were no significant differences regarding mean TPS, TPSR, longitudinal velocity and view point velocity. Using repeated measure of analysis of variances, we observed that S and SR decreased from base to apical level in both groups. The change in the pattern of age adjusted mean S and SR across levels was significantly different between the groups (P < 0.001 for both parameters). We showed changes in S and SR assessed in KD patients versus control subjects in the acute phase of KD. However, we suggest that further studies be undertaken to compare S and SR in the acute phase and thereafter in KD patients.

  8. Risk of Cardiovascular Death in the Remote Period after Myocardial Revascularization and in Association with Renal Dysfunction

    Directory of Open Access Journals (Sweden)

    Ekaterina S. Levitskaya

    2016-03-01

    Full Text Available The aim of the present study was to assess the effectiveness of standard medical therapy in lowering the risk of cardiovascular death (rCVD in the remote period after myocardial revascularization (MR, taking into account the presence of renal dysfunction (RD. Material and Methods: The study included 90 patients with coronary heart disease (CHD and indications for revascularization. We evaluated a drug therapy obtained at different stages of revascularization, as well as the severity of patients’ condition and the prevalence of RD. Results: In the remote period after MR (5.8±0.05 years, 71/78.9% patients participated in the study; death occurred in 10/12.3% patients. The duration of therapy for chronic myocardial ischemia before MR (P=0.005, as well as compliance with prescribed therapy during 6 months (P=0.008 after this procedure, affected CVD in the remote period after MR. Using statins before MR reduced rCVD by 17.2% (P=0.01, beta-blockers -14.95% (P=0.04, and ACE inhibitors (ACEIs - 15.75% (P=0.03. The lack of regular use of acetylsalicylic acid (ASA for 6 months after RM was associated with an increase in rCVD up to 36.2% (P=0.005. Statins and ACEIs are drugs that reduce rCVD in the presence of RD (P<0.05. Conclusion: An efficient drug regimen for patients after MR is important in reducing a long-term prognosis of CVD and for an efficient correction of coronary artery patency.

  9. Impact of post myocardial infarction depression on drug adherence of cardiological medicines

    Directory of Open Access Journals (Sweden)

    Hemanta Dutta

    2015-07-01

    Full Text Available Background: Depressive symptoms are very usual in patients experiencing a history of myocardial infarction (MI. An individual who has developed depression after an episode of MI becomes non compliant with the treatment of cardiology. Aim: To test the impact of post MI depression on drug adherence of cardiological medicines. Settings and design: The study was conducted on patients of acute MI (n=50 attending cardiology outpatient department (OPD of Assam Medical College and Hospital, Dibrugarh at eight weeks after the index event. Methods: Screening was performed by the Primary Care Evaluation of Mental Disorders (PRIME-MD and diagnoses of major depressive disorder were established according to the text revision of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR criteria. The eight-item Morisky Medication Adherence Questionnaire was applied to the patients to assess drug adherence after eight weeks from the MI episode. Results: Statistically significant strong association and correlation were found between post MI depression and drug adherence of cardiological medicines (Wald 9.84, Odd’s ratio 2.054, p=0.002, rho=0.714. Conclusion: The result of analysis has revealed that post MI depression has an unfavourable impact on drug adherence, ultimately contributing to increased risk of cardiological morbidity and death rate. Therefore, routine screening of depressive symptoms should be mandatory in cardiology.

  10. Post-operative cognitive dysfunction in the elderly: A prospective clinical study

    Directory of Open Access Journals (Sweden)

    Nalini Kotekar

    2014-01-01

    Full Text Available Background and Aims: Aging population is a major demographic trend worldwide. Globally, 50% of all the elderly individuals are estimated to undergo atleast one surgical procedure and post-operative cognitive dysfunction (POCD is one of the most common and often poorly understood post-operative complications in this section of the population. This randomised prospective study was conducted to assess the post-operative cognitive status in the elderly undergoing non-cardiac surgery, evaluate the cognitive parameters affected, evaluate the potential risk factors and thereby analyse the potential for implementation of preventive strategies. Methods: This study was conducted on 200 patients aged 60 years or older scheduled for elective non-cardiac surgeries. The baseline cognitive status of the patients was assessed 2 days prior to the date of the surgery. The post-operative cognitive status was assessed on the 3 rd day, 7 th day and after 1 month. Statistical analysis was performed using SAS and SPSS. Results: The incidence of POCD showed a gradual decline from postoperative day 3 to 30. Females were found to be at significant risk in developing POCD. Advancing age and level of education emerged as dominant factors, while type of anaesthesia, duration of surgery, and presence of coexisting comorbidities had no influence on the incidence of cognitive dysfunction. Conclusion: POCD is a definite complication after surgery and anaesthesia in the elderly population. Gender emerged as a significant risk factor with increasing age as a dominating factor contributing to POCD.

  11. Efficacy of post-operative clopidogrel treatment in patients revascularized with coronary artery bypass grafting after myocardial infarction

    DEFF Research Database (Denmark)

    Sørensen, Rikke; Abildstrøm, Steen Z; Hansen, Peter R

    2011-01-01

    OBJECTIVES: The objective of this study was to examine the clinical efficacy of clopidogrel treatment on death and recurrent myocardial infarction (MI) among MI patients revascularized by coronary artery bypass graft surgery (CABG). BACKGROUND: The benefit from post-operative clopidogrel in CABG-...

  12. A systematic review: effect of angiotensin converting enzyme inhibition on left ventricular volumes and ejection fraction in patients with a myocardial infarction and in patients with left ventricular dysfunction

    DEFF Research Database (Denmark)

    Abdulla, Jawdat; Barlera, Simona; Latini, Roberto;

    2006-01-01

    BACKGROUND AND AIM: To summarize and quantify results of echocardiographic studies examining the effect of angiotensin converting enzyme (ACE) inhibition on left ventricular remodelling in patients with acute myocardial infarction (MI) and in patients with left ventricular systolic dysfunction...

  13. Effect of the angiotensin-converting enzyme inhibitor trandolapril on mortality and morbidity in diabetic patients with left ventricular dysfunction after acute myocardial infarction. Trace Study Group

    DEFF Research Database (Denmark)

    Gustafsson, I; Torp-Pedersen, C; Køber, L;

    1999-01-01

    OBJECTIVES: This study evaluated the efficacy of long-term treatment with the angiotensin-converting enzyme (ACE) inhibitor trandolapril in diabetic patients with left ventricular dysfunction after acute myocardial infarction (AMI). BACKGROUND: Patients with diabetes mellitus have a high mortality...... following AMI, probably due to a high risk of congestive heart failure and reinfarction. Because ACE inhibition effectively reduces progression of heart failure, it could be particularly beneficial in diabetic patients after AMI. METHODS: The study is a retrospective analysis using data from.......21 to 0.67]), and no significant reduction of this end point was found in the nondiabetic group. CONCLUSIONS: The ACE inhibition after myocardial infarction complicated by left ventricular dysfunction appears to be of considerable importance in patients with diabetes mellitus by saving lives...

  14. Post-transcriptional gene regulation by RNA-binding proteins in vascular endothelial dysfunction.

    Science.gov (United States)

    Xin, HongBo; Deng, KeYu; Fu, MinGui

    2014-08-01

    Endothelial cell dysfunction is a term which implies the dysregulation of normal endothelial cell functions, including impairment of the barrier functions, control of vascular tone, disturbance of proliferative and migratory capacity of endothelial cells, as well as control of leukocyte trafficking. Endothelial dysfunction is an early step in vascular inflammatory diseases such as atherosclerosis, diabetic vascular complications, sepsis-induced or severe virus infection-induced organ injuries. The expressions of inflammatory cytokines and vascular adhesion molecules induced by various stimuli, such as modified lipids, smoking, advanced glycation end products and bacteria toxin, significantly contribute to the development of endothelial dysfunction. The transcriptional regulation of inflammatory cytokines and vascular adhesion molecules has been well-studied. However, the regulation of those gene expressions at post-transcriptional level is emerging. RNA-binding proteins have emerged as critical regulators of gene expression acting predominantly at the post-transcriptional level in microRNA-dependent or independent manners. This review summarizes the latest insights into the roles of RNA-binding proteins in controlling vascular endothelial cell functions and their contribution to the pathogenesis of vascular inflammatory diseases.

  15. Detection of Left Ventricular Regional Dysfunction and Myocardial Abnormalities Using Complementary Cardiac Magnetic Resonance Imaging in Patients with Systemic Sclerosis without Cardiac Symptoms: A Pilot Study.

    Science.gov (United States)

    Kobayashi, Yasuyuki; Kobayashi, Hitomi; T Giles, Jon; Yokoe, Isamu; Hirano, Masaharu; Nakajima, Yasuo; Takei, Masami

    2016-01-01

    Objective We sought to detect the presence of left ventricular regional dysfunction and myocardial abnormalities in systemic sclerosis (SSc) patients without cardiac symptoms using a complementary cardiac magnetic resonance (CMR) imaging approach. Methods Consecutive patients with SSc without cardiac symptoms and healthy controls underwent CMR on a 1.5 T scanner. The peak systolic regional function in the circumferential and radial strain (Ecc, % and Err, %) were calculated using a feature tracking analysis on the mid-left ventricular slices obtained with cine MRI. In addition, we investigated the myocardial characteristics by contrast MRI. Pharmacological stress and rest perfusion scans were performed to assess perfusion defect (PD) due to micro- or macrovascular impairment, and late gadolinium enhancement (LGE) images were obtained for the assessment of myocarditis and/or fibrosis. Results We compared 15 SSc patients with 10 healthy controls. No statistically significant differences were observed in the baseline characteristics between the patients and healthy controls. The mean peak Err and Ecc of all segments was significantly lower in the patients than the controls (p=0.011 and p=0.003, respectively). Four patients with LGE (28.6%) and seven patients with PD (50.0%) were observed. PD was significantly associated with digital ulcers (p=0.005). Utilizing a linear regression model, the presence of myocardial LGE was significantly associated with the peak Ecc (p=0.024). After adjusting for age, the association between myocardial LGE and the peak Ecc was strengthened. Conclusion A subclinical myocardial involvement, as detected by CMR, was prevalent in the SSc patients without cardiac symptoms. Regional dysfunction might predict the myocardial abnormalities observed in SSc patients without cardiac symptoms.

  16. Induction of Myocardial PDCD4 in Coronary Microembolization-Related Cardiac Dysfunction: Evidence from a Large-Animal Study

    Directory of Open Access Journals (Sweden)

    Qiang Su

    2014-08-01

    Full Text Available Background/Aims: Coronary microembolization (CME has been linked to myocardial inflammation and apoptosis. This study aims to investigate the role of the apoptotic protein PDCD4 in the myocardium after CME in minipigs. Methods: Seventy Bama minipigs were randomized into four groups: control, CME, CME plus PDCD4-siRNA and CME plus control siRNA. CME was induced by injecting polyethylene microspheres into the left anterior descending artery. Cardiac function was evaluated. HE and HBFP staining were used to observe the degree of infarction. Western blotting and qPCR were used to evaluate the expression of PDCD4, TNF-α and caspase-3. The measurements were performed at 0, 3, 6, 9, 12 and 24 h after CME modeling in the CME and control groups. Results: Cardiac function in the CME group was significantly decreased compared with the control group (P0.05. Furthermore, PDCD4-siRNA improved cardiac function and reduced PDCD4 and TNF-α expression compared with the CME plus control siRNA group at 9 h after modeling (P Conclusion: PDCD4 induction may be involved in CME-related cardiac dysfunction, and PDCD4 inhibition via siRNA may attenuate the cardiac impairment and be used as a treatment strategy for CME.

  17. Parathyroid hormone-related protein (PTHrP) signal cascade modulates myocardial dysfunction in the pressure overloaded heart.

    Science.gov (United States)

    Meyer, Rainer; Schreckenberg, Rolf; Kretschmer, Frank; Bittig, Anne; Conzelmann, Charlotte; Grohé, Christian; Schlüter, Klaus-Dieter

    2007-12-01

    Pressure overload induces the cardiac expression of parathyroid hormone-related protein (PTHrP). Plasma levels are elevated in patients with heart disease. It is unknown whether this represents an epiphenomenon or suggests involvement in hypertrophy. To identify a potential role of PTHrP in pressure induced hypertrophy and heart failure. Pressure load was produced via thoracic aortic constriction (TAC) and application of a PTHrP antagonist (PTHrP(7-34)) via osmotic minipumps in mice. Main findings were confirmed in vitro by exposing isolated adult ventricular mice cardiomyocytes to PTHrP(1-34) (100 nmol/l). TAC treated animals developed myocardial hypertrophy within 2 weeks. The heart weight to body weight ratio increased from 5.02+/-0.14 mg/g (sham/vehicle) and 5.16+/-0.19 mg/g (sham/antagonist) to 6.59+/-0.85 mg/g (TAC/vehicle) and 7.07+/-0.80 mg/g (TAC/antagonist) (each n=6-8; pPTHrP(1-34) developed reduced cell shortening. This reduction in cell function was abolished in the co-presence of the antagonist. PTHrP contributes to the progression of cardiac dysfunction in the pressure overloaded heart.

  18. Post-Weaning Protein Malnutrition Increases Blood Pressure and Induces Endothelial Dysfunctions in Rats

    Science.gov (United States)

    Siman, Fabiana D. M.; Silveira, Edna A.; Meira, Eduardo F.; da Costa, Carlos P.; Vassallo, Dalton V.; Padilha, Alessandra S.

    2012-01-01

    Malnutrition during critical periods in early life may increase the subsequent risk of hypertension and metabolic diseases in adulthood, but the underlying mechanisms are still unclear. We aimed to evaluate the effects of post-weaning protein malnutrition on blood pressure and vascular reactivity in aortic rings (conductance artery) and isolated-perfused tail arteries (resistance artery) from control (fed with Labina®) and post-weaning protein malnutrition rats (offspring that received a diet with low protein content for three months). Systolic and diastolic blood pressure and heart rate increased in the post-weaning protein malnutrition rats. In the aortic rings, reactivity to phenylephrine (10−10–3.10−4 M) was similar in both groups. Endothelium removal or L-NAME (10−4 M) incubation increased the response to phenylephrine, but the L-NAME effect was greater in the aortic rings from the post-weaning protein malnutrition rats. The protein expression of the endothelial nitric oxide isoform increased in the aortic rings from the post-weaning protein malnutrition rats. Incubation with apocynin (0.3 mM) reduced the response to phenylephrine in both groups, but this effect was higher in the post-weaning protein malnutrition rats, suggesting an increase of superoxide anion release. In the tail artery of the post-weaning protein malnutrition rats, the vascular reactivity to phenylephrine (0.001–300 µg) and the relaxation to acetylcholine (10−10–10−3 M) were increased. Post-weaning protein malnutrition increases blood pressure and induces vascular dysfunction. Although the vascular reactivity in the aortic rings did not change, an increase in superoxide anion and nitric oxide was observed in the post-weaning protein malnutrition rats. However, in the resistance arteries, the increased vascular reactivity may be a potential mechanism underlying the increased blood pressure observed in this model. PMID:22529948

  19. Post-weaning protein malnutrition increases blood pressure and induces endothelial dysfunctions in rats.

    Science.gov (United States)

    de Belchior, Aucelia C S; Angeli, Jhuli K; Faria, Thaís de O; Siman, Fabiana D M; Silveira, Edna A; Meira, Eduardo F; da Costa, Carlos P; Vassallo, Dalton V; Padilha, Alessandra S

    2012-01-01

    Malnutrition during critical periods in early life may increase the subsequent risk of hypertension and metabolic diseases in adulthood, but the underlying mechanisms are still unclear. We aimed to evaluate the effects of post-weaning protein malnutrition on blood pressure and vascular reactivity in aortic rings (conductance artery) and isolated-perfused tail arteries (resistance artery) from control (fed with Labina®) and post-weaning protein malnutrition rats (offspring that received a diet with low protein content for three months). Systolic and diastolic blood pressure and heart rate increased in the post-weaning protein malnutrition rats. In the aortic rings, reactivity to phenylephrine (10(-10)-3.10(-4) M) was similar in both groups. Endothelium removal or L-NAME (10(-4) M) incubation increased the response to phenylephrine, but the L-NAME effect was greater in the aortic rings from the post-weaning protein malnutrition rats. The protein expression of the endothelial nitric oxide isoform increased in the aortic rings from the post-weaning protein malnutrition rats. Incubation with apocynin (0.3 mM) reduced the response to phenylephrine in both groups, but this effect was higher in the post-weaning protein malnutrition rats, suggesting an increase of superoxide anion release. In the tail artery of the post-weaning protein malnutrition rats, the vascular reactivity to phenylephrine (0.001-300 µg) and the relaxation to acetylcholine (10(-10)-10(-3) M) were increased. Post-weaning protein malnutrition increases blood pressure and induces vascular dysfunction. Although the vascular reactivity in the aortic rings did not change, an increase in superoxide anion and nitric oxide was observed in the post-weaning protein malnutrition rats. However, in the resistance arteries, the increased vascular reactivity may be a potential mechanism underlying the increased blood pressure observed in this model.

  20. Post-weaning protein malnutrition increases blood pressure and induces endothelial dysfunctions in rats.

    Directory of Open Access Journals (Sweden)

    Aucelia C S de Belchior

    Full Text Available Malnutrition during critical periods in early life may increase the subsequent risk of hypertension and metabolic diseases in adulthood, but the underlying mechanisms are still unclear. We aimed to evaluate the effects of post-weaning protein malnutrition on blood pressure and vascular reactivity in aortic rings (conductance artery and isolated-perfused tail arteries (resistance artery from control (fed with Labina® and post-weaning protein malnutrition rats (offspring that received a diet with low protein content for three months. Systolic and diastolic blood pressure and heart rate increased in the post-weaning protein malnutrition rats. In the aortic rings, reactivity to phenylephrine (10(-10-3.10(-4 M was similar in both groups. Endothelium removal or L-NAME (10(-4 M incubation increased the response to phenylephrine, but the L-NAME effect was greater in the aortic rings from the post-weaning protein malnutrition rats. The protein expression of the endothelial nitric oxide isoform increased in the aortic rings from the post-weaning protein malnutrition rats. Incubation with apocynin (0.3 mM reduced the response to phenylephrine in both groups, but this effect was higher in the post-weaning protein malnutrition rats, suggesting an increase of superoxide anion release. In the tail artery of the post-weaning protein malnutrition rats, the vascular reactivity to phenylephrine (0.001-300 µg and the relaxation to acetylcholine (10(-10-10(-3 M were increased. Post-weaning protein malnutrition increases blood pressure and induces vascular dysfunction. Although the vascular reactivity in the aortic rings did not change, an increase in superoxide anion and nitric oxide was observed in the post-weaning protein malnutrition rats. However, in the resistance arteries, the increased vascular reactivity may be a potential mechanism underlying the increased blood pressure observed in this model.

  1. Activation of SHH signaling pathway promotes vasculogenesis in post-myocardial ischemic-reperfusion injury.

    Science.gov (United States)

    Guo, Wei; Yi, Xin; Ren, Faxin; Liu, Liwen; Wu, Suning; Yang, Jun

    2015-01-01

    This study aimed to investigate the potential roles of sonic Hedgehog (SHH) expression in vasculogenesis in post-myocardial ischemic-reperfusion injury (MIRI) and its underlying mechanism. Cardiac microvascular endothelial cells (CMECs) isolated from the SD rat hearts tissues were used to construct the MIRI model. mRNA level of SHH in control cells and MIRI cells was detected using RT-PCR analysis. Furthermore, effects of SHH expression on CMECs viability and apoptosis were analyzed using MTT assay and Annexin-V-FITC kit respectively. Moreover, effects of SHH expression on the pathway signal proteins expression was analyzed using ELISA and western blotting. mRNA level of SHH was significantly decreased compared to the controls (PSHH application compared with the controls (PSHH application, as well as the SHH signal proteins including Patch-1, Gli1, Gli2 and SMO (PSHH application on biological factors levels were reversed by the SHH inhibitor application. This study suggested that SHH over expression may play a pivotal contribute role in vasculogenesis through activating the SHH signals in post-MIRI.

  2. [A case of rupture of the left ventricle free wall with papillary muscle dysfunction following acute myocardial infarction, operated on successfully].

    Science.gov (United States)

    de Lima, R; Perdigão, C; Neves, L; Cravino, J; Dantas, M; Bordalo, A; Pais, F; Diogo, A N; Ferreira, R; Ribeiro, C

    1990-09-01

    The authors present a case of left ventricular free wall rupture post acute myocardial infarction, associated with mitral papillary posterior muscle necrosis, operated by infartectomy and mitral valvular protesis replacement. They refer the various complications occurred during the hospital staying, and discuss its medical and surgical approach. The patient was discharged alive and six months after the infarction keeps a moderate activity.

  3. Cardiac structure and function, remodeling, and clinical outcomes among patients with diabetes after myocardial infarction complicated by left ventricular systolic dysfunction, heart failure, or both

    DEFF Research Database (Denmark)

    Shah, Amil M; Hung, Chung-Lieh; Shin, Sung Hee

    2011-01-01

    The mechanisms responsible for the increased risk of heart failure (HF) post-myocardial infarction (MI) may differ between patients with versus without diabetes. We hypothesized that after high-risk MI, patients with diabetes would demonstrate patterns of remodeling that are suggestive of reduced...

  4. Erectile dysfunction post-radical prostatectomy – a challenge for both patient and physician

    Science.gov (United States)

    Bratu, O; Oprea, I; Marcu, D; Spinu, D; Niculae, A; Geavlete, B; Mischianu, D

    2017-01-01

    Post-radical prostatectomy erectile dysfunction (post RP ED) is a major postoperative complication with a great impact on the quality of life of the patients. Until present, no proper algorithm or guideline based on the clinical trials has been established for the management of post RP ED. According to literature, it is better to initiate a penile rehabilitation program as soon as possible after surgery than doing nothing, in order to prevent and limit the postoperative local hypoxygenation and fibrosis. The results of numerous clinical trials regarding the effectiveness of the phosphodiesterase 5 inhibitors therapy on post RP ED have made them the gold standard treatment. Encouraging results have been achieved in studies with vacuum erectile devices, intraurethral suppositories with alprostadil and intracavernosal injections, but due to their side effects, especially in the cases of intracavernosal injections and intraurethral suppositories, their clinical use was limited therefore making them a second line option for the post RP ED treatment. What should not be forgotten is that penile implant prosthesis has proven very effective, numerous studies confirming high rates of satisfaction for both patients and partners. PMID:28255370

  5. Cobalt Chloride Upregulates Impaired HIF-1α Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats

    Science.gov (United States)

    Wu, Jianjiang; Yang, Long; Xie, Peng; Yu, Jin; Yu, Tian; Wang, Haiying; Maimaitili, Yiliyaer; Wang, Jiang; Ma, Haiping; Yang, Yining; Zheng, Hong

    2017-01-01

    Previous studies from our group have demonstrated that sevoflurane post-conditioning (SPC) protects against myocardial ischemia reperfusion injury via elevating the intranuclear expression of hypoxia inducible factor-1 alpha (HIF-1α). However, diabetic SPC is associated with decreased myocardial protection and disruption of the HIF-1 signaling pathway. Previous studies have demonstrated that cobalt chloride (CoCl2) can upregulate HIF-1α expression under diabetic conditions, but whether myocardial protection by SPC can be restored afterward remains unclear. We established a rat model of type 2 diabetes and a Langendorff isolated heart model of ischemia-reperfusion injury. Prior to reperfusion, 2.4% sevoflurane was used as a post-conditioning treatment. The diabetic rats were treated with CoCl2 24 h before the experiment. At the end of reperfusion, tests were performed to assess myocardial function, infarct size, mitochondrial morphology, nitric oxide (NO), Mitochondrial reactive oxygen species (ROS), mitochondrial respiratory function and enzyme activity, HIF-1α, vascular endothelial growth factor (VEGF) and endothelial NO synthase (eNOS) protein levels. In addition, myocardial protection by SPC was monitored after the blood glucose levels were lowered by insulin. The diabetic state was associated with deficient SPC protection and decreased HIF-1α expression. After treating the diabetic rats with CoCl2, SPC significantly upregulated the expression of HIF-1α, VEGF and eNOS, which markedly improved cardiac function, NO, mitochondrial respiratory function, and enzyme activity and decreased the infarction areas and ROS. In addition, these effects were not influenced by blood glucose levels. This study proved that CoCl2activates the HIF-1α signaling pathway, which restores SPC-dependent myocardial protection under diabetic conditions, and the protective effects of SPC were independent of blood glucose levels. PMID:28659817

  6. ECG marker of adverse electrical remodeling post-myocardial infarction predicts outcomes in MADIT II study.

    Directory of Open Access Journals (Sweden)

    Larisa G Tereshchenko

    Full Text Available BACKGROUND: Post-myocardial infarction (MI structural remodeling is characterized by left ventricular dilatation, fibrosis, and hypertrophy of the non-infarcted myocardium. OBJECTIVE: The goal of our study was to quantify post-MI electrical remodeling by measuring the sum absolute QRST integral (SAI QRST. We hypothesized that adverse electrical remodeling predicts outcomes in MADIT II study participants. METHODS: Baseline orthogonal ECGs of 750 MADIT II study participants (448 [59.7%] ICD arm were analyzed. SAI QRST was measured as the arithmetic sum of absolute QRST integrals over all three orthogonal ECG leads. The primary endpoint was defined as sudden cardiac death (SCD or sustained ventricular tachycardia (VT/ventricular fibrillation (VF with appropriate ICD therapies. All-cause mortality served as a secondary endpoint. RESULTS: Adverse electrical remodeling in post-MI patients was characterized by wide QRS, increased magnitudes of spatial QRS and T vectors, J-point deviation, and QTc prolongation. In multivariable Cox regression analysis after adjustment for age, QRS duration, atrial fibrillation, New York Heart Association heart failure class and blood urea nitrogen, SAI QRST predicted SCD/VT/VF (HR 1.33 per 100 mV*ms (95%CI 1.11-1.59; P = 0.002, and all-cause death (HR 1.27 per 100 mV*ms (95%CI 1.03-1.55, P = 0.022 in both arms. No interaction with therapy arm and bundle branch block (BBB status was found. CONCLUSIONS: In MADIT II patients, increased SAI QRST is associated with increased risk of sustained VT/VF with appropriate ICD therapies and all-cause death in both ICD and in conventional medical therapy arms, and in patients with and without BBB. Further studies of SAI QRST are warranted.

  7. Relation between preoperative renal dysfunction and cardiovascular events (stroke, myocardial infarction, or heart failure or death) within three months of isolated coronary artery bypass grafting.

    Science.gov (United States)

    Holzmann, Martin J; Sartipy, Ulrik

    2013-11-01

    Renal dysfunction is related to long-term mortality and myocardial infarction after coronary artery bypass grafting (CABG). We aimed to investigate the association between preoperative renal dysfunction and early risk of stroke, myocardial infarction, or heart failure after CABG. From the Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies registry, we included all 36,284 patients who underwent primary isolated CABG from 2000 to 2008 in Sweden. The Swedish National Inpatient Registry was used to obtain the primary end point, which was rehospitalization for stroke, myocardial infarction, or heart failure ≤90 days after CABG. Logistic regression models were used to estimate the risk for the primary outcome and the secondary outcome of death from any cause, while adjusting for confounders. During 90 days of follow-up, there were 2,462 cardiovascular events and 617 deaths. In total, 17% of patients developed acute kidney injury postoperatively. Odds ratios with 95% confidence intervals for cardiovascular events after adjustment for age, gender, atrial fibrillation, left ventricular ejection fraction, diabetes mellitus, peripheral vascular disease, and history of myocardial infarction, heart failure, or stroke was 1.24 (1.06 to 1.45) in patients with an estimated glomerular filtration rate of 15 to 45 ml/min/1.73 m(2) but became nonsignificant after acute kidney injury was introduced into the statistical model. The risk of death was significantly increased in patients with estimated glomerular filtration rate of 15 to 45 ml/min/1.73 m(2) (odds ratio 1.76, 95% confidence interval 1.38 to 2.25) even after adjustment for all confounders. Renal dysfunction was associated with all-cause mortality but not with cardiovascular events during the first 3 postoperative months after primary isolated CABG.

  8. Post-operative orofacial pain, temporomandibular dysfunction and trigeminal sensitivity after recent pterional craniotomy: preliminary study.

    Science.gov (United States)

    Brazoloto, Thiago Medina; de Siqueira, Silvia Regina Dowgan Tesseroli; Rocha-Filho, Pedro Augusto Sampaio; Figueiredo, Eberval Gadelha; Teixeira, Manoel Jacobsen; de Siqueira, José Tadeu Tesseroli

    2017-05-01

    Surgical trauma at the temporalis muscle is a potential cause of post-craniotomy headache and temporomandibular disorders (TMD). The aim of this study was to evaluate the prevalence of pain, masticatory dysfunction and trigeminal somatosensory abnormalities in patients who acquired aneurysms following pterional craniotomy. Fifteen patients were evaluated before and after the surgical procedure by a trained dentist. The evaluation consisted of the (1) research diagnostic criteria for TMD, (2) a standardized orofacial pain questionnaire and (3) a systematic protocol for quantitative sensory testing (QST) for the trigeminal nerve. After pterional craniotomy, 80% of the subjects, 12 patients, developed orofacial pain triggered by mandibular function. The pain intensity was measured by using the visual analog scale (VAS), and the mean pain intensity was 3.7. The prevalence of masticatory dysfunction was 86.7%, and there was a significant reduction of the maximum mouth opening. The sensory evaluation showed tactile and thermal hypoesthesia in the area of pterional access in all patients. There was a high frequency of temporomandibular dysfunction, postoperative orofacial pain and trigeminal sensory abnormalities. These findings can help to understand several abnormalities that can contribute to postoperative headache or orofacial pain complaints after pterional surgeries.

  9. Association between diffuse myocardial fibrosis by cardiac magnetic resonance contrast-enhanced T(1) mapping and subclinical myocardial dysfunction in diabetic patients: a pilot study.

    NARCIS (Netherlands)

    Ng, A.C.; Auger, D.; Delgado, V.; Elderen, S.G. van; Bertini, M.; Siebelink, H.M.; Geest, R.J. van der; Bonetti, C.; Velde, E.T. van der; Roos, A. de; Smit, J.W.A.; Leung, D.Y.; Bax, J.J.; Lamb, H.J.

    2012-01-01

    BACKGROUND: Diabetic patients have increased interstitial myocardial fibrosis on histological examination. Magnetic resonance imaging (MRI) T(1) mapping is a previously validated imaging technique that can quantify the burden of global and regional interstitial fibrosis. However, the association bet

  10. [Surface recording of abnormal post-QRS micropotentials. Description and frequency in ventricular tachycardias after myocardial infarction].

    Science.gov (United States)

    Varenne, A; Blanc, P; Camous, J P; Grangier, L; Morand, P

    1986-10-01

    In order to study abnormal post-QRS micropotentials, so called late potentials, and to determine their frequency in post myocardial infarction ventricular tachycardia (VT), high amplification electrocardiogrammes were recorded in 180 patients classified in 3 different groups: Group A comprising 36 patients who developed sustained VT after myocardial infarction; Group B comprising 124 patients with myocardial infarction uncomplicated by VT. This group was subdivided into subgroup B1 (retrospective study of 35 patients with chronic myocardial infarction, dating on average 10 months--range 7 days to 8 years) and subgroup B2 (prospective study of 89 patients investigated on the 7th and 60th days after infarction); Group C comprising 20 young, normal control subjects. Using computer assisted high amplification electrocardiography, all patients underwent at least 3 successive recordings of the following parameters: averaging 100 cycles; sampling: 1 kHz; band pass 20-300 Hz and 80-300 Hz; gain setting 10,000 and 25,000. Late potentials usually appears, after the end of the S wave, as high frequency oscillations with an amplitude (10 to 20 microV) significantly greater than that of the background noise. Our recordings also showed: the frequent presence, especially in intraventricular blocks, of fragmentation of the end of the R wave and of the S wave or terminal potentials; the presence of an abnormal giant low frequency high amplitude wave (40 to 80 microV) in 5 patients with a large left ventricular aneurysm.(ABSTRACT TRUNCATED AT 250 WORDS)

  11. Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy

    Science.gov (United States)

    Milani-Nejad, Nima; Schultz, Eric J.; Slabaugh, Jessica L.; Janssen, Paul M. L.; Rafael-Fortney, Jill A.

    2016-01-01

    Mutations in several members of the dystrophin glycoprotein complex lead to skeletal and cardiomyopathies. Cardiac care for these muscular dystrophies consists of management of symptoms with standard heart medications after detection of reduced whole heart function. Recent evidence from both Duchenne muscular dystrophy patients and animal models suggests that myocardial dysfunction is present before myocardial damage or deficiencies in whole heart function, and that treatment prior to heart failure symptoms may be beneficial. To determine whether this same early myocardial dysfunction is present in other muscular dystrophy cardiomyopathies, we conducted a physiological assessment of cardiac function at the tissue level in the δ-sarcoglycan null mouse model (Sgcd−/−) of Limb-girdle muscular dystrophy type 2F. Baseline cardiac contractile force measurements using ex vivo intact linear muscle preparations, were severely depressed in these mice without the presence of histopathology. Virotherapy withclaudin-5 prevents the onset of cardiomyopathy in another muscular dystrophy model. After virotherapy with claudin-5, the cardiac contractile force deficits in Sgcd−/− mice are no longer significant. These studies suggest that screening Limb-girdle muscular dystrophy patients using methods that detect earlier functional changes may provide a longer therapeutic window for cardiac care. PMID:27999547

  12. Tissue Doppler imaging for detection of radial and longitudinal myocardial dysfunction in a family of cats affected by dystrophin-deficient hypertrophic muscular dystrophy.

    Science.gov (United States)

    Chetboul, Valérie; Blot, Stephane; Sampedrano, Carolina Carlos; Thibaud, Jean-Laurent; Granger, Nicolas; Tissier, Renaud; Bruneval, Patrick; Gaschen, Frederic; Gouni, Vassiliki; Nicolle, Audrey P; Pouchelon, Jean-Louis

    2006-01-01

    Diagnosis of feline hypertrophic cardiomyopathy currently is based on the presence of myocardial hypertrophy detected using conventional echocardiography. The accuracy of tissue Doppler imaging (TDI) for earlier detection of the disease has never been described. The objective of this sudy was to quantify left ventricular free wall (LVFW) velocities in cats with hypertrophic muscular dystrophy (HFMD) during preclinical cardiomyopathy using TDI. The study animals included 22 healthy controls and 7 cats belonging to a family of cats with HFMD (2 affected adult males, 2 heterozygous adult females, one 2.5-month-old affected male kitten, and 2 phenotypically normal female kittens from the same litter). All cats were examined via conventional echocardiography and 2-dimensional color TDI. No LVFW hypertrophy was detected in the 2 carriers or in the affected kitten when using conventional echocardiography and histologic examination, respectively. The LVFW also was normal for 1 affected male and at the upper limit of normal for the 2nd male. Conversely, LVFW dysfunction was detected in all affected and carrier cats with HFMD when using TDI. TDI consistently detects LVFW dysfunction in cats with HFMD despite the absence of myocardial hypertrophy. Therefore, TDI appears more sensitive than conventional echocardiography in detecting regional myocardial abnormalities.

  13. Myocardial Contractile Dysfunction is Present Without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and is Prevented after Claudin-5 Virotherapy

    Directory of Open Access Journals (Sweden)

    Nima Milani-Nejad

    2016-12-01

    Full Text Available AbstractMutations in several members of the dystrophin glycoprotein complex lead to skeletal and cardiomyopathies. Cardiac care for these muscular dystrophies consists of management of symptoms with standard heart medications after detection of reduced whole heart function. Recent evidence from both Duchenne muscular dystrophy patients and animal models suggests that myocardial dysfunction is present before myocardial damage or deficiencies in whole heart function, and that treatment prior to heart failure symptoms may be beneficial. To determine whether this same early myocardial dysfunction is present in other muscular dystrophy cardiomyopathies, we conducted a physiological assessment of cardiac function at the tissue level in the δ-sarcoglycan null mouse model (Sgcd-/- of Limb-girdle muscular dystrophy type 2F. Baseline cardiac contractile force measurements using ex vivo intact linear muscle preparations, were severely depressed in these mice without the presence of histopathology. Virotherapy with claudin-5 prevents the onset of cardiomyopathy in another muscular dystrophy model. After virotherapy with claudin-5, the cardiac contractile force deficits in Sgcd-/- mice are no longer significant. These studies suggest that screening Limb-girdle muscular dystrophy patients using methods that detect earlier functional changes may provide a longer therapeutic window for cardiac care.

  14. Galectin-3 is expressed in the myocardium very early post-myocardial infarction.

    Science.gov (United States)

    Hashmi, Satwat; Al-Salam, Suhail

    2015-01-01

    Galectin-3 (GAL-3) plays a regulatory role in several diverse biological processes and disease states. It is associated with heart failure and increased risk of death in a number of studies. We aim to study the direct effects of ischemia on GAL-3 levels in the heart very early in the course of events following myocardial infarction (MI). Male C57B6/J mice were used for permanently ligating the left anterior descending artery of the heart to create ischemia/infarction in the anterior wall of left ventricle (LV). Heart samples were processed for immunohistochemical and immunofluorescent labeling, enzyme-linked immunosorbent assay, and quantitative reverse transcriptase polymerase chain reaction to identify GAL-3 levels in the heart during the first 24 h following MI. GAL-3 mRNA was significantly increased at 60min (P=.032), 4 h (P=.012), and 24 h (P=.00) post-MI groups in the infarcted LV as compared to sham. Thirty minutes post-MI GAL-3 mRNA is higher than the sham and almost reaching statistical significance (P=.056). GAL-3 protein was significantly increased in the LV at 30 min (P=.021), 60 min (P=.029), 4 h (P=.015), and 24 h (P=.01) post-MI compared to corresponding sham-operated mice. Plasma GAL-3 levels are also significantly raised at 24-h post-MI. GAL-3 is colocalized with cardiomyocytes and endothelial cells in the ischemic area of the LV. GAL-3 is also colocalized with hypoxia-inducible factor-1 alpha (HIF-1α). We show for the first time that GAL-3 is increased at both transcriptional and translational levels in the LV in early ischemic period, which can possibly be a part of the prosurvival gene expression profile transcribed by HIF-1α. This is significant because it can help in understanding the mechanism of very early response of the myocardium following acute infarction and help devise ways to save the viable tissue before permanent damage sets in. Copyright © 2014 Elsevier Inc. All rights reserved.

  15. Effects of renal sympathetic denervation on post-myocardial infarction cardiac remodeling in rats.

    Directory of Open Access Journals (Sweden)

    Jialu Hu

    Full Text Available OBJECTIVE: To investigate the therapeutic effects of renal denervation (RD on post- myocardial infarction (MI cardiac remodeling in rats, the most optimal time for intervention and the sustainability of these effects. METHODS: One hundred SPF male Wistar rats were randomly assigned to N group (Normal, n=10, MI group(MI, n=20,RD group (RD, n=10, RD3+MI (MI three days after RD, n=20, MI1+RD (RD one day after MI, n=20, MI7+RD (RD seven days after MI, n=20. MI was produced through thoracotomic ligation of the anterior descending artery. RD was performed through laparotomic stripping of the renal arteriovenous adventitial sympathetic nerve. Left ventricular function, hemodynamics, plasma BNP, urine volume, urine sodium excretion and other indicators were measured four weeks after MI. RESULTS: (1 The left ventricular function of the MI group significantly declined (EF<40%, plasma BNP was elevated, urine output was significantly reduced, and 24-hour urine sodium excretion was significantly reduced. (2 Denervation can be achieved by surgically stripping the arteriovenous adventitia, approximately 3 mm from the abdominal aorta. (3 In rats with RD3+MI, MI1+RD and MI7+RD, compared with MI rats respectively, the LVEF was significantly improved (75 ± 8.4%,69 ± 3.8%,73 ± 5.5%, hemodynamic indicators were significantly improved, plasma BNP was significantly decreased, and the urine output was significantly increased (21.3 ± 5 ml,23.8 ± 5.4 ml,25.2 ± 8.7 ml. However, the urinary sodium excretion also increased but without significant difference. CONCLUSIONS: RD has preventive and therapeutic effects on post-MI cardiac remodeling.These effects can be sustained for at least four weeks, but there were no significant differences between denervation procedures performed at different times in the course of illness. Cardiac function, hemodynamics, urine volume and urine sodium excretion in normal rats were not affected by RD.

  16. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation.

    Science.gov (United States)

    Paulus, Walter J; Tschöpe, Carsten

    2013-07-23

    Over the past decade, myocardial structure, cardiomyocyte function, and intramyocardial signaling were shown to be specifically altered in heart failure with preserved ejection fraction (HFPEF). A new paradigm for HFPEF development is therefore proposed, which identifies a systemic proinflammatory state induced by comorbidities as the cause of myocardial structural and functional alterations. The new paradigm presumes the following sequence of events in HFPEF: 1) a high prevalence of comorbidities such as overweight/obesity, diabetes mellitus, chronic obstructive pulmonary disease, and salt-sensitive hypertension induce a systemic proinflammatory state; 2) a systemic proinflammatory state causes coronary microvascular endothelial inflammation; 3) coronary microvascular endothelial inflammation reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes; 4) low PKG activity favors hypertrophy development and increases resting tension because of hypophosphorylation of titin; and 5) both stiff cardiomyocytes and interstitial fibrosis contribute to high diastolic left ventricular (LV) stiffness and heart failure development. The new HFPEF paradigm shifts emphasis from LV afterload excess to coronary microvascular inflammation. This shift is supported by a favorable Laplace relationship in concentric LV hypertrophy and by all cardiac chambers showing similar remodeling and dysfunction. Myocardial remodeling in HFPEF differs from heart failure with reduced ejection fraction, in which remodeling is driven by loss of cardiomyocytes. The new HFPEF paradigm proposes comorbidities, plasma markers of inflammation, or vascular hyperemic responses to be included in diagnostic algorithms and aims at restoring myocardial PKG activity.

  17. Meta-analysis of transcranial magnetic stimulation to treat post-stroke dysfunction

    Institute of Scientific and Technical Information of China (English)

    Yang Tian; Lianguo Kang; Hongying Wang; Zhenyi Liu

    2011-01-01

    OBJECTIVE: To evaluate the effects of transcranial magnetic stimulation (TMS) on post-stroke dysfunction.DATA SOURCES: A computer-based online search of the VIP and PubMed databases was performed to identify TMS studies published between January 1989 and December 2010 using the Key Words "transcranial magnetic stimulation, stroke" in Chinese and English.A total of 61 articles were collected.STUDY SELECTION: Repetitive articles were excluded.Articles published recently in the authoritative journals of the same domain were selected.The full-text of selected articles was searched.A total of seven articles were randomized controlled experiments regarding the application of TMS in the treatment of post-stroke dysfunction.The methodology quality of included articles was evaluated according to standards of Cochrane Reviewer's Handbook system and analyzed using RevMand4.2 software.MAIN OUTCOME MEASURES: Therapeutic effects and difference evaluation indices were represented by odds ratios, weighted mean difference (WMD) and 95% confidence interval (CI).Potential publication bias was described using a funnel plot.RESULTS: A total of seven randomized, controlled studies were included involving 281 patients.Following TMS treatment, meta-analysis results revealed that scores in the Mini-Mental State Examination were higher in the TMS group compared with the control group [WMD = 3.96, 95% CI (2.44, 5.49), P = 0.08]; scores in the Hamilton Rating Scale for Depression were significantly lower in the TMS group compared with the control group [WMD = -6.21, 95% CI (-7.55, -4.87), P = 0.92]; scores in National Institutes of Health Stroke Scale were lower following TMS treatment compared with the control group [WMD = -0.89, 95% CI (-1.98, 0.19), P = 0.04].Performance of patients undergoing TMS treatment was better than the controls in the line bisection test [WMD = -0.78, 95% CI (-1.43, -0.12), P = 0.005] and line cancellation test [WMD = -0.47, 95% CI (-0.78, -0.15), P < 0.000 01

  18. Level of complement activity predicts cardiac dysfunction after acute myocardial infarction treated with primary percutaneous coronary intervention

    DEFF Research Database (Denmark)

    Haahr-Pedersen, Sune; Bjerre, Mette; Flyvbjerg, Allan

    2009-01-01

    The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human myocardial I...

  19. Hippocampal Dysfunction Effects on Context Memory: Possible Etiology for Post-traumatic Stress Disorder

    Science.gov (United States)

    Acheson, Dean T.; Gresack, Jodi E.; Risbrough, Victoria B.

    2011-01-01

    Hippocampal volume reductions and functional impairments are reliable findings in post-traumatic stress disorder (PTSD) imaging studies. However, it is not clear if and how hippocampal dysfunction contributes to the etiology and maintenance of PTSD. Individuals with PTSD are often described as showing fear responses to trauma reminders outside of contexts in which these cues would reasonably predict danger. Animal studies suggest that the hippocampus is required to form and recall associations between contextual stimuli and aversive events. For example, the hippocampus is critical for encoding memories in which a complex configuration of multiple cues is associated with the aversive event. Conversely, the hippocampus is not required for associations with discrete cues. In animal studies, if configural memory is disrupted, learning strategies using discrete cue associations predominate. These data suggest poor hippocampal function could bias the organism towards forming multiple simple cue associations during trauma, thus increasing the chances of fear responses in multiple environments (or contexts) in which these cues may be present. Here we will examine clinical and animal literature to support a theory of hippocampal dysfunction as a primary contributory factor to the etiology of PTSD, and discuss future research required to test these hypotheses. PMID:21596050

  20. Clinical significance of late high-degree atrioventricular block in patients with left ventricular dysfunction after an acute myocardial infarction--a Cardiac Arrhythmias and Risk Stratification After Acute Myocardial Infarction (CARISMA) substudy

    DEFF Research Database (Denmark)

    Gang, Uffe Jakob Ortved; Jøns, Christian; Jørgensen, Rikke Mørch;

    2011-01-01

    High-degree atrioventricular block (HAVB) is a frequent complication in the acute stages of a myocardial infarction associated with an increased rate of mortality. However, the incidence and clinical significance of HAVB in late convalescent phases of an AMI is largely unknown. The aim of this st...... of this study was to assess the incidence and prognostic value of late HAVB documented by continuous electrocardiogram (ECG) monitoring in post-AMI patients with reduced left ventricular function....

  1. Predictors and prognostic impact of recurrent myocardial infarction in patients with left ventricular dysfunction, heart failure, or both following a first myocardial infarction

    DEFF Research Database (Denmark)

    Thune, Jens Jakob; Signorovitch, James E; Kober, Lars;

    2011-01-01

    IMS: Recurrent myocardial infarction (MI) is common after a first MI and is associated with increased morbidity and mortality. Predictors and prognosis of a recurrent MI with contemporary management are not well known. METHODS AND RESULTS: We assessed the predictors and prognostic impact of a fir...

  2. Long-term prognostic importance of resting heart rate in patients with left ventricular dysfunction in connection with either heart failure or myocardial infarction: the DIAMOND study

    DEFF Research Database (Denmark)

    Fosbøl, Emil Loldrup; Seibaek, Marie; Brendorp, Bente

    2010-01-01

    dysfunction in connection with either heart failure (HF) or myocardial infarction (MI). METHODS: In the Danish Investigations and Arrhythmia ON Dofetilide (DIAMOND) study; patients with left ventricular dysfunction were randomized to Dofetilide (class III antiarrhythmic drug) or placebo. One part of the study......BACKGROUND: Elevated resting heart rate is associated with increased mortality in a variety of cardiac diseases, but comparisons between different clinical settings are lacking. We investigated the long-term prognostic importance of resting heart rate in patients hospitalized with left ventricular...... increment in baseline heart rate of 10 bpm was associated with an increase in mortality in both MI-patients (hazard ratio, 1.14; 95%-confidence interval (CI): 1.09-1.19; Pheart rate on short-term prognosis...

  3. [The role of B type natriuretic peptide in the assessment of post myocardial infarction prognosis].

    Science.gov (United States)

    Ben Halima, A; Ibn el Hadj, Z; Chrigui, R; Kammoun, I; Lefi, A; Chine, S; Gargouri, S; Keskes, H; Kachboura, S

    2006-10-01

    Recently cardiac peptides have received close attention as cardiovascular markers. Brain (B type) natriuretic peptide is a neurohormone synthesized predominantly in ventricular myocardium. Previous studies have shown that this hormone can provide prognostic information in patients with myocardial infarction. The aim of this review is to evaluate the impact of plasma levels of BNP on prediction of left ventricular ejection fraction and remodelling and major cardiac events after myocardial infarction.

  4. Matrix cross-linking lysyl oxidases are induced in response to myocardial infarction and promote cardiac dysfunction

    NARCIS (Netherlands)

    González-Santamaría, J.; Villalba, M.; Busnadiego, O.; López-Olañeta, M.M.; Sandoval, P.; Snabel, J.; López-Cabrera, M.; Erler, J.T.; Hanemaaijer, R.; Lara-Pezzi, E.; Rodríguez-Pascual, F.

    2016-01-01

    Aims After myocardial infarction (MI), extensive remodelling of the extracellular matrix contributes to scar formation. While aiming to preserve tissue integrity, this fibrotic response is also associated with adverse events, including a markedly increased risk of heart failure, ventricular arrhythm

  5. Matrix cross-linking lysyl oxidases are induced in response to myocardial infarction and promote cardiac dysfunction

    DEFF Research Database (Denmark)

    González-Santamaría, José; Villalba, María; Busnadiego, Oscar

    2016-01-01

    AIMS: After myocardial infarction (MI), extensive remodelling of the extracellular matrix contributes to scar formation. While aiming to preserve tissue integrity, this fibrotic response is also associated with adverse events, including a markedly increased risk of heart failure, ventricular arrh...

  6. Low thyroid function leads to cardiac atrophy with chamber dilatation, impaired myocardial blood flow, loss of arterioles, and severe systolic dysfunction.

    Science.gov (United States)

    Tang, Yi-Da; Kuzman, James A; Said, Suleman; Anderson, Brent E; Wang, Xuejun; Gerdes, A Martin

    2005-11-15

    Although thyroid dysfunction has been linked to heart failure, it is not clear whether hypothyroidism alone can cause heart failure. Hypothyroidism was induced in adult rats by treatment with 0.025% propylthiouracil (PTU) for 6 weeks (PTU-S) and 1 year (PTU-L). Echocardiographic measurements, left ventricular (LV) hemodynamics, isolated myocyte length (KOH method), myocardial blood flow (fluorescent microspheres), arteriolar morphometry, and gene expression (Western blot) were determined. Heart weight, heart rate, LV systolic blood pressure, LV ejection fraction, LV fractional shortening, and systolic wall thickness were reduced in PTU-S and PTU-L rats. LV internal diameter in systole increased by 40% in PTU-S and 86% in PTU-L. LV internal dimension in diastole was increased in PTU-S and PTU-L rats, but only PTU-L rats showed a significant increase in myocyte length due to series sarcomere addition. Resting and maximum (adenosine) myocardial blood flow were reduced in both PTU-S and PTU-L rats. Impaired blood flow was due to a large reduction in arteriolar length density and small arterioles in PTU-S and PTU-L (Pcardiac mass. Chamber dilatation in PTU-L rats was due to series sarcomere addition, typical of heart failure. Hypothyroidism resulted in impaired myocardial blood flow due to a dramatic loss of arterioles. Thus, we have identified 2 important new mechanisms by which low thyroid function may lead to heart failure.

  7. The need for standardisation of cardiac FDG PET imaging in the evaluation of myocardial viability in patients with chronic ischaemic left ventricular dysfunction

    Energy Technology Data Exchange (ETDEWEB)

    Kuuti, J. [Turku Univ. (Finland). Turku PET Centre; Schelbert, H.R. [UCLA School of Medicine, Los Angeles, CA (United States). Dept. of Molecular and Medical Pharmacology; Bax, J.J. [Leiden University Medical Center (Netherlands). Dept. of Cardilogy

    2002-09-01

    The evaluation of myocardial glucose utilisation with fluorine-18 fluorodeoxyglucose (FDG) and positron emission tomography is currently considered the most reliable tool for the identification of myocardial viability. However, the investigations using FDG imaging to predict improvement in left ventricular (LV) function after revascularisation have reported wide ranges for sensitivity (71%-100%) and, in particular, for specificity (33%-91%). The variable results may be related to differences in study populations but also to differences in the imaging protocols employed. Detailed analysis of the published studies has revealed differences in study populations, patient selection criteria, the methods for assessing changes in LV function post revascularisation and the timing of these assessments. Even more importantly, protocols have varied substantially with regard to imaging equipment, perfusion tracers, metabolic conditions, data analysis and interpretation of results. In addition, evaluation of patients with insulin resistance appears to represent a specific challenge. This review examines the different study protocols and methodologies used for myocardial FDG imaging in order to draw conclusions concerning optimal imaging protocols. It appears that the optimisation and standardisation of study protocols and analysis of FDG images for the assessment of myocardial viability are critical. In addition, multi-centre trials seem warranted on prediction of long-term function, congestive heart failure symptoms, survival and quality of life.

  8. Executive Dysfunctions: The role in Attention Deficit Hyperactivity and Post-traumatic Stress neuropsychiatric disorders

    Directory of Open Access Journals (Sweden)

    Lía Martínez

    2016-08-01

    Full Text Available Executive functions (EFs is an umbrella term for various cognitive processes controlled by a complex neural activity, which allow the production of different types of behaviors seeking to achieve specific objectives, one of them being inhibitory control. There is a wide consensus that clinical and behavioral alterations associated with EF, such as inhibitory control, are present in various neuropsychiatric disorders. This paper reviews the research literature on the relationship between executive dysfunction, frontal-subcortical neural circuit changes, and the psychopathological processes associated with Attention Deficit Hyperactivity Disorder (ADHD and Post-traumatic Stress Disorder (PTSD. A revision on the role of frontal-subcortical neural circuits and their presumable abnormal functioning and the high frequency of neuropsychiatric symptoms could explain the difficulties with putting effector mechanisms into action, giving individuals the necessary tools to act efficiently in their environment. Although neuronal substrate data about ADHD and PTSD has been reported in the literature, it is isolated. Therefore, this review highlights the overlapping of neural substrates in the symptomatology of ADHD and PTSD disorders concerning EFs, especially in the inhibitory component. Thus, the changes related to impaired EF that accompany disorders like ADHD and PTSD could be explained by disturbances that have a direct or indirect impact on the functioning of these loops. Initially, the theoretical model of EF according to current neuropsychology will be presented, focusing on the inhibitory component. In a second stage, this component will be analyzed for each of the disorders of interest, considering the clinical aspects, the etiology and the neurobiological basis. Additionally, commonalities between the two neuropsychiatric conditions will be taken into consideration from the perspectives of cognitive and emotional inhibition. Finally, the

  9. Executive Dysfunctions: The Role in Attention Deficit Hyperactivity and Post-traumatic Stress Neuropsychiatric Disorders

    Science.gov (United States)

    Martínez, Lía; Prada, Edward; Satler, Corina; Tavares, Maria C. H.; Tomaz, Carlos

    2016-01-01

    Executive functions (EFs) is an umbrella term for various cognitive processes controlled by a complex neural activity, which allow the production of different types of behaviors seeking to achieve specific objectives, one of them being inhibitory control. There is a wide consensus that clinical and behavioral alterations associated with EF, such as inhibitory control, are present in various neuropsychiatric disorders. This paper reviews the research literature on the relationship between executive dysfunction, frontal-subcortical neural circuit changes, and the psychopathological processes associated with attention deficit hyperactivity disorder (ADHD) and post-traumatic stress disorder (PTSD). A revision on the role of frontal-subcortical neural circuits and their presumable abnormal functioning and the high frequency of neuropsychiatric symptoms could explain the difficulties with putting effector mechanisms into action, giving individuals the necessary tools to act efficiently in their environment. Although, neuronal substrate data about ADHD and PTSD has been reported in the literature, it is isolated. Therefore, this review highlights the overlapping of neural substrates in the symptomatology of ADHD and PTSD disorders concerning EFs, especially in the inhibitory component. Thus, the changes related to impaired EF that accompany disorders like ADHD and PTSD could be explained by disturbances that have a direct or indirect impact on the functioning of these loops. Initially, the theoretical model of EF according to current neuropsychology will be presented, focusing on the inhibitory component. In a second stage, this component will be analyzed for each of the disorders of interest, considering the clinical aspects, the etiology and the neurobiological basis. Additionally, commonalities between the two neuropsychiatric conditions will be taken into consideration from the perspectives of cognitive and emotional inhibition. Finally, the implications and future

  10. Executive Dysfunctions: The Role in Attention Deficit Hyperactivity and Post-traumatic Stress Neuropsychiatric Disorders.

    Science.gov (United States)

    Martínez, Lía; Prada, Edward; Satler, Corina; Tavares, Maria C H; Tomaz, Carlos

    2016-01-01

    Executive functions (EFs) is an umbrella term for various cognitive processes controlled by a complex neural activity, which allow the production of different types of behaviors seeking to achieve specific objectives, one of them being inhibitory control. There is a wide consensus that clinical and behavioral alterations associated with EF, such as inhibitory control, are present in various neuropsychiatric disorders. This paper reviews the research literature on the relationship between executive dysfunction, frontal-subcortical neural circuit changes, and the psychopathological processes associated with attention deficit hyperactivity disorder (ADHD) and post-traumatic stress disorder (PTSD). A revision on the role of frontal-subcortical neural circuits and their presumable abnormal functioning and the high frequency of neuropsychiatric symptoms could explain the difficulties with putting effector mechanisms into action, giving individuals the necessary tools to act efficiently in their environment. Although, neuronal substrate data about ADHD and PTSD has been reported in the literature, it is isolated. Therefore, this review highlights the overlapping of neural substrates in the symptomatology of ADHD and PTSD disorders concerning EFs, especially in the inhibitory component. Thus, the changes related to impaired EF that accompany disorders like ADHD and PTSD could be explained by disturbances that have a direct or indirect impact on the functioning of these loops. Initially, the theoretical model of EF according to current neuropsychology will be presented, focusing on the inhibitory component. In a second stage, this component will be analyzed for each of the disorders of interest, considering the clinical aspects, the etiology and the neurobiological basis. Additionally, commonalities between the two neuropsychiatric conditions will be taken into consideration from the perspectives of cognitive and emotional inhibition. Finally, the implications and future

  11. Systolic Myocardial Dysfunction in Patients with Type 2 Diabetes Mellitus: Identification at MR Imaging with Cine Displacement Encoding with Stimulated Echoes

    Science.gov (United States)

    Ernande, Laura; Thibault, Hélène; Bergerot, Cyrille; Moulin, Phillippe; Wen, Han; Derumeaux, Geneviève

    2012-01-01

    Purpose: To determine if cine displacement encoding with stimulated echoes (DENSE) can help to identify and determine the patterns of subclinical myocardial systolic dysfunction in patients with type 2 diabetes mellitus (DM) when compared with cine DENSE in control patients. Materials and Methods: After obtaining approval from the institutional ethics committee and written informed consent from the patients, 37 patients with type 2 DM without overt heart disease and 23 age-matched control patients were prospectively included in the study. The patients underwent standard cine magnetic resonance (MR) imaging with two-dimensional cine DENSE acquisitions. Circumferential (Ecc) and radial (Err) systolic strains were measured on short-axis views at basal, mid, and apical left ventricular levels. Longitudinal strain (Ell) was measured on four- and two-chamber views. Statistical testing included the intraclass correlation coefficient and multiple linear regression analysis. Results: The intraobserver intraclass correlation coefficient values were 0.85, 0.95, and 0.90, and the interobserver intraclass correlation coefficient values were 0.79, 0.91 and 0.80 for Ecc, Err, and Ell, respectively. The left ventricular ejection fraction was in the reference range and similar between the groups, and the patients with DM showed a decrease in Ecc (−14.4% ± 1.6 vs −17.0% ± 1.6, P Cine DENSE, a motion-encoding MR imaging technique for myocardial strain assessment with high spatial resolution, appears to be useful in the identification of subclinical myocardial dysfunction in patients with DM. © RSNA, 2012 Supplemental material: http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.12112571/-/DC1 PMID:22929334

  12. Clinical significance of late high-degree atrioventricular block in patients with left ventricular dysfunction after an acute myocardial infarction--a Cardiac Arrhythmias and Risk Stratification After Acute Myocardial Infarction (CARISMA) substudy

    DEFF Research Database (Denmark)

    Gang, Uffe Jakob Ortved; Jøns, Christian; Jørgensen, Rikke Mørch;

    2011-01-01

    High-degree atrioventricular block (HAVB) is a frequent complication in the acute stages of a myocardial infarction associated with an increased rate of mortality. However, the incidence and clinical significance of HAVB in late convalescent phases of an AMI is largely unknown. The aim of this st......High-degree atrioventricular block (HAVB) is a frequent complication in the acute stages of a myocardial infarction associated with an increased rate of mortality. However, the incidence and clinical significance of HAVB in late convalescent phases of an AMI is largely unknown. The aim...... of this study was to assess the incidence and prognostic value of late HAVB documented by continuous electrocardiogram (ECG) monitoring in post-AMI patients with reduced left ventricular function....

  13. Intracoronary cardiosphere-derived cells after myocardial infarction: evidence of therapeutic regeneration in the final 1-year results of the CADUCEUS trial (CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction).

    Science.gov (United States)

    Malliaras, Konstantinos; Makkar, Raj R; Smith, Rachel R; Cheng, Ke; Wu, Edwin; Bonow, Robert O; Marbán, Linda; Mendizabal, Adam; Cingolani, Eugenio; Johnston, Peter V; Gerstenblith, Gary; Schuleri, Karl H; Lardo, Albert C; Marbán, Eduardo

    2014-01-21

    This study sought to report full 1-year results, detailed magnetic resonance imaging analysis, and determinants of efficacy in the prospective, randomized, controlled CADUCEUS (CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction) trial. Cardiosphere-derived cells (CDCs) exerted regenerative effects at 6 months in the CADUCEUS trial. Complete results at the final 1-year endpoint are unknown. Autologous CDCs (12.5 to 25 × 10(6)) grown from endomyocardial biopsy specimens were infused via the intracoronary route in 17 patients with left ventricular dysfunction 1.5 to 3 months after myocardial infarction (MI) (plus 1 infused off-protocol 14 months post-MI). Eight patients were followed as routine-care control patients. In 13.4 months of follow-up, safety endpoints were equivalent between groups. At 1 year, magnetic resonance imaging revealed that CDC-treated patients had smaller scar size compared with control patients. Scar mass decreased and viable mass increased in CDC-treated patients but not in control patients. The single patient infused 14 months post-MI responded similarly. CDC therapy led to improved regional function of infarcted segments compared with control patients. Scar shrinkage correlated with an increase in viability and with improvement in regional function. Scar reduction correlated with baseline scar size but not with a history of temporally remote MI or time from MI to infusion. The changes in left ventricular ejection fraction in CDC-treated subjects were consistent with the natural relationship between scar size and ejection fraction post-MI. Intracoronary administration of autologous CDCs did not raise significant safety concerns. Preliminary indications of bioactivity include decreased scar size, increased viable myocardium, and improved regional function of infarcted myocardium at 1 year post-treatment. These results, which are consistent with therapeutic regeneration, merit further investigation in future trials

  14. Thymol, a dietary monoterpene phenol abrogates mitochondrial dysfunction in β-adrenergic agonist induced myocardial infarcted rats by inhibiting oxidative stress.

    Science.gov (United States)

    Nagoor Meeran, M F; Jagadeesh, G S; Selvaraj, P

    2016-01-25

    Mitochondrial dysfunction has been suggested to be one of the important pathological events in isoproterenol (ISO), a synthetic catecholamine and β-adrenergic agonist induced myocardial infarction (MI). In this context, we have evaluated the impact of thymol against ISO induced oxidative stress and calcium uniporter malfunction involved in the pathology of mitochondrial dysfunction in rats. Male albino Wistar rats were pre and co-treated with thymol (7.5 mg/kg body weight) daily for 7 days. Isoproterenol (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce MI. To explore the extent of cardiac mitochondrial damage, the activities/levels of cardiac marker enzymes, mitochondrial lipid peroxidation products, antioxidants, lipids, calcium, adenosine triphosphate and multi marker enzymes were evaluated. Isoproterenol induced myocardial infarcted rats showed a significant increase in the activities of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, lipids, calcium, and a significant decrease in the activities/levels of heart mitochondrial superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, isocitrate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase, and adenosine triphosphate. Thymol pre and co-treatment showed near normalized effects on all the biochemical parameters studied. Transmission electron microscopic findings and mitochondrial swelling studies confirmed our biochemical findings. The in vitro study also revealed the potent free-radical scavenging activity of thymol. Thus, thymol attenuates the involvement of ISO against oxidative stress and calcium uniporter malfunction associated with mitochondrial dysfunction in rats.

  15. Continuous Care Model and the Self-Management in Post-Myocardial Infarction Patients: A Randomized Controlled Trial

    Directory of Open Access Journals (Sweden)

    Akbari

    2016-09-01

    Full Text Available Background Self-management after myocardial infarction is fundamental to effective medical treatment. Objectives The current study aimed to investigate the effects of applying the continuous care model on self-management of a sample of Iranian patients with post-myocardial infarction. Methods Sixty hospitalized patients were randomly allocated into control (n = 30 and intervention (n = 30 groups. Before the intervention and at the end of it, self-management of both groups was evaluated by chronic disease self-management questionnaire. The continuous care model was performed for the intervention group for three months. The data were analyzed by SPSS version 16. In addition to descriptive statistical tests, Chi-square, the exact Fisher, Willcoxon and Mann-Whitney, and analysis of covariance (ANCOVA tests were used. The significant level was set at P 0.05. At the end of the intervention, in all self-management sub-dimensions expect for shortness of breath, the status of intervention group improved significantly more than that of the control group (P < 0.005. Moreover, mean of changes in all sub-dimensions of self-management showed no significant difference, but fatigue and health care utilization between the two groups had significant difference. Conclusions The continuous care model can be considered as a useful tool to improve patients’ self-management after myocardial infarction.

  16. Negative impact of β-arrestin-1 on post-myocardial infarction heart failure via cardiac and adrenal-dependent neurohormonal mechanisms.

    Science.gov (United States)

    Bathgate-Siryk, Ashley; Dabul, Samalia; Pandya, Krunal; Walklett, Karlee; Rengo, Giuseppe; Cannavo, Alessandro; De Lucia, Claudio; Liccardo, Daniela; Gao, Erhe; Leosco, Dario; Koch, Walter J; Lymperopoulos, Anastasios

    2014-02-01

    β-Arrestin (βarr)-1 and β-arrestin-2 (βarrs) are universal G-protein-coupled receptor adapter proteins that negatively regulate cardiac β-adrenergic receptor (βAR) function via βAR desensitization and downregulation. In addition, they mediate G-protein-independent βAR signaling, which might be beneficial, for example, antiapoptotic, for the heart. However, the specific role(s) of each βarr isoform in cardiac βAR dysfunction, the molecular hallmark of chronic heart failure (HF), remains unknown. Furthermore, adrenal βarr1 exacerbates HF by chronically enhancing adrenal production and hence circulating levels of aldosterone and catecholamines. Herein, we sought to delineate specific roles of βarr1 in post-myocardial infarction (MI) HF by testing the effects of βarr1 genetic deletion on normal and post-MI cardiac function and morphology. We studied βarr1 knockout (βarr1KO) mice alongside wild-type controls under normal conditions and after surgical MI. Normal (sham-operated) βarr1KO mice display enhanced βAR-dependent contractility and post-MI βarr1KO mice enhanced overall cardiac function (and βAR-dependent contractility) compared with wild type. Post-MI βarr1KO mice also show increased survival and decreased cardiac infarct size, apoptosis, and adverse remodeling, as well as circulating catecholamines and aldosterone, compared with post-MI wild type. The underlying mechanisms, on one hand, improved cardiac βAR signaling and function, as evidenced by increased βAR density and procontractile signaling, via reduced cardiac βAR desensitization because of cardiac βarr1 absence, and, on the other hand, decreased production leading to lower circulating levels of catecholamines and aldosterone because of adrenal βarr1 absence. Thus, βarr1, via both cardiac and adrenal effects, is detrimental for cardiac structure and function and significantly exacerbates post-MI HF.

  17. Fluvastatin attenuates myocardial interstitial fibrosis and cardiac dysfunction in diabetic rats by inhibiting over-expression of connective tissue growth factor

    Institute of Scientific and Technical Information of China (English)

    DAI Qi-ming; LU Jing; LIU Nai-feng

    2011-01-01

    Background Diabetic myocardiopathy is characterized by myocardial interstitial fibrosis and cardiac dysfunction.Statins were found to exert protective effects on cardiovascular disease by suppressing activation of small G proteins,independently of their lipid-lowering effect. The study investigated the effect of fluvastatin on myocardial interstitial fibrosis, cardiac function and mechanism of its action in diabetic rats.Methods Twenty-four male SD rats were randomly assigned to 3 groups: control rats (n=8), streptozotocin (STZ)-induced diabetic rats (n=8), and diabetic rats treated with fluvastatin (administered fluvastatin orally, 10 mg/kg body weight per day, n=8). Twelve weeks later, miniature cardiac catheter was inserted into the left ventricle to conduct hemodynamic examination. Then myocardium tissues were collected, collagen content was detected by picro-sirius red staining, real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of connective tissue growth factor (CTGF), and Western blotting was used to detect the protein expression of CTGF. Rho activity was determined by pull-down assay.Results After 12 weeks, the left ventricular systolic pressure (LVSP) and maximum rate of left ventricular (LV) pressure rise and fall (+dP/dt max and -dP/dr max) were significantly lower and left ventricular end diastolic pressure (LVEDP) was higher in the diabetic rats than those in the control rats (P <0.01). Moreover, in LV myocardial tissue of diabetic rats the collagen content, fibronectin, mRNA and protein expression of CTGF and the activity of RhoA were all significantly increased compared with the control rats (P <0.01). Administration of fluvastain obviously improved the cardiac function of diabetic rats, attenuated fibronectin expression, mRNA and protein expression of CTGF and the activity of RhoA in LV myocardium of diabetic rats.Conclusions Fluvastatin attenuates cardiac dysfunction and

  18. Long-term survival after mitral valve surgery for post-myocardial infarction papillary muscle rupture

    NARCIS (Netherlands)

    Bouma, Wobbe; Wijdh-den Hamer, Inez J.; Koene, Bart M.; Kuijpers, Michiel; Natour, Ehsan; Erasmus, Michiel E.; Jainandunsing, Jayant S.; van der Horst, Iwan C. C.; Gorman, Joseph H.; Gorman, Robert C.; Mariani, Massimo A.

    2015-01-01

    Background: Papillary muscle rupture (PMR) is a rare, but dramatic mechanical complication of myocardial infarction (MI), which can lead to rapid clinical deterioration and death. Immediate surgical intervention is considered the optimal and most rational treatment, despite high risks. In this study

  19. Mitral valve repair for post-myocardial infarction papillary muscle rupture

    NARCIS (Netherlands)

    Bouma, Wobbe; Wijdh-den Hamer, Inez J.; Klinkenberg, Theo J.; Kuijpers, Michiel; Bijleveld, Aanke; van der Horst, Iwan C. C.; Erasmus, Michiel E.; Gorman, Joseph H.; Gorman, Robert C.; Mariani, Massimo A.

    2013-01-01

    Papillary muscle rupture (PMR) is a rare, but serious mechanical complication of myocardial infarction (MI). Although mitral valve replacement is usually the preferred treatment for this condition, mitral valve repair may offer an improved outcome. In this study, we sought to determine the outcome o

  20. Early exercise training normalizes myofilament function and attenuates left ventricular pump dysfunction in mice with a large myocardial infarction

    NARCIS (Netherlands)

    M.C. de Waard (Monique); J. van der Velden (Jolanda); V. Bito (Virginie); S. Ozdemir (Semir); L. Biesmans (Liesbeth); N.M. Boontje (Nicky); D.H. Dekkers (Dick); K. Schoonderwoerd (Kees); J.C.H. Schuurbiers (Johan); R. de Crom (Rini); G.J.M. Stienen (Ger); K.R. Sipido (Karin); J.M.J. Lamers (Jos); D.J.G.M. Duncker (Dirk)

    2007-01-01

    textabstractThe extent and mechanism of the cardiac benefit of early exercise training following myocardial infarction (MI) is incompletely understood, but may involve blunting of abnormalities in Ca-handling and myofilament function. Consequently, we investigated the effects of 8-weeks of voluntary

  1. Effect of Metformin on Metabolites and Relation With Myocardial Infarct Size and Left Ventricular Ejection Fraction After Myocardial Infarction

    NARCIS (Netherlands)

    Eppinga, Ruben N; Kofink, Daniel; Dullaart, Robin P F; Dalmeijer, Geertje W; Lipsic, Erik; van Veldhuisen, Dirk J; van der Horst, Iwan C C; Asselbergs, Folkert W; van der Harst, Pim

    2017-01-01

    BACKGROUND: Left ventricular ejection fraction (LVEF) and infarct size (ISZ) are key predictors of long-term survival after myocardial infarction (MI). However, little is known about the biochemical pathways driving LV dysfunction after MI. To identify novel biomarkers predicting post-MI LVEF and IS

  2. Delayed diagnosis of post-traumatic acute myocardial infarction complicated by congestive heart failure.

    Science.gov (United States)

    Tsai, Tsung-Neng; Yang, Shih-Ping; Tsao, Tien-Ping; Huang, Kuo-An; Cheng, Shu-Meng

    2005-11-01

    A 53-year-old man experienced persistent chest pain followed by slight shortness of breath after being hit in the chest by a stranger. Chest X-ray study showed no rib fractures but electrocardiography indicated acute anterior wall myocardial infarction. Echocardiography revealed akinesia in both the interventricular septum and anterior left ventricular wall. Emergency cardiac catheterization demonstrated total occlusion of the proximal left anterior descending coronary artery, 9 h after the event. He was successfully treated with coronary angioplasty and stenting procedures. However, poor left ventricular function was observed 3 months after the event despite medications. We conclude that evaluation for possible myocardial injury should be considered soon after blunt chest trauma for early treatment to improve prognosis.

  3. Acute suprachoroidal haemorrhage post-tenecteplase thrombolysis for myocardial infarction: management considerations.

    Science.gov (United States)

    Trikha, Sameer; Lockwood, Alastair; Puvanachandra, Narman; Kirwan, James

    2010-05-13

    We report a case of a 63-year-old man who received intravenous tenecteplase as thrombolytic therapy for an inferior ST elevation myocardial infarction. Three hours later he complained of blurred vision in the right eye and on examination had sustained a suprachoroidal haemorrhage. With conservative treatment the haemorrhage resolved, leading to a normalisation of visual acuity. To the authors' knowledge, no case reports exist of this rare complication following intravenous tenecteplase. We discuss implications for further thrombolysis and anticoagulation.

  4. Acute suprachoroidal haemorrhage post-tenecteplase thrombolysis for myocardial infarction: management considerations

    OpenAIRE

    2010-01-01

    We report a case of a 63-year-old man who received intravenous tenecteplase as thrombolytic therapy for an inferior ST elevation myocardial infarction. Three hours later he complained of blurred vision in the right eye and on examination had sustained a suprachoroidal haemorrhage. With conservative treatment the haemorrhage resolved, leading to a normalisation of visual acuity. To the authors’ knowledge, no case reports exist of this rare complication following intravenous tenecteplase. We di...

  5. A Novel Method in the Stratification of Post-Myocardial-Infarction Patients Based on Pathophysiology.

    Directory of Open Access Journals (Sweden)

    Ben He

    Full Text Available We proposed that the severity of ST-segment elevation myocardial infarction (STEMI could be classified based on pathophysiological changes.First-STEMI patients were classified within hospitalization. Grade 0: no detectable myocardial necrosis; Grade 1: myocardial necrosis without functional and morphological abnormalities; Grade 2: myocardial necrosis with reduced LVEF; Grade 3: reduced LVEF on the basis of cardiac remodeling; Grade 4: mitral regurgitation additional to the Grade-3 criteria.Of 180 patients, 1.7, 43.9, 26.1, 23.9 and 4.4% patients were classified as Grade 0 to 4, respectively. The classification is an independent predicator of 90-day MACEs (any death, resuscitated cardiac arrest, acute heart failure and stroke: the rate was 0, 5.1, 8.5, 48.8 and 75% from Grade 0 to 4 (p < 0.001, respectively. The Grade-2 patients were more likely to have recovered left ventricular ejection fraction than the Grade-3/4 patients did after 90 days (48.9% vs. 19.1%, p < 0.001. Avoiding complicated quantification, the classification served as a good reflection of infarction size as measured by cardiac magnetic resonance imaging (0 ± 0, 15.68 ± 8.48, 23.68 ± 9.32, 36.12 ± 11.35 and 40.66 ± 14.33% of the left ventricular mass by Grade 0 to 4, P < 0.001, and with a comparable prognostic value (AUC 0.819 vs. 0.813 for infarction size, p = 0.876 by C-statistics for MACEs.The new classification represents an easy and objective method to scale the cardiac detriments for STEMI patients.

  6. Reperfusion Therapy in Integrative Medicine:the Most Basic Treatment for Preventing Ventricular Remodeling in Post-myocardial Infarction Patients

    Institute of Scientific and Technical Information of China (English)

    WANG Shuo-ren

    2007-01-01

    @@ Acute myocardial infarction (AMI) is the severest pathological basis of ventricular remodeling (VR) in coronary heart disease(CHD).VR is a process of ventricular changes in size,shape,and tissue structure caused by increasing of myocardial load or myocardial damage,including myocardial infarction,poisoning,inflammation,and metabolist abnormality.

  7. EFFECTS OF Β-ADRENOBLOCKERS ON MYOCARDIAL REMODELING, IMMUNO-INFLAMMATORY REACTIONS AND ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH ISCHEMIC HEART DISEASE AND CHRONIC HEART FAILURE

    Directory of Open Access Journals (Sweden)

    A. N. Zakirova

    2015-12-01

    Full Text Available Aim. To assess the effect of β-adrenoblockers (BAB on myocardial remodeling, immuno-inflammatory reactions and endothelial dysfunction in patients with ischemic heart disease and chronic heart failure (CHF.Material and methods. 84 patients with ischemic CHF of II-IV functional class were involved in the study. They were randomized in two groups. The first group was presented with 43 patients receiving carvedilol in addition to standard therapy for 24 weeks; the second group was presented with 41patients receiving metoprolol. Echocardiography, 6-minute walk test were applied. Blood levels of primary and secondary lipid peroxidation (LP products, cytokines, endothelin-1 (ET-1, intercellular adhesive molecule (VCAM-1 were determined.Results. Both of BAB improved the clinical condition and physical working ability of patients with CHF. Carvedilol in comparison with metoprolol was more effective in myocardial remodeling prevention, inhibition of pro-inflammatory cytokines [tumor necrosis factor alpha (TNF-α, interleukins (IL-1β IL-6] and LP. Besides carvedilol increased in endothelium-dependent vasodilatation and reduced in ET-1 and VCAM-1 levels.Conclusion. Long-term carvedilol treatment has anti-inflammatory, antioxidant and endothelium-protective effects as well as improves haemodynamics. 

  8. Post-prostatectomy erectile dysfunction: contemporary approaches from a US perspective

    Directory of Open Access Journals (Sweden)

    Hamilton Z

    2014-05-01

    Full Text Available Zachary Hamilton,1 Moben Mirza,2 1Department of Urology, 2Division of Urologic Oncology, Department of Urology, University of Kansas, Kansas City, KS, USA Abstract: Success of cancer surgery often leads to life-changing side effects, and surgical treatment for malignant urologic disease often results in erectile dysfunction (ED. Patients that undergo surgical prostatectomy or cystoprostatectomy will often experience impairment of erections due to disruption of blood and nerve supply. Surgical technique, nerve sparing status, patient age, comorbid conditions, and pretreatment potency status all have an effect on post-surgical ED. Regardless of surgical technique, prostatectomy results in disruption of normal anatomy and nerve supply to the penis, which governs the functional aspects of erection. A variety of different treatment options are available for men who develop ED after prostatectomy, including vacuum erection device, oral phosphodiesterase 5 inhibitors (PDE5I, intracorporal injections, and penile prosthesis. The vacuum erection device creates an artificial erection by forming a vacuum via suction of air to draw blood into the penis. The majority of men using the vacuum erection device daily after prostatectomy, regardless of nerve-sparing status, have erections sufficient for intercourse. Phosphodiesterase 5 inhibitors remain a common treatment option for post-surgical ED and are the mainstay of therapy. They work through cyclic adenosine monophosphate and cyclic guanine monophosphate pathways and are recommended in all forms of ED. Intracorporal injections or intraurethral use of vasoactive substances may be a good second-line therapy in men who do not experience improvement with oral medications. Surgical placement of a penile prosthesis is typically the treatment strategy of choice after other options have failed. Semi-rigid and inflatable devices are available with high satisfaction rates. With careful patient counseling and proper

  9. Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Xian-Liang Tang

    Full Text Available Although statins impart a number of cardiovascular benefits, whether statin therapy during the peri-infarct period improves subsequent myocardial structure and function remains unclear. Thus, we evaluated the effects of atorvastatin on cardiac function, remodeling, fibrosis, and apoptosis after myocardial infarction (MI. Two groups of rats were subjected to permanent coronary occlusion. Group II (n = 14 received oral atorvastatin (10 mg/kg/d daily for 3 wk before and 4 wk after MI, while group I (n = 12 received equivalent doses of vehicle. Infarct size (Masson's trichrome-stained sections was similar in both groups. Compared with group I, echocardiographic left ventricular ejection fraction (LVEF and fractional area change (FAC were higher while LV end-diastolic volume (LVEDV and LV end-systolic and end-diastolic diameters (LVESD and LVEDD were lower in treated rats. Hemodynamically, atorvastatin-treated rats exhibited significantly higher dP/dt(max, end-systolic elastance (Ees, and preload recruitable stroke work (PRSW and lower LV end-diastolic pressure (LVEDP. Morphometrically, infarct wall thickness was greater in treated rats. The improvement of LV function by atorvastatin was associated with a decrease in hydroxyproline content and in the number of apoptotic cardiomyocyte nuclei. We conclude that atorvastatin therapy during the peri-infarct period significantly improves LV function and limits adverse LV remodeling following MI independent of a reduction in infarct size. These salubrious effects may be due in part to a decrease in myocardial fibrosis and apoptosis.

  10. Influence of high energy phosphate metabolism in postischemic myocardial dysfunction using magnetic resonance spectroscopy; Influencia dos fosfatos de alta energia na funcao ventricular em pacientes com infarto do miocardio avaliada pela resonancia magnetica

    Energy Technology Data Exchange (ETDEWEB)

    Kalil Filho, Roberto [Sao Paulo Univ., SP (Brazil). Faculdade de Medicina. Hospital das Clinicas

    1998-05-01

    The recovery of left ventricular function after reperfusion is delayed in general by several hours, days or weeks and this phenomenon is known as myocardial stunning. One of the theories to explain the pathogenesis of this postischemic myocardial dysfunction is the production of not enough energy by mitochondria, leading to decreased adenosine-triphosphate (ATP) levels. We evaluated the influence of high energy phosphate metabolism in postischemic myocardial dysfunction, using magnetic resonance spectroscopy in patients with acute anterior wall myocardial infarction, successfully reperfused, within the first six hours from the onset of the symptoms. Twenty-nine patients were studied in the acute phase (on average four days after the onset of myocardial infarction) and 21 repeated the examination in the follow-up phase (average 39 days). Regional left ventricular function was evaluated by cine-resonance and high energy phosphate metabolism by phosphorus-31 spectroscopy, using the phosphocreatine {beta} ATP (P Cr/{beta}ATP) ratio. The existence of myocardial stunning was suggested by the improvement of the related regional contractility during the follow-up. The contractility improved in the septal wall from 2.46{+-} 0.68 to 1.54 {+-} 0.78 (p<0.001), in the anteroseptal wall from 2.0 {+-} 0.89 to 1.40 {+-} 0.75 (p<0.001) and in the anterior wall from 2.37 {+-} 0.71 to 1.41 {+-} 0.59 (p<0.001). The P Cr/{beta}ATP ratio did not change from acute to follow-up phase (1.51 {+-} 0.17 vs. 1.53 {+-} 0.17; p = 0.6). This study suggests that decreased high energy phosphate metabolism after reperfusion does not have an important role in the genesis of the myocardial stunning in patients with acute anterior wall myocardial infarction. (author) 25 refs., 9 figs., 1 tab.

  11. Systemic and Cardiac Depletion of M2 Macrophage through CSF-1R Signaling Inhibition Alters Cardiac Function Post Myocardial Infarction.

    Science.gov (United States)

    Leblond, Anne-Laure; Klinkert, Kerstin; Martin, Kenneth; Turner, Elizebeth C; Kumar, Arun H; Browne, Tara; Caplice, Noel M

    2015-01-01

    The heart hosts tissue resident macrophages which are capable of modulating cardiac inflammation and function by multiple mechanisms. At present, the consequences of phenotypic diversity in macrophages in the heart are incompletely understood. The contribution of cardiac M2-polarized macrophages to the resolution of inflammation and repair response following myocardial infarction remains to be fully defined. In this study, the role of M2 macrophages was investigated utilising a specific CSF-1 receptor signalling inhibition strategy to achieve their depletion. In mice, oral administration of GW2580, a CSF-1R kinase inhibitor, induced significant decreases in Gr1lo and F4/80hi monocyte populations in the circulation and the spleen. GW2580 administration also induced a significant depletion of M2 macrophages in the heart after 1 week treatment as well as a reduction of cardiac arginase1 and CD206 gene expression indicative of M2 macrophage activity. In a murine myocardial infarction model, reduced M2 macrophage content was associated with increased M1-related gene expression (IL-6 and IL-1β), and decreased M2-related gene expression (Arginase1 and CD206) in the heart of GW2580-treated animals versus vehicle-treated controls. M2 depletion was also associated with a loss in left ventricular contractile function, infarct enlargement, decreased collagen staining and increased inflammatory cell infiltration into the infarct zone, specifically neutrophils and M1 macrophages. Taken together, these data indicate that CSF-1R signalling is critical for maintaining cardiac tissue resident M2-polarized macrophage population, which is required for the resolution of inflammation post myocardial infarction and, in turn, for preservation of ventricular function.

  12. Effect of streptokinase on reperfusion after acute myocardial infarction and its complications: an ex-post facto study.

    Science.gov (United States)

    Taheri, Leila; Boroujeni, Ali Zargham; Kargar Jahromi, Marzieh; Charkhandaz, Maryam; Hojat, Mohsen

    2015-01-01

    Emergency treatment of patients with acute myocardial infarction is very important. Streptokinase in Iran is often as the only clot-busting medication is used. The purpose of using streptokinase medication is to revive the ischemic heart tissue, although has dangerous complications too. Therefore, the present study aimed to determine the effect of streptokinase on reperfusion after acute myocardial infarction and its complications, has been designed and conducted. This is an Ex-post facto study. The study population included patients who suffer from acute myocardial infarction. The sample size was 300 patients, and 2 groups were matched, in variables of age, sex, underlying disease, frequencies and area of MI. Data collection did by researcher making questionnaire, that accept face and content validity by 10 expert researcher, the reliability was conducted with Spearman's test (r=0.85) by Test-retest method. Data analysis did by SPSS software: V 12. Mean of EF in SK group was (46.15±8.11) and in control group was (43.11±12.57). Significant relationship was seen between SK, arrhythmia occurring and improve EF reperfusion by chi-square test (p=0.028), (p=0.020).The most arrhythmia in SK group was Ventricular Tachycardia (20.7%). Significant statistical relation between SK and mortality were found by Chi-square test (p=0.001). But a meaningful statistical relation was not found between SK and pulmonary edema incidence (p=0.071). Nurses of CCU should be aware about SK complications such as hypotension, bleeding and arrhythmias. Proposed compare SK and tissue plasminogen drug in reperfusion and complications effect.

  13. Adenosine A2A  receptor agonist prevents cardiac remodeling and dysfunction in spontaneously hypertensive male rats after myocardial infarction

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    da Silva JS

    2017-03-01

    Full Text Available Jaqueline S da Silva,1 Daniele Gabriel-Costa,1 Roberto T Sudo,1 Hao Wang,2 Leanne Groban,2 Emanuele B Ferraz,3 José Hamilton M Nascimento,3 Carlos Alberto M Fraga,1 Eliezer J Barreiro,1 Gisele Zapata-Sudo1 1Research Program Development of Drugs, Institute of Biomedical Sciences, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil; 2Department of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, NC, USA; 3Institute of Biophysics Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil Background: This work evaluated the hypothesis that 3,4-methylenedioxybenzoyl-2- thienylhydrazone (LASSBio-294, an agonist of adenosine A2A  receptor, could be beneficial for preventing cardiac dysfunction due to hypertension associated with myocardial infarction (MI. Methods: Male spontaneously hypertensive rats (SHR were randomly divided into four groups (six animals per group: sham-operation (SHR-Sham, and myocardial infarction rats (SHR-MI were treated orally either with vehicle or LASSBio-294 (10 and 20 mg.kg-1.d-1 for 4 weeks. Echocardiography and in vivo hemodynamic parameters measured left ventricle (LV structure and function. Exercise tolerance was evaluated using a treadmill test. Cardiac remodeling was accessed by LV collagen deposition and tumor necrosis factor α expression. Results: Early mitral inflow velocity was significantly reduced in the SHR-MI group, and there was significant recovery in a dose-dependent manner after treatment with LASSBio-294. Exercise intolerance observed in the SHR-MI group was prevented by 10 mg.kg-1.d-1 of LASSBio-294, and exercise tolerance exceeded that of the SHR-Sham group at 20 mg.kg-1.d-1. LV end-diastolic pressure increased after MI, and this was prevented by 10 and 20 mg.kg-1.d-1 of LASSBio-294. Sarcoplasmic reticulum Ca2+ ATPase levels were restored in a dose-dependent manner after treatment with LASSBio-294. Fibrosis and inflammatory processes were also

  14. Attenuation of cardiac dysfunction and remodeling of myocardial infarction by microRNA-130a is mediated by suppression of PTEN and activation of PI3K dependent signaling

    Science.gov (United States)

    Lu, Chen; Wang, Xiaohui; Ha, Tuanzhu; Hu, Yuanping; Liu, Li; Zhang, Xia; Yu, Honghui; Miao, Jonathan; Kao, Race; Kalbfleisch, John; Williams, David; Li, Chuanfu

    2015-01-01

    Objective Activation of PI3K/Akt signaling protects the myocardium from ischemia/reperfusion injury. MicroRNAs have been demonstrated to play an important role in the regulation of gene expression at the post-transcriptional level. In this study, we examined whether miR-130a will attenuate cardiac dysfunction and remodeling after myocardial infarction (MI) via PI3K/Akt dependent mechanism. Approaches and Results To determine the role of miR-130a in the proliferation and migration of endothelial cells, HUVECs were transfected with miR-130a mimics before the cells were subjected to scratch-induced wound injury. Transfection of miR-130a mimics stimulated the migration of endothelial cells into the wound area and increased phosphor-Akt levels. To examine the effect of miR-130a on cardiac dysfunction and remodeling after MI, Lentivirus expressing miR-130a (LmiR-130a) was delivered into mouse hearts seven days before the mice were subjected to MI. Cardiac function was assessed by echocardiography before and for up to 21 days after MI. Ejection fraction (EF%) and fractional shortening (FS%) in the LmiR-130a transfected MI hearts were significantly greater than in LmiR-control and untransfected control MI groups. LmiR-130a transfection increased capillary number and VEGF expression, and decreased collagen deposition in the infarcted myocardium. Importantly, LmiR-130a transfection significantly suppressed PTEN expression and increased the levels of phosphorylated Akt in the myocardium. However, treatment of LmiR-130a-transfected mice with LY294002, a PI3K inhibitor, completely abolished miR-130a-induced attenuation of cardiac dysfunction after MI. Conclusions miR-130a plays a critical role in attenuation of cardiac dysfunction and remodeling after MI. The mechanisms involve activation of PI3K/Akt signaling via suppression of PTEN expression. PMID:26458524

  15. OSM mitigates post-infarction cardiac remodeling and dysfunction by up-regulating autophagy through Mst1 suppression.

    Science.gov (United States)

    Hu, Jianqiang; Zhang, Lei; Zhao, Zhijing; Zhang, Mingming; Lin, Jie; Wang, Jiaxing; Yu, Wenjun; Man, Wanrong; Li, Congye; Zhang, Rongqing; Gao, Erhe; Wang, Haichang; Sun, Dongdong

    2016-11-04

    The incidence and prevalence of heart failure (HF) in the world are rapidly rising possibly attributed to the worsened HF following myocardial infarction (MI) in recent years. Here we examined the effects of oncostatin M (OSM) on postinfarction cardiac remodeling and the underlying mechanisms involved. MI model was induced using left anterior descending coronary artery (LAD) ligation. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated MI. Our results revealed that OSM alleviated left ventricular remodeling, promoted cardiac function, restored mitochondrial cristae density and architecture disorders after 4weeks of MI. Enhanced autophagic flux was indicated in cardiomyocytes transduced with Ad-GFP -LC3 in the OSM treated group as compared with the MI group. OSM receptor Oβ knockout blocked the beneficial effects of OSM in postinfarction cardiac remodeling and cardiomyocytes autophagy. OSM pretreatment significantly alleviated left ventricular remodeling and dysfunction in Mst1 transgenic mice, while it failed to reverse further the postinfarction left ventricular dilatation and cardiac function in the Mst1 knockout mice. Our data revealed that OSM alleviated postinfarction cardiac remodeling and dysfunction by enhancing cardiomyocyte autophagy. OSM holds promise as a therapeutic target in treating HF after MI through Oβ receptor by inhibiting Mst1 phosphorylation.

  16. Regional Coherence Alterations Revealed by Resting-State fMRI in Post-Stroke Patients with Cognitive Dysfunction.

    Directory of Open Access Journals (Sweden)

    Cheng-Yu Peng

    Full Text Available Post-stroke cognitive dysfunction greatly influences patients' quality of life after stroke. However, its neurophysiological basis remains unknown. This study utilized resting-state functional magnetic resonance imaging (fMRI to investigate the alterations in regional coherence in patients after subcortical stroke.Resting-state fMRI measurements were acquired from 16 post-stroke patients with poor cognitive function (PSPC, 16 post-stroke patients with good cognitive function (PSGC and 30 well-matched healthy controls (HC. Regional homogeneity (ReHo was used to detect alterations in regional coherence. Abnormalities in regional coherence correlated with scores on neuropsychological scales.Compared to the HC and the PSGC, the PSPC showed remarkably decreased ReHo in the bilateral anterior cingulate cortex and the left posterior cingulate cortex/precuneus. ReHo in the bilateral anterior cingulate cortex positively correlated with the scores on the Symbol Digit Modalities Test (r = 0.399, P = 0.036 and the Complex Figure Test-delayed recall subtest (r = 0.397, P = 0.036 in all post-stroke patients. Moreover, ReHo in the left posterior cingulate cortex/precuneus positively correlated with the scores on the Forward Digit Span Test (r = 0.485, P = 0.009 in all post-stroke patients.Aberrant regional coherence was observed in the anterior and posterior cingulate cortices in post-stroke patients with cognitive dysfunction. ReHo could represent a promising indicator of neurobiological deficiencies in post-stroke patients.

  17. Differential prognostic importance of QRS duration in heart failure and acute myocardial infarction associated with left ventricular dysfunction

    DEFF Research Database (Denmark)

    Fosbøl, Emil Loldrup; Seibaek, Marie; Brendorp, Bente;

    2007-01-01

    randomised 3028 patients to dofetilide (class III antiarrhythmic) or placebo. The study consisted of two almost identical trials conducted simultaneously. One trial included 1518 patients with chronic HF and the other trial 1510 patients with a recent MI. All patients had left ventricular dysfunction...

  18. Serum Klotho (but not haplotypes associate with the post-myocardial infarction status of older adults

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    Roberta S. Paula

    Full Text Available OBJECTIVES: The number of deaths from vascular diseases is incredibly high worldwide, and reliable markers for major events are still needed. The current cross-sectional study investigated the association of Klotho haplotypes and Klotho serum levels with classic risk factors and a clinical history of vascular events. METHODS: Clinical, anthropometric, biochemical and nutritional assessments were conducted with 168 older adults, complemented by genotyping (rs9536314 and rs9527025 and the detection of serum Klotho (ELISA. RESULTS: Klotho levels and haplotypes did not associate with most classic risk factors for vascular events, including markers such as C-reactive protein and homocysteine. A positive association was only found between Klotho levels and the previous occurrence of a myocardial infarction by both correlational (p=0.006 and variance analyses (p<0.001, and these associations were independent of the context. CONCLUSION: Our results suggest that serum Klotho is higher in individuals with a clinical history of myocardial infarction but not with a history of coronary artery disease or stroke. None of the Klotho haplotypes were associated with the variables investigated herein.

  19. Human bone marrow-derived adult stem cells for post-myocardial infarction cardiac repair: current status and future directions.

    Science.gov (United States)

    Wei, H M; Wong, P; Hsu, L F; Shim, W

    2009-10-01

    Stem cell-based cell therapy has emerged as a potentially therapeutic option for patients with acute myocardial infarction (AMI) and heart failure. With the completion of a number of trials using bone marrow (BM)-derived adult stem cells, critical examination of the overall clinical benefits, limitations and potential side effects of this revolutionary treatment will pave the way for future clinical research. At present, clinical trials have been conducted almost exclusively using BM stem cells. The primary endpoints of these trials are mainly safety and feasibility, with secondary endpoints in the efficacy of post-myocardial infarction (MI) cardiac repair. Intervention with BM-derived cells was mainly carried out by endogenously-mobilised BM cells with granulocyte-colony stimulating factor, and more frequently, by intracoronary infusion or direct intramyocardial injection of autologous BM cells. While these studies have been proven safe and feasible without notable side effects, mixed outcomes in terms of clinical benefits have been reported. The major clinical benefits observed are improved cardiac contractile function and suppressed left ventricular negative remodelling, including reduced infarct size and improved cardiac perfusion of infarct zone. Moderate and transient clinical benefits have been mostly observed in studies with intracoronary infusion or direct intramyocardial injection of BM cells. These effects are widely considered to be indirect effects of implanted cells in association with paracrine factors, cell fusion, passive ventricular remodelling, or the responses of endogenous cardiac stem cells. In contrast, evidence of cardiac regeneration characterised by differentiation of implanted stem cells into cardiomyocytes and other cardiac cell lineages, is weak or lacking. To elucidate a clear risk-benefit of this exciting therapy, future studies on the mechanisms of cardiac cell therapy will need to focus on confirming the ideal cell types in relation

  20. Severe right ventricular dysfunction is an independent predictor of pre- and post-transplant mortality among candidates for heart transplantation.

    Science.gov (United States)

    Ravis, Eleonore; Theron, Alexis; Mancini, Julien; Jaussaud, Nicolas; Morera, Pierre; Chalvignac, Virginie; Guidon, Catherine; Grisoli, Dominique; Gariboldi, Vlad; Riberi, Alberto; Habib, Gilbert; Mouly-Bandini, Annick; Collart, Frederic

    2017-03-01

    Heart transplantation is the gold-standard treatment for end-stage heart failure. However, the shortage of grafts has led to longer waiting times and increased mortality for candidates without priority. To study waiting-list and post-transplant mortality, and their risk factors among patients registered for heart transplantation without initial high emergency procedure. All patients registered on the heart transplantation waiting list (2004-2015) without initial high emergency procedure were included. Clinical, biological, echocardiographic and haemodynamic data were collected. Waiting list and 1-year post-transplant survival were analysed with a Kaplan-Meier model. Of 221 patients enrolled, 168 (76.0%) were men. Mean age was 50.0±12.0 years. Forty-seven patients died on the waiting list, resulting in mortality rates of 11.2±2.7% at 1 year, 31.9±5.4% at 2 years and 49.4±7.1% at 3 years. Median survival was 36.0±4.6 months. In the multivariable analysis, left ventricular ejection fractionright ventricular systolic dysfunction (HR: 2.89, 95% CI: 1.41-5.92; P=0.004) were associated with increased waiting-list mortality. The post-transplant survival rate was 73.1±4.4% at 1 year. Pretransplant severe right ventricular dysfunction and age>50 years were strong predictors of death after transplantation (HR: 5.38, 95% CI: 1.38-10.24 [P=0.020] and HR: 6.16, 95% CI: 1.62-9.32 [P=0.0130], respectively). Mortality among candidates for heart transplantation remains high. Patients at highest risk of waiting-list mortality have to be promoted, but without compromising post-transplant outcomes. For this reason, candidates with severe right ventricular dysfunction are of concern, because, for them, transplantation is hazardous. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  1. [Effectiveness of the physical training of post-myocardial infarction patients with differing exertion tolerances].

    Science.gov (United States)

    Barats, S S; Lipchenko, A A; Vetrov, A V

    1986-01-01

    A total of 159 men after myocardial infarction were examined. Of them 73 were engaged in physical training for 11 mos. Its efficacy was analysed after the results of bicycle ergometry taking account of initial exercise tolerance. A positive effect of physical training was noted both in the patients with high and low exercise tolerance. Raised physical working capacity was observed in parallel with the improved indices of the left ventricular contractility in accordance with the results of two-dimensional echocardiography. The authors also observed a favorable effect of physical training on lipoprotein metabolism, in particular a decrease in the value of the apo B/apo AI ratio was noted that might suggest a decrease in the inflow of cholesterol to the vascular wall and an enhanced outflow from it.

  2. EFFECT IMBALANCE AQUEOUS BODY FLUIDS, AND RENAL DYSFUNCTION, CARDIOVASCULAR SURVIVAL IN PATIENTS AFTER AN ACUTE CORONARY SYNDROME, MYOCARDIAL REVASCULARIZATION

    Directory of Open Access Journals (Sweden)

    E. S. Levitskaya

    2017-01-01

    Full Text Available Objective. Analysis imbalance aqueous body fluids on the prognosis of cardiovascular events in the late period after an acute coronary syndrome (ACS and myocardial revascularization based on indicators of renal function.Materials and methods. The study included 120 patients with ACS, including unstable angina was diagnosed in 68 patients, 52 patients — acute myocardial infarction. All patients underwent myocardial revascularization. To register the presence of albuminuria in the range of 30-300 mg/l, and glomerular filtration rate (GFR. It makes calculations indicators aqueous body fluids — the total volume of water (TVW, the total fluid, intracellular fluid (IF, extracellular fluid. The endpoint of the study was the presence of cardiovascular complications within 6 months after ACS.Results. It is found that the presence and magnitude of albuminuria was significantly increase the risk of the end point of the study. In patients with GFR less than 60 mL/min/1,73m2 studied the risk is higher by 17.1%, compared with patients with a GFR above this limit. Analysis of the distribution of the water body fluids showed a significant increase in the average TVW and IF. Through statistical analysis of survival found an increased risk of cardiovascular complications in the late period after ACS in patients who have an increase IF on the stage of development of coronary catastrophe.Conclusion. The study demonstrated the predictive value to stratify cardiovascular disease risk, not only the presence of albuminuria, but its level and value of GFR less than 60 mL/min/1,73m2. Redistribution of aqueous body fluids in the form of increased IF is a marker of adverse cardiovascular events in the late period after ACS. These data indicate the need for a comprehensive and integrated analysis of existing pathogenetic changes occurring in ACS, as well as the status of the patients premorbid factor for improving risk stratification of cardiovascular

  3. Reperfusion-induced myocardial dysfunction is prevented by endogenous annexin-A1 and its N-terminal-derived peptide Ac-ANX-A1(2-26).

    Science.gov (United States)

    Qin, Chengxue; Buxton, Keith D; Pepe, Salvatore; Cao, Anh H; Venardos, Kylie; Love, Jane E; Kaye, David M; Yang, Yuan H; Morand, Eric F; Ritchie, Rebecca H

    2013-01-01

    Annexin-A1 (ANX-A1) is an endogenous, glucocorticoid-regulated anti-inflammatory protein. The N-terminal-derived peptide Ac-ANX-A1(2-26) preserves cardiomyocyte viability, but the impact of ANX-A1-peptides on cardiac contractility is unknown. We now test the hypothesis that ANX-A1 preserves post-ischaemic recovery of left ventricular (LV) function. Ac-ANX-A1(2-26) was administered on reperfusion, to adult rat cardiomyocytes as well as hearts isolated from rats, wild-type mice and mice deficient in endogenous ANX-A1 (ANX-A1(-/-)). Myocardial viability and recovery of LV function were determined. Ischaemia-reperfusion markedly impaired both cardiomyocyte viability and recovery of LV function by 60%. Treatment with exogenous Ac-ANX-A1(2-26) at the onset of reperfusion prevented cardiomyocyte injury and significantly improved recovery of LV function, in both intact rat and wild-type mouse hearts. Ac-ANX-A1(2-26) cardioprotection was abolished by either formyl peptide receptor (FPR)-nonselective or FPR1-selective antagonists, Boc2 and cyclosporin H, but was relatively insensitive to the FPR2-selective antagonist QuinC7. ANX-A1-induced cardioprotection was associated with increased phosphorylation of the cell survival kinase Akt. ANX-A1(-/-) exaggerated impairment of post-ischaemic recovery of LV function, in addition to selective LV FPR1 down-regulation. These data represent the first evidence that ANX-A1 affects myocardial function. Our findings suggest ANX-A1 is an endogenous regulator of post-ischaemic recovery of LV function. Furthermore, the ANX-A1-derived peptide Ac-ANX-A1(2-26) on reperfusion rescues LV function, probably via activation of FPR1. ANX-A1-based therapies may thus represent a novel clinical approach for the prevention and treatment of myocardial reperfusion injury. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

  4. A comparison of the efficacy of surgical renal denervation and pharmacologic therapies in post-myocardial infarction heart failure.

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    Jialu Hu

    Full Text Available OBJECTIVE: Although renal denervation (RD has been shown to be effective in treating post- myocardial Infarction (MI heart failure (HF in animal models and clinical trials, its utility as a standalone treatment without traditional drug treatment for post-MI HF still needs to be investigated. METHODS: Rats were randomly assigned into seven experimental groups: N group (control group with no MI and no RD, n = 10, MI group (MI, n = 20, RD group (renal denervation, n = 10, RD-3d+MI group (RD performed three days before MI, n = 15, β-blocker-3d+MI group (Metoprolol treated three days before MI, n = 15, ACEI-3d+MI group (Perindopril treated three days before MI, n = 15, and ARB-3d+MI group (Losartan treated three days before MI, n = 15. Cardiac function, autonomic nervous system parameters, and neuroendocrine activities were evaluated 8 weeks post MI. RESULTS: Compared to β-blockers, ACEIs, and ARBs, RD alone provided significantly better cardiac remodeling and function, enhanced water and sodium excretion, and improved autonomic modulation. CONCLUSIONS: In this post-MI HF animal model, surgical RD provides effective autonomic modulation, inhibition of the RAAS, improved cardiac remodeling, and preserved renal function, without affecting normal circulation and cardiopulmonary function in normal rats. Compared to β-blocker, ACEI, and ARB single-drug therapies, RD alone is more efficacious. These results suggest that RD may be an effective treatment option for HF, especially in patients who have contraindications to drug therapy.

  5. Magnetic resonance imaging in the assessment of the myocardial viability; Ressonancia magnetica cardiaca na avaliacao da viabilidade miocardica

    Energy Technology Data Exchange (ETDEWEB)

    Andrade, Joalbo; Baptista, Luciana; Favaro, Daniele; Loureiro, Ricardo; Parga Filho, Jose; Avila, Luiz F.; Rochitte, Carlos E.; Piva, Rosa M.V.; Castro, Claudio C. [Hospital das Clinicas, Sao Paulo, SP (Brazil). Instituto do Coracao. Secao de Ressonancia Magnetica]. E-mail: jmtandrade@hotmail.com; Cerri, Giovanni G. [Hospital das Clinicas, Sao Paulo, SP (Brazil). Instituto do Coracao. Div. de Diagnostico por Imagem

    2003-07-01

    The assessment of myocardial viability in patients with coronary artery disease and ventricular dysfunction is important in order to differentiate viable from nonviable myocardium. Magnetic resonance imaging allows assessment of myocardial viability by evaluating the contractility of the heart and the analysis of post-gadolinium images using a T1-weighted spoiled gradient echo sequences with a preparation inversion pulse to null the normal myocardial signal. The aim of this study is to describe the magnetic resonance imaging technical parameters and image acquisition approach using a recently validated gadolinium-enhanced technique for the assessment of myocardial viability. (author)

  6. Evaluation of mouse models of myocardial dysfunction and myocardial fibrosis by speckle tracking imaging%斑点追踪成像评估小鼠心肌功能不全及纤维化的研究

    Institute of Scientific and Technical Information of China (English)

    褚明; 雍永宏; 洪牮; 王瑛璎; 姚静; 许迪

    2013-01-01

    Objective To investigate the value of two-dimensional speckle tracking imaging (STI) in assessing regional myocardial dysfunction and myocardial fibrosis in a mouse model of myocardial infarction.Methods Twenty C57/B6 mice were randomly divided into two groups:myocardial infarction (MI) group (n =10) and sham-operation (SO) group (n =10).Echocardiography was performed four weeks after surgery.High frame rate two dimensional images were recorded in the left ventricular short axis views at the papillary muscle level and analysised at EchoPac workstation.Peak radical strain (PRS) and peak radical strain rate (PRSR) of each segment were measured at systolic period.Percent segmental fibrosis (PSF) was assessed from histological left ventricular cross sections stained by Masson trichrome.Results Compared with SO group,PRS and PRSR decreased significantly in all segments of MI group (P < 0.01),especially in anterosepetal,anterior and lateral segments (P <0.05).PSF of anterosepetal,anterior,lateral and posterior segments in MI group increased significantly than those in SO group(P <0.01),and were negatively correlated with PRS and PRSR of these segments(r =-0.88,P <0.001 ; r =-0.77,P <0.001).Conclusions STI could accurately quantify regional myocardial function in a mouse model of myocardial infarction.Segmental radial strain and strain rate measured by STI were significantly correlated with PSF,which can be a non-invasive tool for monitoring myocardial fibrosis after myocardial infarction.%目的 探讨二维超声斑点追踪成像技术评估小鼠心肌梗死模型局部心肌功能不全及心肌纤维化程度的应用价值.方法 20只C57/B6小鼠随机分成两组:心肌梗死手术模型(MI)组10只和假手术(SO)组,10只.实验小鼠于术后4周行超声心动图检查,应用EchoPac工作站分析左室乳头肌短轴观高帧频图像,测量各节段收缩期峰值径向应变(peak radical strain,PRS)及峰值径向应变率(peak radical strain

  7. A follow-up study on post myocardial infarction depression in a tertiary healthcare centre of Assam

    Directory of Open Access Journals (Sweden)

    Hemanta Dutta

    2016-01-01

    Full Text Available Background: Major depressive disorder is widely prevalent in post myocardial infarction (MI period. Various studies have reported a significant relationship between these two major disease states. Aim: To examine depression after MI and its socio-demographic variation. Methods: The study was a follow up study on patients of acute MI (n=50 attending cardiology outpatient department of the Assam Medical College Hospital in four to six weeks after the index event. Screening was done by the Primary Care Evaluation of Mental Disorders and diagnoses of major depressive disorder were established according to the text revision of the fourth edition of the Diagnostic and Statistical Manual for Mental Disorders criteria. Severity of the depression was assessed by the Beck Depression Inventory. Study populations were again reassessed after eight weeks from the index event. Statistical software packages like SPSS-20, XLSTAT, and Microsoft Office Access were used for analysis. Results: Twenty eight and 32% of the study subjects were depressed on their first and second visit respectively. Conclusion: Similar pattern of post MI depression is found in our state likewise in correlation to western and Indian studies which were conducted in different states. So we recommend vigilance from the clinician’s side while handling cases of MI.

  8. Untangling the relationship between medication adherence and post-myocardial infarction outcomes: medication adherence and clinical outcomes.

    Science.gov (United States)

    Choudhry, Niteesh K; Glynn, Robert J; Avorn, Jerry; Lee, Joy L; Brennan, Troyen A; Reisman, Lonny; Toscano, Michele; Levin, Raisa; Matlin, Olga S; Antman, Elliott M; Shrank, William H

    2014-01-01

    Patients who adhere to medications experience better outcomes than their nonadherent counterparts. However, these observations may be confounded by patient behaviors. The level of adherence necessary for patients to derive benefit and whether adherence to all agents is important for diseases that require multiple drugs remain unclear. This study quantifies the relationship between medication adherence and post-myocardial infarction (MI) adverse coronary events. This is a secondary analysis of the randomized MI FREEE trial. Patients who received full prescription coverage were classified as adherent (proportion of days covered ≥80%) or not based upon achieved adherence in the 6 months after randomization. First major vascular event or revascularization rates were compared using multivariable Cox models adjusting for comorbidity and health-seeking behavior. Compared with patients randomized to usual care, full coverage patients adherent to statin, β-blocker, or angiotensin-converting enzyme inhibitor/angiotensin receptor blocker were significantly less likely to experience the study's primary outcome (hazard ratio [HR] range 0.64-0.81). In contrast, nonadherent patients derived no benefit (HR range 0.98-1.04, P ≤ .01 for the difference in HRs between adherent and nonadherent patients). Partially adherent patients had no reduction in clinical outcomes for any of the drugs evaluated, although their achieved adherence was higher than that among controls. Achieving high levels of adherence to each and all guideline-recommended post-MI secondary prevention medication is associated with improved event-free survival. Lower levels of adherence appear less protective. © 2014.

  9. 缬沙坦或卡托普利或二者联合治疗心肌梗塞伴心力衰竭和(或)左心室功能障碍的评价%Evaluation of Valsartan, Captopril or Both in Myocardial Infarction Complicated by Heart Failure, Left Ventricular Dysfunction, or Both

    Institute of Scientific and Technical Information of China (English)

    钱卫民

    2005-01-01

    Pfeffer MA, McMurray JV, Velazquez E J, et al. Valsartan, Captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both [J]. N Engl J Med, 2003, 349 (20) : 1893-1905.

  10. ST-elevated acute myocardial infarction happening 1 month post stent implantation: late thrombosis in-stents or new lesions?

    Institute of Scientific and Technical Information of China (English)

    SONG Guang-yuan; YANG Yue-jin; XU Bo; LI Jian-jun; GAO Run-lin; QIAO Shu-bin; YUAN Jin-qing; TANG Yi-da; YOU Shi-jie; PEI Han-jun; ZHAO Zhen-yan; WANG Xi-mei; WU Yong-jian

    2009-01-01

    Background ST-elevated acute myocardial infarction (STEAMI) happening in the first month post percutaneous coronary intervention (PCI) is almost related to acute thrombosis or subacute thrombosis in-stents. This study aimed to investigate the possible causes of myocardial infarction one month later. Methods Patients who had a history of successful PCI, and received coronary angiography or re-PCI due to STEAMI were included in this study. The AMI-related lesions and previous angiographic findings such as the number of lesions, the degree of the stenosis, the type of stents and acute results of last PCI were recorded. If the AMI-related lesion was localized in-stents or at the edge of stents (distance apart from the edge <5 mm), it was defined to be late thrombosis; otherwise as a new-lesion induced AMI. Results One hundred and ninety-two patients aged 40-79 years were included in this study. New lesions, as the cause of STEAMI, were found in 144 patients (Group A, 75%), and late thrombosis in 48 patients (Group B, 25%). Almost all newly built thromboses were found at the sites of previous insignificant lesions (diameter stenosis <50%). There was a significant difference in the average time from previous PCI to AMI ((30.1+12.4) vs (20.3+11.9) months) between the two groups. Diabetes mellitus (DM) and drug-eluting stent (DES) utilization were associated with markedly higher morbidity of late thrombosis in adjusted Logistic regression (hazard ratio (HR) 3.4, 95% confidence interval (CI) 1.1-10.9 and 5.3, 95% CI 1.1-26.5). Conclusions STEAMIs happening 1 month after PCI are more likely to develop from previous insignificant lesion rupture than from late thrombosis in-stents. Moreover, DM and DES are associated with the high incidence of latethrombosis, which may indicate that intensive antiplatelet therapy should be considered in patients with diabetes.

  11. Have we given up on intra-aortic balloon counterpulsation in post-myocardial infarction cardiogenic shock?

    Science.gov (United States)

    Acharji, Subasit; Mathur, Atish; Lakshmanadoss, Umashankar; Prasad, Hari; Singh, Maninder; Kaluski, Edo

    2013-11-01

    The recently published Intra-aortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial concluded that intra-aortic counterpulsation (IACP) does not reduce 30-day mortality in patients with cardiogenic shock (CS) complicating acute myocardial infarction (AMI) for whom early revascularization strategy was planned. The study resulted in downgrading IACP in post-AMI CS patients by certain professional organizations like the European Society of Cardiology. Although this is the largest and most important CS study of this decade, it suffers from considerable shortcomings: (1) time intervals from chest-pain onset or AMI recognition to revascularization, enrollment, and IACP initiation are not disclosed; (2) 86.6% of the treatment arm initiated IACP only post-percutaneous coronary intervention (PCI), and 4.3 % did not receive IACP at all; (3) 17.4% of the control arm crossed over to IACP or other mechanical support, mostly due to protocol violations; (4) there is no adjudication of the mortality events; (5) follow-up is limited to 30 days; and (5) both methodology (especially IACP device size) and quality of IACP are not evaluated and documented. Because the study assessed mostly the efficacy and safety of IACP initiated post-PCI, the study conclusions should not be extrapolated to IACP pre-PCI or during PCI in CS. Moreover, IACP had a favorable effect on the mortality of younger patients. Intra-aortic counterpulsation should remain the first line of mechanical circulatory support for the hemodynamically compromised AMI patients with or without CS who are undergoing primary PCI. Early upgrade to more advanced mechanical circulatory support should be considered for selective suitable candidates who remain in refractory CS despite revascularization and IACP.

  12. Endothelial dysfunction, carotid artery plaque burden, and conventional exercise-induced myocardial ischemia as predictors of coronary artery disease prognosis

    Directory of Open Access Journals (Sweden)

    Ishihara Masayuki

    2008-12-01

    Full Text Available Abstract Background While both flow-mediated vasodilation (FMD in the brachial artery (BA, which measures endothelium-dependent vasodilatation, and intima-media thickness (IMT in the carotid artery are correlated with the prognosis of coronary artery disease (CAD, it is not clear which modality is a better predictor of CAD. Furthermore, it has not been fully determined whether either of these modalities is superior to conventional ST-segment depression on exercise stress electrocardiogram (ECG as a predictor. Thus, the goal of the present study was to compare the predictive value of FMD, IMT, and stress ECG for CAD prognosis. Methods and Results A total of 103 consecutive patients (62 ± 9 years old, 79 men with clinically suspected CAD had FMD and nitroglycerin-induced dilation (NTG-D in the BA, carotid artery IMT measurement using high-resolution ultrasound, and exercise treadmill testing. The 73 CAD patients and 30 normal coronary patients were followed for 50 ± 15 months. Fifteen patients had coronary events during this period (1 cardiac death, 2 non-fatal myocardial infarctions, 3 acute heart failures, and 9 unstable anginas. On Kaplan-Meier analysis, only FMD and stress ECG were significant predictors for cardiac events. Conclusion Brachial endothelial function as reflected by FMD and conventional exercise stress testing has comparable prognostic value, whereas carotid artery plaque burden appears to be less powerful for predicting future cardiac events.

  13. Permeabilized myocardial fibers as model to detect mitochondrial dysfunction during sepsis and melatonin effects without disruption of mitochondrial network.

    Science.gov (United States)

    Doerrier, Carolina; García, José A; Volt, Huayqui; Díaz-Casado, María E; Luna-Sánchez, Marta; Fernández-Gil, Beatriz; Escames, Germaine; López, Luis C; Acuña-Castroviejo, Darío

    2016-03-01

    Analysis of mitochondrial function is crucial to understand their involvement in a given disease. High-resolution respirometry of permeabilized myocardial fibers in septic mice allows the evaluation of the bioenergetic system, maintaining mitochondrial ultrastructure and intracellular interactions, which are critical for an adequate functionality. OXPHOS and electron transport system (ETS) capacities were assessed using different substrate combinations. Our findings show a severe septic-dependent impairment in OXPHOS and ETS capacities with mitochondrial uncoupling at early and late phases of sepsis. Moreover, sepsis triggers complex III (CIII)-linked alterations in supercomplexes structure, and loss of mitochondrial density. In these conditions, melatonin administration to septic mice prevented sepsis-dependent mitochondrial injury in mitochondrial respiration. Likewise, melatonin improved cytochrome b content and ameliorated the assembly of CIII in supercomplexes. These results support the use of permeabilized fibers to identify properly the respiratory deficits and specific melatonin effects in sepsis. Copyright © 2015 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

  14. An Altered Pattern of Myocardial Histopathological and Molecular Changes Underlies the Different Characteristics of Type-1 and Type-2 Diabetic Cardiac Dysfunction

    Directory of Open Access Journals (Sweden)

    Tamás Radovits

    2015-01-01

    Full Text Available Increasing evidence suggests that both types of diabetes mellitus (DM lead to cardiac structural and functional changes. In this study we investigated and compared functional characteristics and underlying subcellular pathological features in rat models of type-1 and type-2 diabetic cardiomyopathy. Type-1 DM was induced by streptozotocin. For type-2 DM, Zucker Diabetic Fatty (ZDF rats were used. Left ventricular pressure-volume analysis was performed to assess cardiac function. Myocardial nitrotyrosine immunohistochemistry, TUNEL assay, hematoxylin-eosin, and Masson’s trichrome staining were performed. mRNA and protein expression were quantified by qRT-PCR and Western blot. Marked systolic dysfunction in type-1 DM was associated with severe nitrooxidative stress, apoptosis, and fibrosis. These pathological features were less pronounced or absent, while cardiomyocyte hypertrophy was comparable in type-2 DM, which was associated with unaltered systolic function and increased diastolic stiffness. mRNA-expression of hypertrophy markers c-fos, c-jun, and β-MHC, as well as pro-apoptotic caspase-12, was elevated in type-1, while it remained unaltered or only slightly increased in type-2 DM. Expression of the profibrotic TGF-β1 was upregulated in type-1 and showed a decrease in type-2 DM. We compared type-1 and type-2 diabetic cardiomyopathy in standard rat models and described an altered pattern of key pathophysiological features in the diabetic heart and corresponding functional consequences.

  15. Influence of age on the prognostic importance of left ventricular dysfunction and congestive heart failure on long-term survival after acute myocardial infarction. TRACE Study Group

    DEFF Research Database (Denmark)

    Køber, L; Torp-Pedersen, C; Ottesen, M;

    1996-01-01

    The aim of this study was to assess the importance of congestive heart failure and left ventricular (LV) systolic dysfunction after an acute myocardial infarction (AIM) on long-term mortality in different age groups. A total of 7,001 consecutive enzyme-confirmed AMIs (6,676 patients) were screened...... for entry into the TRAndolapril Cardiac Evaluation (TRACE) study. Medical history, echocardiographic estimation of LV systolic function determined as wall motion index, infarct complications, and survival were documented for all patients. To study the importance of congestive heart failure and wall motion......%, and 55%, respectively. The risk ratios (and 95% confidence limits) associated with congestive heart failure in the same 4 age strata were 1.9 (1.3 to 2.9), 2.8 (2.1 to 3.7), 1.8 (1.5 to 2.2) and 1.8 (1.5 to 2.2), respectively. The risk ratios associated with decreasing wall motion index were 6.5 (3...

  16. Hyperglycemia, acute insulin resistance, and renal dysfunction in the early phase of ST-elevation myocardial infarction without previously known diabetes: impact on long-term prognosis.

    Science.gov (United States)

    Lazzeri, Chiara; Valente, Serafina; Chiostri, Marco; Attanà, Paola; Mattesini, Alessio; Nesti, Martina; Gensini, Gian Franco

    2014-11-01

    We evaluated the relationship between admission renal function (as assessed by estimated glomerular filtration rate (eGFR)), hyperglycemia, and acute insulin resistance, indicated by the homeostatic model assessment (HOMA) index, and their impact on long-term prognosis in 825 consecutive patients with ST-elevation myocardial infarction (STEMI) without previously known diabetes who underwent primary percutaneous coronary intervention (PCI). Admission eGFR showed a significant indirect correlation with admission glycemia (Spearman's ρ -0.23, P renal function and glucose values and acute insulin resistance in the early phase of STEMI was detectable, since a significant, indirect correlation between eGFR, insulin values, and glycemia was observed. Patients with renal dysfunction (eGFR renal function (eGFR ≥60 ml/min/1.73 m(2)). The prognostic role of glucose values for 1-year mortality was confined to patients with eGFR ≥60 ml/min/m(2), who represent the large part of our population and are thought to be at lower risk. In these patients, an independent relationship between 1-year mortality and glucose values was detectable not only for admission glycemia but also for glucose values measured at discharge.

  17. Effect on short- and long-term major adverse cardiac events of statin treatment in patients with acute myocardial infarction and renal dysfunction.

    Science.gov (United States)

    Lim, Sang Yup; Bae, Eun Hui; Choi, Joon Seok; Kim, Chang Seong; Park, Jeong Woo; Ma, Seong Kwon; Jeong, Myung Ho; Kim, Soo Wan

    2012-05-15

    The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) reduce major adverse cardiac events (MACE) and mortality in patients with acute coronary syndrome. We investigated the effectiveness of statin therapy in reducing MACE in patients with acute myocardial infarction (AMI) and renal dysfunction (RD). In the present retrospective study of 12,853 patients with AMI, the patients were categorized into 4 groups: group I, statin therapy and no RD (estimated glomerular filtration rate ≥60 ml/min/1.73 m(2)); group II, neither statin therapy nor RD; group III, statin therapy and RD; group IV, no statin therapy but RD. The primary end points were death and complications during the hospital course. The secondary end points were MACE during 1 year of follow-up after AMI. Significant differences in the composite MACE during 12 months of follow-up were observed among the 4 groups (group I, 11.7%; group II, 19.0%; group III, 26.7%; and group IV, 45.5%; p <0.001). In a Cox proportional hazards model, mortality at 12 months increased stepwise from group II to IV compared to group I. Moreover, MACE-free survival in the severe RD group (estimated glomerular filtration rate <30 mL/min/1.73 m(2)) was also greater in the statin-treated group. In conclusion, statin therapy reduced MACE at 1 year of follow-up in patients with AMI regardless of RD.

  18. Rat adipose tissue-derived stem cells transplantation attenuates cardiac dysfunction post infarction and biopolymers enhance cell retention.

    Directory of Open Access Journals (Sweden)

    Maria E Danoviz

    Full Text Available BACKGROUND: Cardiac cell transplantation is compromised by low cell retention and poor graft viability. Here, the effects of co-injecting adipose tissue-derived stem cells (ASCs with biopolymers on cell cardiac retention, ventricular morphometry and performance were evaluated in a rat model of myocardial infarction (MI. METHODOLOGY/PRINCIPAL FINDINGS: 99mTc-labeled ASCs (1x10(6 cells isolated from isogenic Lewis rats were injected 24 hours post-MI using fibrin a, collagen (ASC/C, or culture medium (ASC/M as vehicle, and cell body distribution was assessed 24 hours later by gamma-emission counting of harvested organs. ASC/F and ASC/C groups retained significantly more cells in the myocardium than ASC/M (13.8+/-2.0 and 26.8+/-2.4% vs. 4.8+/-0.7%, respectively. Then, morphometric and direct cardiac functional parameters were evaluated 4 weeks post-MI cell injection. Left ventricle (LV perimeter and percentage of interstitial collagen in the spare myocardium were significantly attenuated in all ASC-treated groups compared to the non-treated (NT and control groups (culture medium, fibrin, or collagen alone. Direct hemodynamic assessment under pharmacological stress showed that stroke volume (SV and left ventricle end-diastolic pressure were preserved in ASC-treated groups regardless of the vehicle used to deliver ASCs. Stroke work (SW, a global index of cardiac function, improved in ASC/M while it normalized when biopolymers were co-injected with ASCs. A positive correlation was observed between cardiac ASCs retention and preservation of SV and improvement in SW post-MI under hemodynamic stress. CONCLUSIONS: We provided direct evidence that intramyocardial injection of ASCs mitigates the negative cardiac remodeling and preserves ventricular function post-MI in rats and these beneficial effects can be further enhanced by administering co-injection of ASCs with biopolymers.

  19. Rat Adipose Tissue-Derived Stem Cells Transplantation Attenuates Cardiac Dysfunction Post Infarction and Biopolymers Enhance Cell Retention

    Science.gov (United States)

    Danoviz, Maria E.; Nakamuta, Juliana S.; Marques, Fabio L. N.; dos Santos, Leonardo; Alvarenga, Erica C.; dos Santos, Alexandra A.; Antonio, Ednei L.; Schettert, Isolmar T.; Tucci, Paulo J.; Krieger, Jose E.

    2010-01-01

    Background Cardiac cell transplantation is compromised by low cell retention and poor graft viability. Here, the effects of co-injecting adipose tissue-derived stem cells (ASCs) with biopolymers on cell cardiac retention, ventricular morphometry and performance were evaluated in a rat model of myocardial infarction (MI). Methodology/Principal Findings 99mTc-labeled ASCs (1×106 cells) isolated from isogenic Lewis rats were injected 24 hours post-MI using fibrin a, collagen (ASC/C), or culture medium (ASC/M) as vehicle, and cell body distribution was assessed 24 hours later by γ-emission counting of harvested organs. ASC/F and ASC/C groups retained significantly more cells in the myocardium than ASC/M (13.8±2.0 and 26.8±2.4% vs. 4.8±0.7%, respectively). Then, morphometric and direct cardiac functional parameters were evaluated 4 weeks post-MI cell injection. Left ventricle (LV) perimeter and percentage of interstitial collagen in the spare myocardium were significantly attenuated in all ASC-treated groups compared to the non-treated (NT) and control groups (culture medium, fibrin, or collagen alone). Direct hemodynamic assessment under pharmacological stress showed that stroke volume (SV) and left ventricle end-diastolic pressure were preserved in ASC-treated groups regardless of the vehicle used to deliver ASCs. Stroke work (SW), a global index of cardiac function, improved in ASC/M while it normalized when biopolymers were co-injected with ASCs. A positive correlation was observed between cardiac ASCs retention and preservation of SV and improvement in SW post-MI under hemodynamic stress. Conclusions We provided direct evidence that intramyocardial injection of ASCs mitigates the negative cardiac remodeling and preserves ventricular function post-MI in rats and these beneficial effects can be further enhanced by administrating co-injection of ASCs with biopolymers. PMID:20711471

  20. Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic rats

    Science.gov (United States)

    Kip, Gülay; Çelik, Ali; Bilge, Mustafa; Alkan, Metin; Kiraz, Hasan Ali; Özer, Abdullah; Şıvgın, Volkan; Erdem, Özlem; Arslan, Mustafa; Kavutçu, Mustafa

    2015-01-01

    Objective Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R). Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods Diabetes was induced with streptozotocin (55 mg/kg) in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC), diabetes plus ischaemia-reperfusion (DIR), and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD)) after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg); the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group) in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT) and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA) levels were evaluated in the lung tissues of all rats. Results Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively). The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively). The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT activity

  1. Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic rats

    Directory of Open Access Journals (Sweden)

    Gülay Kip

    2015-09-01

    Full Text Available Objective: Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R. Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods: Diabetes was induced with streptozotocin (55 mg/kg in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC, diabetes plus ischaemia-reperfusion (DIR, and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg; the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA levels were evaluated in the lung tissues of all rats. Results: Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively. The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively. The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT

  2. Post-Weaning Protein Malnutrition Increases Blood Pressure and Induces Endothelial Dysfunctions in Rats

    OpenAIRE

    Aucelia C S de Belchior; Angeli, Jhuli K.; Thaís de O Faria; Siman, Fabiana D. M.; Edna A Silveira; Eduardo F Meira; da Costa, Carlos P.; Dalton V Vassallo; Alessandra S Padilha

    2012-01-01

    Malnutrition during critical periods in early life may increase the subsequent risk of hypertension and metabolic diseases in adulthood, but the underlying mechanisms are still unclear. We aimed to evaluate the effects of post-weaning protein malnutrition on blood pressure and vascular reactivity in aortic rings (conductance artery) and isolated-perfused tail arteries (resistance artery) from control (fed with Labina®) and post-weaning protein malnutrition rats (offspring that received a diet...

  3. Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group

    DEFF Research Database (Denmark)

    Flather, M D; Yusuf, S; Køber, L

    2000-01-01

    enrolled patients within a week after acute myocardial infarction. Data were combined by use of the Peto-Yusuf method. FINDINGS: Overall 12,763 patients were randomly assigned treatment or placebo and followed up for an average of 35 months. In the three post-infarction trials (n=5,966), mortality...

  4. Sevoflurane postconditioning affects post-ischaemic myocardial mitochondrial ATP-sensitive potassium channel function and apoptosis in ageing rats.

    Science.gov (United States)

    Jiang, Jing-Jing; Li, Chao; Li, Heng; Zhang, Lei; Lin, Zong-Hang; Fu, Bao-Jun; Zeng, Yin-Ming

    2016-05-01

    This study investigated the effect of sevoflurane postconditioning on post-ischaemic cardiac function, infarct size, myocardial mitochondrial ATP-sensitive potassium channel (mitoKATP) function and apoptosis in ageing rats to determine the possible mechanism underlying the cardioprotective property of sevoflurane. Ageing rat hearts were isolated and attached to a Langendorff apparatus. The hearts were then exposed or not to sevoflurane postconditioning in the presence or absence of 100 μmol/L 5-hydroxydecanoate (5-HD), a selective mitoKATP inhibitor. The infarct size was measured by triphenyltetrazolium chloride (TTC) staining. Mitochondrial morphology was observed by electron microscopy and scored using FlaMeng semiquantitative analysis. In addition, the expression levels of Bax, Bcl-2, and cytochrome-C (Cyt-C) were determined by Western blot analysis at the end of reperfusion. Sevoflurane postconditioning increased coronary flow, improved functional recovery, reduced Bax/Bcl-2 and Cyt-C phosphorylation levels, and decreased mitochondrial lesion severity and the extent of apoptosis. The protective effects of sevoflurane postconditioning were prevented by the mitoKATP inhibitor 5-HD. Sevoflurane postconditioning significantly protected the function of ageing hearts that were subjected to ischaemia and reperfusion, and these protective effects were mediated by mitoKATP opening. © 2016 John Wiley & Sons Australia, Ltd.

  5. Race and Sex Differences in Post-Myocardial Infarction Angina Frequency and Risk of 1-Year Unplanned Rehospitalization.

    Science.gov (United States)

    Hess, Connie N; Kaltenbach, Lisa A; Doll, Jacob A; Cohen, David J; Peterson, Eric D; Wang, Tracy Y

    2017-02-07

    Race and sex disparities in in-hospital treatment and outcomes of patients with acute myocardial infarction (MI) have been described, but little is known about race and sex differences in post-MI angina and long-term risk of unplanned rehospitalization. We examined race and sex differences in post-MI angina frequency and 1-year unplanned rehospitalization to identify factors associated with unplanned rehospitalization, testing for whether race and sex modify these relationships. Using TRANSLATE-ACS (Treatment With Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events after Acute Coronary Syndrome) data, we examined 6-week and 1-year angina frequency and 1-year unplanned rehospitalization stratified by race and sex among MI patients treated with percutaneous coronary intervention. We used multivariable logistic regression to assess factors associated with unplanned rehospitalization and tested for interactions among angina frequency, race, and sex. A total of 11 595 MI patients survived to 1 year postdischarge; there were 66.6% white male patients, 24.3% white female patients, 5.3% black male patients, and 3.8% black female patients. Overall, 29.7% had angina at 6 weeks, and 20.6% had angina at 1 year postdischarge. Relative to white patients, black patients were more likely to have angina at 6 weeks (female: 44.2% versus 31.8%; male: 33.5% versus 27.1%; both Pyear (female: 49.4% versus 38.9%; male: 46.3% versus 31.1%; both Pyear unplanned rehospitalization were highest among black female patients (44.1%), followed by white female patients (38.4%), black male patients (36.4%), and white male patients (30.2%, Pyear postdischarge angina, with black and female patients more likely to have angina and to be rehospitalized. Better treatment of post-MI angina may improve patient quality of life and quality of care and help to lower rates of rehospitalization overall and particularly among black and female patients, given

  6. Effect of Post-Reconstruction Gaussian Filtering on Image Quality and Myocardial Blood Flow Measurement with N-13 Ammonia PET

    Directory of Open Access Journals (Sweden)

    Hyeon Sik Kim

    2014-10-01

    Full Text Available Objective(s: In order to evaluate the effect of post-reconstruction Gaussian filtering on image quality and myocardial blood flow (MBF measurement by dynamic N-13 ammonia positron emission tomography (PET, we compared various reconstruction and filtering methods with image characteristics. Methods: Dynamic PET images of three patients with coronary artery disease (male-female ratio of 2:1; age: 57, 53, and 76 years were reconstructed, using filtered back projection (FBP and ordered subset expectation maximization (OSEM methods. OSEM reconstruction consisted of OSEM_2I, OSEM_4I, and OSEM_6I with 2, 4, and 6 iterations, respectively. The images, reconstructed and filtered by Gaussian filters of 5, 10, and 15 mm, were obtained, as well as non-filtered images. Visual analysis of image quality (IQ was performed using a 3-grade scoring system by 2 independent readers, blinded to the reconstruction and filtering methods of stress images. Then, signal-to-noise ratio (SNR was calculated by noise and contrast recovery (CR. Stress and rest MBF and coronary flow reserve (CFR were obtained for each method. IQ scores, stress and rest MBF, and CFR were compared between the methods, using Chi-square and Kruskal-Wallis tests. Results: In the visual analysis, IQ was significantly higher by 10 mm Gaussian filtering, compared to other sizes of filter (PP=0.923 and 0.855 for readers 1 and 2, respectively. SNR was significantly higher in 10 mm Gaussian filter. There was a significant difference in stress and rest MBF between several vascular territories. However CFR was not significantly different according to various filtering methods. Conclusion: Post-reconstruction Gaussian filtering with a filter size of 10 mm significantly enhances the IQ of N-13 ammonia PET-CT, without changing the results of CFR calculation. .

  7. Myocardial contrast defect associated with thrombotic coronary occlusion: Pre-autopsy diagnosis of a cardiac death with post-mortem CT angiography

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Heon; Cha, Jang Gyu [Dept. of Radiology, Soonchunhyang University Hospital, Bucheon (Korea, Republic of); Park, Hye Jin; Lee, Soo Kyoung; Yang, Kyung Moo [Dept. of Forensic Medicine, National Forensic Service, Wonju (Korea, Republic of)

    2015-10-15

    We report the case of a female who died of suspected acute myocardial infarction. Post-mortem CT angiography (PMCTA) was performed with intravascular contrast infusion before the standard autopsy, and it successfully demonstrated the complete thrombotic occlusion of a coronary artery and also a corresponding perfusion defect on myocardium. We herein describe the PMCTA findings of a cardiac death with special emphasis on the potential benefits of this novel CT technique in forensic practice.

  8. Restoration of radiation therapy-induced salivary gland dysfunction in mice by post therapy IGF-1 administration

    Directory of Open Access Journals (Sweden)

    Grundmann Oliver

    2010-08-01

    Full Text Available Abstract Background Radiotherapy for head and neck cancer results in severe and chronic salivary gland dysfunction in most individuals. This results in significant side effects including xerostomia, dysphagia, and malnutrition which are linked to significant reductions in patients' quality of life. Currently there are few xerostomia treatment approaches that provide long-term results without significant side effects. To address this problem we investigated the potential for post-therapeutic IGF-1 to reverse radiation-induced salivary gland dysfunction. Methods FVB mice were treated with targeted head and neck radiation and significant reductions in salivary function were confirmed 3 days after treatment. On days 4-8 after radiation, one group of mice was injected intravenously with IGF-1 while a second group served as a vehicle control. Stimulated salivary flow rates were evaluated on days 30, 60, and 90 and histological analysis was performed on days 9, 30, 60, and 90. Results Irradiated animals receiving vehicle injections have 40-50% reductions in stimulated salivary flow rates throughout the entire time course. Mice receiving injections of IGF-1 have improved stimulated salivary flow rates 30 days after treatment. By days 60-90, IGF-1 injected mice have restored salivary flow rates to unirradiated control mice levels. Parotid tissue sections were stained for amylase as an indicator of functioning acinar cells and significant reductions in total amylase area are detected in irradiated animals compared to unirradiated groups on all days. Post-therapeutic injections of IGF-1 results in increased amylase-positive acinar cell area and improved amylase secretion. Irradiated mice receiving IGF-1 show similar proliferation indices as untreated mice suggesting a return to tissue homeostasis. Conclusions Post-therapeutic IGF-1 treatment restores salivary gland function potentially through normalization of cell proliferation and improved expression of

  9. Impact of the combined presence of left ventricular systolic and renal dysfunction on the 5-year outcome after ST-elevation myocardial infarction

    Directory of Open Access Journals (Sweden)

    Savić Lidija

    2015-01-01

    Full Text Available Background/Aim. The coincidence of left ventricular systolic dysfunction (LVSD and renal dysfunction (RD is a strong independent predictor of adverse events in the short-term and mid-term follow-ups of patients with ST-elevation myocardial infarction (STEMI treated with primary percutaneous coronary intervention (pPCI. The aim of this study was primarily to assess the prognostic impact of the LVSD-RD combination on the 5-year all-cause mortality in patients with STEMI treated with pPCI, as well as to assess the prognostic impact of the LVSD-RD combination on the occurrence of major adverse cardiovascular events (MACEs: cardiovascular death, reinfarction, stroke and target vessel revascularization in these patients. Methods. We analyzed 951 patients divided into 4 groups according to the presence of LVSD (ejection fraction < 40% and/or baseline RD (creatinine clearance < 60 mL/min: group I (no LVSD, no RD; group II (LVSD, no RD; group III (RD, no LVSD; group IV (LVSD+RD. Results. The 5-year mortality rates were 2.3%, 17.6%, 11.7% and 38.3%, while the 5-year MACE rates were 8.8%, 28.4%, 18.3% and 44.4% in the groups I, II, III and IV, respectively (p < 0.001. The highest percentage of lethal outcomes and MACE was registered in the first year of follow-up in all the groups. The 1-year landmark analysis confirmed that the patients with LVSD-RD combination had the highest percentage of lethal outcomes in the period of 1 to 5 years (p = 0.028. There was a strong trend toward the significance in the occurrence of MACE among the analyzed groups in the period of 1 to 5 years (p = 0.085. In the Cox regression model the LVSD-RD combination was a strong independent predictor of 5-year mortality and the occurrence of MACE: mortality hazard ratio (HR 4.5 (95%CI 1.9-10.8; MACE HR 2.5 (95%CI 1.4-4.5. Conclusion. The strong negative independent prognostic impact of the LVSD-RD combination persisted in the long-term follow-up of the patients with STEMI treated

  10. Global and regional left ventricular strain indices in post-myocardial infarction patients with ventricular arrhythmias and moderately abnormal ejection fraction.

    Science.gov (United States)

    Nguyen, Bich Lien; Capotosto, Lidia; Persi, Alessandro; Placanica, Attilio; Rafique, Asim; Piccirillo, Gianfranco; Gaudio, Carlo; Gang, Eli S; Siegel, Robert J; Vitarelli, Antonio

    2015-02-01

    The aim of the study described here was to compare myocardial strains in ischemic heart patients with and without sustained ventricular tachycardia (VT) and moderately abnormal left ventricular ejection fraction (LVEF) to investigate which index could better predict VT on the basis of the analysis of global and regional left ventricular (LV) dysfunction. We studied 467 patients with previous myocardial infarction and LVEF >35%. Fifty-one patients had documented VT, and 416 patients presented with no VT. LV volumes and score index were obtained by 2-D echocardiography. Longitudinal, radial and circumferential strains were determined. Strains of the infarct, border and remote zones were also obtained. There were no differences in standard LV 2-D parameters between patients with and those without VT. Receiver operating characteristic values were -12.7% for global longitudinal strain (area under the curve [AUC] = 0.72), -4.8% for posterior-inferior wall circumferential strain (AUC = 0.80), 61 ms for LV mechanical dispersion (AUC = 0.84), -10.1% for longitudinal strain of the border zone (AUC = 0.86) and -9.2% for circumferential strain of the border zone (AUC = 0.89). In patients with previous myocardial infarction and moderately abnormal LVEF, peri-infarct circumferential strain was the strongest predictor of documented ventricular arrhythmias among all strain quantitative indices. Additionally, strain values from posterior-inferior wall infarctions had a higher association with arrhythmic events compared with global strain.

  11. Stress-induced myocardial ischemia is associated with early post-stress left ventricular mechanical dyssynchrony as assessed by phase analysis of {sup 201}Tl gated SPECT myocardial perfusion imaging

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    Chen, Chien-Cheng; Shen, Thau-Yun [Show Chwan Memorial Hospital, Department of Cardiology, Changhua (China); Chang, Ming-Che [Changhua Christian Hospital, Department of Nuclear Medicine, Changhua (China); Hung, Guang-Uei [Chang Bing Show Chwan Memorial Hospital, Department of Nuclear Medicine, Changhua (China); China Medical University, Department of Biomedical Imaging and Radiological Science, Taichung (China); Chen, Wan-Chen [Chang Bing Show Chwan Memorial Hospital, Department of Nuclear Medicine, Changhua (China); Kao, Chia-Hung [China Medical University, Department of Biomedical Imaging and Radiological Science, Taichung (China); Chen, Ji [Emory University School of Medicine, Department of Radiology and Imaging Sciences, Atlanta, GA (United States)

    2012-12-15

    In {sup 201}Tl SPECT myocardial perfusion imaging (MPI) data are acquired shortly after the stress injection to assess early post-stress left ventricle (LV) function. The purpose of this study was to use {sup 201}Tl SPECT MPI to investigate whether stress-induced myocardial ischemia is associated with LV mechanical dyssynchrony. Enrolled in the study were 75 patients who were referred for dipyridamole stress and rest {sup 201}Tl gated SPECT MPI. The early post-stress scan was started 5 min after injection, and followed by the rest scan 4 h later. The patients were divided into three groups: ischemia group (N = 25, summed stress score, SSS, {>=}5, summed rest score, SRS, <5), infarct group (N = 16, SSS {>=}5, SRS {>=}5) and normal group (N = 34, SSS <5, SRS <5). LV dyssynchrony parameters were calculated by phase analysis, and compared between the stress and rest images. In the ischemia group, LV dyssynchrony was significantly larger during stress than during rest. On the contrary, LV dyssynchrony during stress was significantly smaller than during rest in the normal and infarct groups. LV dyssynchrony during rest was significantly larger in the infarct group than in the normal and ischemia groups. There were no significant differences in LV dyssynchrony during rest between the normal and ischemia groups. Stress-induced myocardial ischemia caused dyssynchronous contraction in the ischemic region, leading to a deterioration in LV synchrony. Normal myocardium had more synchronous contraction during stress. The different dyssynchrony pattern between ischemic and normal myocardium early post-stress may aid the diagnosis of coronary artery disease using {sup 201}Tl gated SPECT MPI. (orig.)

  12. Activation of mitochondrial STAT-3 and reduced mitochondria damage during hypothermia treatment for post-cardiac arrest myocardial dysfunction.

    Science.gov (United States)

    Huang, Chien-Hua; Tsai, Min-Shan; Chiang, Chih-Yen; Su, Yu-Jen; Wang, Tzung-Dau; Chang, Wei-Tien; Chen, Huei-Wen; Chen, Wen-Jone

    2015-11-01

    While therapeutic hypothermia improves the outcomes of individuals in cardiac arrest, the hemodynamic responses and mechanisms which underlie hypothermia-induced cardioprotection are not fully understood. Therefore, we investigated the mechanism by which induced hypothermia preserves cardiac function and protects against mitochondrial damage following cardiac arrest. Cardiac arrest was induced in adult male Wistar rats by asphyxiation for 8.5 min. Following resuscitation, the animals were randomly assigned to a hypothermia (32 °C) or normothermia (37 °C) group. Monitoring results showed that cardiac output at the fourth hour after resuscitation was significantly better in rats treated with hypothermia when compared to rats treated with normothermia (P mitochondrial permeability transition pores occurred less frequently in the hypothermic group. While complex I/III activity in the electron transport reaction was damaged after cardiac arrest and resuscitation, the degree of injury was ameliorated by hypothermia treatment (P mitochondrial integrity and electron transport activity.

  13. Cortical neuron loss in post-traumatic higher brain dysfunction using (123)I-iomazenil SPECT.

    Science.gov (United States)

    Nakagawara, Jyoji; Kamiyama, Kenji; Takahashi, Masaaki; Nakamura, Hirohiko

    2013-01-01

    In patients with higher brain dysfunction (HBD) after mild traumatic brain injury (MTBI), diagnostic imaging of cortical neuron loss in the frontal lobes was studied using SPECT with (123)I-iomazenil (IMZ), as a radioligand for central benzodiazepine receptor (BZR). Statistical imaging analysis using three-dimensional stereotactic surface projections (3D-SSP) for (123)I-IMZ SPECT was performed in 17 patients. In all patients with HBD defined by neuropsychological tests, cortical neuron loss was indicated in the bilateral medial frontal lobes in 14 patients (83 %). A comparison between the group of 17 patients and the normal database demonstrated common areas of cortical neuron loss in the bilateral medial frontal lobes involving the medial frontal gyrus (MFG) and the anterior cingulate gyrus (ACG). In an assessment of cortical neuron loss in the frontal medial cortex using the stereotactic extraction estimation (SEE) method (level 3), significant cortical neuron loss was observed within bilateral MFG in 9 patients and unilateral MFG in 4, and bilateral ACG in 12 and unilateral ACG in 3. Fourteen patients showed significant cortical neuron loss in bilateral MFG or ACG. In patients with MTBI, HBD seemed to correlate with selective cortical neuron loss within the bilateral MFG or ACG where the responsible lesion could be. 3D-SSP and SEE level 3 analysis for (123)I-IMZ SPECT could be valuable for diagnostic imaging of HBD after MTBI.

  14. Safe Oral Triiodo-L-Thyronine Therapy Protects from Post-Infarct Cardiac Dysfunction and Arrhythmias without Cardiovascular Adverse Effects.

    Directory of Open Access Journals (Sweden)

    Viswanathan Rajagopalan

    Full Text Available A large body of evidence suggests that thyroid hormones (THs are beneficial for the treatment of cardiovascular disorders. We have shown that 3 days of triiodo-L-thyronine (T3 treatment in myocardial infarction (MI rats increased left ventricular (LV contractility and decreased myocyte apoptosis. However, no clinically translatable protocol is established for T3 treatment of ischemic heart disease. We hypothesized that low-dose oral T3 will offer safe therapeutic benefits in MI.Adult female rats underwent left coronary artery ligation or sham surgeries. T3 (~6 μg/kg/day was available in drinking water ad libitum immediately following MI and continuing for 2 month(s (mo. Compared to vehicle-treated MI, the oral T3-treated MI group at 2 mo had markedly improved anesthetized Magnetic Resonance Imaging-based LV ejection fraction and volumes without significant negative changes in heart rate, serum TH levels or heart weight, indicating safe therapy. Remarkably, T3 decreased the incidence of inducible atrial tachyarrhythmias by 88% and improved remodeling. These were accompanied by restoration of gene expression involving several key pathways including thyroid, ion channels, fibrosis, sympathetic, mitochondria and autophagy.Low-dose oral T3 dramatically improved post-MI cardiac performance, decreased atrial arrhythmias and cardiac remodeling, and reversed many adverse changes in gene expression with no observable negative effects. This study also provides a safe and effective treatment/monitoring protocol that should readily translate to humans.

  15. Post-ischaemic angiogenic therapy using in vivo prevascularized ascorbic acid-enriched myocardial artificial grafts improves heart function in a rat model.

    Science.gov (United States)

    Martinez, Eliana C; Wang, Jing; Lilyanna, Shera; Ling, Lieng H; Gan, Shu U; Singh, Rajeev; Lee, Chuen N; Kofidis, Theo

    2013-03-01

    Angiogenesis plays a key role in post-ischaemic myocardial repair. We hypothesized that epicardial implantation of an ascorbic acid (AA)-enriched myocardial artificial graft (MAG), which has been prevascularized in the recipients' own body, promotes restoration of the ischaemic heart. Gelatin patches were seeded with GFP-luciferase-expressing rat cardiomyoblasts and enriched with 5 μm AA. Grafts were prevascularized in vivo for 3 days, using a renal pouch model in rats. The MAG patch was then implanted into the same rat's ischaemic heart following myocardial infarction (MI). MAG-treated animals (MAG group, n = 6) were compared to untreated infarcted animals as injury controls (MI group, n = 6) and sham-operated rats as healthy controls (healthy group, n = 7). In vivo bioluminescence imaging indicated a decrease in donor cell survival by 83% during the first week post-implantation. Echocardiographic and haemodynamic assessment 4 weeks after MI revealed that MAG treatment attenuated left ventricular (LV) remodelling (LV end-systolic volume, 0.31 ± 0.13 vs 0.81 ± 0.01 ml, p hearts, attenuated LV remodelling and preserved LV function.

  16. Impact of general versus epidural anesthesia on early post-operative cognitive dysfunction following hip and knee surgery

    Directory of Open Access Journals (Sweden)

    Mandal Sripurna

    2011-01-01

    Full Text Available Background : Post-operative cognitive dysfunction is the subtle cerebral complication temporally seen following surgery. The aim of this study was to compare the influence of either general anesthesia (GA or epidural anesthesia (EA on the early post-operative neurocognitive outcome in elderly (>59 years subjects undergoing hip and knee surgery. Methods : A total of 60 patients were recruited in a prospective, randomized, parallel-group study, comparable by age and sex. They were enrolled and randomized to receive either EA (n = 30 or GA (n = 30. All of them were screened using the Mini Mental State Examination (MMSE, with components of the Kolkata Cognitive Screening Battery. The operated patients were re-evaluated 1 week after surgery using the same scale. The data collected were analyzed to assess statistical significance. Results : We observed no statistical difference in cognitive behavior in either group pre-operatively, which were comparable with respect to age, sex and type of surgery. Grossly, a significant difference was seen between the two groups with respect to the perioperative changes in verbal fluency for categories and MMSE scores. However, these differences were not significant after the application of the Bonferroni correction for multiple analyses, except the significant differences observed only in the MMSE scores. Conclusions : We observed a difference in cognitive outcome with GA compared with EA. Certain aspects of the cognition were affected to a greater extent in this group of patients undergoing hip and knee surgery.

  17. The effect of treatment with carvedilol in patients with left ventricular dysfunction after acute myocardial infarction%卡维地洛治疗急性心肌梗死患者左室功能的疗效观察

    Institute of Scientific and Technical Information of China (English)

    贺礼荣

    2013-01-01

    Object To explore the effect of treatment with carvedilol in patients with left ventricular dysfunction after acute myocardial infarction . Method From 2005.1 to 2009.7, 100 cases with acute myocardial infarction were randomly divided into two groups.carvedilol group (50 cases) and metoprolol group (50 cases) . The left ventricular systolic function and diastolic function of both group were recorded by echocardiography at the time both within 24 hours when the patient was hospitalized and one month after the end of treatment .Result The left ventricular systolic function of the carvedilol group improved more than the metoprolol group (P0.05)。结论在治疗1个月后,卡维地洛和美托洛尔均显著改善左心室功能,但卡维地洛疗效更好。

  18. POST-REPERFUSION LIVER BIOPSY AND ITS VALUE IN PREDICTING MORTALITY AND GRAFT DYSFUNCTION AFTER LIVER TRANSPLANTATION.

    Science.gov (United States)

    Zanchet, Marcos Vinícius; Silva, Larissa Luvison Gomes da; Matias, Jorge Eduardo Fouto; Coelho, Júlio Cezar Uili

    2016-01-01

    The outcome of the patients after liver transplant is complex and to characterize the risk for complications is not always easy. In this context, the hepatic post-reperfusion biopsy is capable of portraying alterations of prognostic importance. To compare the results of liver transplantation, correlating the different histologic features of the hepatic post-reperfusion biopsy with graft dysfunction, primary non-function and patient survival in the first year after transplantation. From the 377 transplants performed from 1996 to 2008, 164 patients were selected. Medical records were reviewed and the following clinical outcomes were registered: mortality in 1, 3, 6 and 12 months, graft dysfunction in varied degrees and primary graft non-function. The post-reperfusion biopsies had been examined by a blinded pathologist for the outcomes. The following histological variables had been evaluated: ischemic alterations, congestion, steatosis, neutrophilic exudate, monomorphonuclear infiltrate and necrosis. The variables associated with increased mortality were: steatosis (p=0.02209), monomorphonuclear infiltrate (p=0.03935) and necrosis (ptransplant. A evolução dos pacientes após transplante hepático é complexa e caracterizar o risco para complicações nem sempre é fácil. Nesse contexto, a biópsia hepática pós-reperfusão é capaz de retratar alterações de importância prognóstica. Avaliar os resultados no primeiro ano após transplante hepático, correlacionando as alterações histológicas à biópsia hepática pós-reperfusão com a sobrevida, a disfunção e o não-funcionamento primário do enxerto. Dos 377 transplantes ocorridos de 1996 a 2008, 164 pacientes foram selecionados para estudo. Os seguintes desfechos clínicos foram registrados: mortalidade em 1, 3, 6 e 12 meses, disfunção do enxerto em graus variados e o não-funcionamento primário do enxerto. As biópsias pós-reperfusão foram examinadas por um patologista sem conhecimento dos

  19. Depression: links with ischemic heart disease and erectile dysfunction.

    Science.gov (United States)

    Roose, Steven P

    2003-01-01

    This article examines the relationships among depression, ischemic heart disease, and erectile dysfunction. Depression is an independent risk factor for the development of ischemic heart disease, and depression in the post-myocardial infarction patient is associated with increased morbidity and mortality. Ischemic heart disease and erectile dysfunction are also frequently comorbid and share many common risk factors including age, hypertension, diabetes, dyslipidemia, obesity, sedentary lifestyle, and smoking. Depression and erectile dysfunction often occur together; however, the causal relation may be difficult to determine because erectile dysfunction may be a symptom of depression, social distress accompanying erectile dysfunction may precipitate depressive symptoms, or both conditions may result from a common factor such as vascular disease.

  20. Impact of proton pump inhibitor treatment on gastrointestinal bleeding associated with non-steroidal anti-inflammatory drug use among post-myocardial infarction patients taking antithrombotics

    DEFF Research Database (Denmark)

    Olsen, Anne-Marie Schjerning; Lindhardsen, Jesper; Gislason, Gunnar H.

    2015-01-01

    administrative registry data from all hospitals in Denmark between 1997 and 2011. The study included patients aged 30 years and over admitted with a first myocardial infarction who survived at least 30 days after discharge. The association between PPIs and risk of gastrointestinal bleeding according to NSAID...... of NSAID, and type of PPI used. FUNDING, COMPETING INTERESTS, DATA SHARING: AMSO has received a grant from the Danish Council of Independent Research (grant 12-132760). GHG is supported by an unrestricted research scholarship from the Novo Nordisk Foundation....... plus antithrombotic therapy was estimated using adjusted time dependent Cox regression models. STUDY ANSWER AND LIMITATIONS: The use of PPIs was independently associated with decreased risk of gastrointestinal bleeding in post-myocardial infarction patients taking antithrombotics and treated...

  1. Sphingosine 1-Phosphate Receptor Modulator Fingolimod (FTY720) Attenuates Myocardial Fibrosis in Post-heterotopic Heart Transplantation.

    Science.gov (United States)

    Ahmed, Naseer; Linardi, Daniele; Muhammad, Nazeer; Chiamulera, Cristiano; Fumagalli, Guido; Biagio, Livio San; Gebrie, Mebratu A; Aslam, Muhammad; Luciani, Giovanni Battista; Faggian, Giuseppe; Rungatscher, Alessio

    2017-01-01

    Background and Objective: Sphingosine 1-phosphate (S1P), and S1P receptor modulator fingolimod have been suggested to play important cardioprotective role in animal models of myocardial ischemia/reperfusion injuries. To understand the cardioprotective function of S1P and its mechanism in vivo, we analyzed apoptotic, inflammatory biomarkers, and myocardial fibrosis in an in vivo heterotopic rat heart transplantation model. Methods: Heterotopic heart transplantation is performed in 60 Sprague-Dawley (SD) rats (350-400 g). The heart transplant recipients (n = 60) are categorized into Group A (control) and Group B (fingolimod treated 1 mg/kg intravenous). At baseline with 24 h after heart transplantation, blood and myocardial tissue are collected for analysis of myocardial biomarkers, apoptosis, inflammatory markers, oxidative stress, and phosphorylation of Akt/Erk/STAT-3 signaling pathways. Myocardial fibrosis was investigated using Masson's trichrome staining and L-hydroxyline. Results: Fingolimod treatment activates both Reperfusion Injury Salvage Kinase (RISK) and Survivor Activating Factor Enhancement (SAFE) pathways as evident from activation of anti-apoptotic and anti-inflammatory pathways. Fingolimod treatment caused a reduction in myocardial oxidative stress and hence cardiomyocyte apoptosis resulting in a decrease in myocardial reperfusion injury. Moreover, a significant (p < 0.001) reduction in collagen staining and hydroxyproline content was observed in fingolimod treated animals 30 days after transplantation demonstrating a reduction in cardiac fibrosis. Conclusion: S1P receptor activation with fingolimod activates anti-apoptotic and anti-inflammatory pathways, leading to improved myocardial salvage causing a reduction in cardiac fibrosis.

  2. The incidence and prognostic significance of new-onset atrial fibrillation in patients with acute myocardial infarction and left ventricular systolic dysfunction: a CARISMA substudy

    DEFF Research Database (Denmark)

    Jons, Christian; Jacobsen, Uffe G; Joergensen, Rikke Moerch;

    2011-01-01

    The incidence and risk associated with new-onset atrial fibrillation (AF) occurring after discharge in patients with acute myocardial infarction (MI) remains unknown.......The incidence and risk associated with new-onset atrial fibrillation (AF) occurring after discharge in patients with acute myocardial infarction (MI) remains unknown....

  3. Mitral regurgitation in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: prognostic significance and relation to ventricular size and function

    DEFF Research Database (Denmark)

    Amigoni, Maria; Meris, Alessandra; Thune, Jens Jakob

    2007-01-01

    AIMS: Mitral regurgitation (MR) confers independent risk in patients with acute myocardial infarction. We utilized data from the VALsartan In Acute myocardial iNfarcTion echo study to relate baseline MR to left ventricular (LV) size, shape, and function, and to assess the relationship between bas...

  4. Skipping breakfast is associated with reproductive dysfunction in post-adolescent female college students.

    Science.gov (United States)

    Fujiwara, Tomoko; Nakata, Rieko

    2010-12-01

    Although increasing attention has been paid to the adverse effects of skipping breakfast on quality of life, there are very few reports concerning the relationship between skipping breakfast and reproductive function. Therefore, we examined this issue by conducting a questionnaire survey of female college students aged from 18 to 20 years old. The 5 annual surveys of questionnaire demonstrated that the severity of dysmenorrhea was significantly higher in the population that skipped breakfast. The incidence of irregular menses was also higher in the population that skipped breakfast, although there was no difference in the incidence of premenstrual symptoms. The group that skipped breakfast showed a tendency to suffer from constipation. In addition, despite no difference in body mass index, there was a significantly higher incidence of a self-perception of poor general health among the group that skipped breakfast. These findings suggest that skipping breakfast is associated with menstrual disorders, and affects the physical condition of female college students who are undergoing post-adolescent maturation. Since these menstrual disorders may influence the quality of life of young women not only in the present but also in the future, skipping breakfast should be re-evaluated from the perspective of future reproductive function.

  5. uPA, uPAR and TGFβ₁ expression during early and late post myocardial infarction period in rat myocardium.

    Science.gov (United States)

    Stavropoulou, Anastasia; Philippou, Anastassios; Halapas, Antonios; Sourla, Antigone; Pissimissis, Nikolaos; Koutsilieris, Michael

    2010-01-01

    The expression patterns of transforming growth factor beta 1 (TGFβ₁), urokinase-type plasminogen activator (uPA) and uPA receptor (uPAR) were analysed after artery ligation-induced myocardial infarction (MI) in the rat myocardium. uPA and uPAR expressions were significantly increased both at transcriptional and protein level during early phase post MI period (uPA at 1 hour and uPAR at 24 hours post infarction). TGFβ1 mRNA expression profile revealed a significant increase of TGFβ1 expression from day 4 up to 8 weeks post infarction. These data suggest that the need for an increasing TGFβ₁ bioavailability during the post-infarction period in rat myocardium is achieved in the early post MI period by an increased expression of uPA/uPAR proteolytic system (indirect activation of latent TGFβ₁) and in the late post MI period by direct regulation of TGFβ₁ expression. It is therefore concluded that differential regulation of the TGFβ₁ bioavailability may be a crucial step of the repair mechanisms during the post MI infarction period in the rat myocardium.

  6. Is there still a role for treatment with beta-adrenoceptor antagonists in post-myocardial infarction patients with well-preserved left ventricular systolic function?

    Science.gov (United States)

    Horowitz, John D; Arstall, Margaret A; Zeitz, Christopher J; Beltrame, John F

    2008-01-01

    The utility of beta-adrenoceptor antagonists post myocardial infarction was established in the pre-thrombolytic era. Evidence for improvement in long-term prognosis with metoprolol, timolol and propranolol in particular derives from reduction in event rates in patients who have had substantial left ventricular damage at the time of infarction and probably correlates largely with the more recently demonstrated salutary effects of this group of drugs in patients with chronic heart failure. In all other respects, evidence for beneficial effects of beta-adrenoceptor antagonists in peri-infarct and post-infarct therapeutics is equivocal. They appear to exert no major influence on outcomes in patients with unstable angina, nor do they markedly alter early clinical course in uncomplicated acute myocardial infarction, irrespective of other interventions. Furthermore, the limited available analyses suggest no discernible beneficial effect on long-term outcomes post-uncomplicated infarction. It is possible that in such patients, current recommendations for 'routine' long-term beta-adrenoceptor blockade can no longer be justified.

  7. Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos Myocardial dysfunction and abnormalities in intracellular calcium handling in obese rats

    Directory of Open Access Journals (Sweden)

    Ana Paula Lima-Leopoldo

    2011-09-01

    these factors in the development of myocardial dysfunction induced by obesity is still not clear. OBJECTIVE: The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca2+ handling and the β-adrenoceptor system. METHODS: Male 30-day-old Wistar rats were fed with standard food (C and a cycle of five hypercaloric diets (Ob for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers. RESULTS: Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca2+ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation. CONCLUSION: Obesity promotes cardiac dysfunction related to changes in intracellular Ca2+ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2 activation via Ca2+ calmodulin kinase.

  8. Impaired oxidative metabolism and calcium mishandling underlie cardiac dysfunction in a rat model of post-acute isoproterenol-induced cardiomyopathy.

    Science.gov (United States)

    Willis, B Cicero; Salazar-Cantú, Ayleen; Silva-Platas, Christian; Fernández-Sada, Evaristo; Villegas, César A; Rios-Argaiz, Eduardo; González-Serrano, Pilar; Sánchez, Luis A; Guerrero-Beltrán, Carlos E; García, Noemí; Torre-Amione, Guillermo; García-Rivas, Gerardo J; Altamirano, Julio

    2015-03-01

    Stress-induced cardiomyopathy, triggered by acute catecholamine discharge, is a syndrome characterized by transient, apical ballooning linked to acute heart failure and ventricular arrhythmias. Rats receiving an acute isoproterenol (ISO) overdose (OV) suffer cardiac apex ischemia-reperfusion damage and arrhythmia, and then undergo cardiac remodeling and dysfunction. Nevertheless, the subcellular mechanisms underlying cardiac dysfunction after acute damage subsides are not thoroughly understood. To address this question, Wistar rats received a single ISO injection (67 mg/kg). We found in vivo moderate systolic and diastolic dysfunction at 2 wk post-ISO-OV; however, systolic dysfunction recovered after 4 wk, while diastolic dysfunction worsened. At 2 wk post-ISO-OV, cardiac function was assessed ex vivo, while mitochondrial oxidative metabolism and stress were assessed in vitro, and Ca(2+) handling in ventricular myocytes. These were complemented with sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA), phospholamban (PLB), and RyR2 expression studies. Ex vivo, basal mechanical performance index (MPI) and oxygen consumption rate (MVO2) were unchanged. Nevertheless, upon increase of metabolic demand, by β-adrenergic stimulation (1-100 nM ISO), the MPI versus MVO2 relation decreased and shifted to the right, suggesting MPI and mitochondrial energy production uncoupling. Mitochondria showed decreased oxidative metabolism, membrane fragility, and enhanced oxidative stress. Myocytes presented systolic and diastolic Ca(2+) mishandling, and blunted response to ISO (100 nM), and all these without apparent changes in SERCA, PLB, or RyR2 expression. We suggest that post-ISO-OV mitochondrial dysfunction may underlie decreased cardiac contractility, mainly by depletion of ATP needed for myofilaments and Ca(2+) transport by SERCA, while exacerbated oxidative stress may enhance diastolic RyR2 activity.

  9. Unusual towering elevation of troponin I after ST-elevation myocardial infarction and intensive monitoring with echocardiography post-percutaneous coronary intervention: a case report

    Directory of Open Access Journals (Sweden)

    Suryadevara Ramya

    2010-05-01

    Full Text Available Abstract Introduction The elevation of troponin levels directly corresponds to the extent of myocardial injury. Here we present a case of a robust rise in cardiac biomarkers that correspond to extensive damage to the myocardium but did not spell doom for our patient. It is important to note that, to the best of our knowledge, this is the highest level of troponin I ever reported in the literature after a myocardial injury in an acute setting. Case presentation A 53-year-old African American man with an unknown medical history presented to the emergency room of our hospital with chest pain associated with diaphoresis and altered mental status. He required emergency intubation due to acute respiratory failure and circulatory collapse within 10 minutes of his arrival. He was started on heparin and eptifibatide (Integrilin drips but he was taken immediately for cardiac catheterization, which showed a total occlusion of his proximal left anterior descending, diffuse left circumflex disease and severe left ventricular dysfunction with segmental wall motion abnormality. He remained hypotensive throughout the procedure and an intra-aortic balloon pump was inserted for circulatory support. His urinary toxicology examination result was positive for cocaine metabolites. Serial echocardiograms showed an akinetic apex, a severely hypokinetic septum, and severe systolic dysfunction of his left ventricle. Our patient stayed at the Coronary Care Unit for a total of 15 days before he was finally discharged. Conclusion Studies demonstrate that an increase of 1 ng/ml in the cardiac troponin I level is associated with a significant increase in the risk ratio for death. The elevation of troponin I to 515 ng/ml in our patient is an unusual robust presentation which may reflect a composite of myocyte necrosis and reperfusion but without short-term mortality. Nevertheless, prolonged close monitoring is required for better outcome. We also emphasize the need for the

  10. Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications

    Directory of Open Access Journals (Sweden)

    Byoung-Joon Song

    2014-01-01

    Full Text Available Mitochondria are critically important in providing cellular energy ATP as well as their involvement in anti-oxidant defense, fat oxidation, intermediary metabolism and cell death processes. It is well-established that mitochondrial functions are suppressed when living cells or organisms are exposed to potentially toxic agents including alcohol, high fat diets, smoking and certain drugs or in many pathophysiological states through increased levels of oxidative/nitrative stress. Under elevated nitroxidative stress, cellular macromolecules proteins, DNA, and lipids can undergo different oxidative modifications, leading to disruption of their normal, sometimes critical, physiological functions. Recent reports also indicated that many mitochondrial proteins are modified via various post-translation modifications (PTMs and primarily inactivated. Because of the recently-emerging information, in this review, we specifically focus on the mechanisms and roles of five major PTMs (namely oxidation, nitration, phosphorylation, acetylation, and adduct formation with lipid-peroxides, reactive metabolites, or advanced glycation end products in experimental models of alcoholic and nonalcoholic fatty liver disease as well as acute hepatic injury caused by toxic compounds. We also highlight the role of the ethanol-inducible cytochrome P450-2E1 (CYP2E1 in some of these PTM changes. Finally, we discuss translational research opportunities with natural and/or synthetic anti-oxidants, which can prevent or delay the onset of mitochondrial dysfunction, fat accumulation and tissue injury.

  11. Dysfunction of pre- and post-operative cardiac autonomic nervous system in elderly patients with diabetes mellitus.

    Science.gov (United States)

    Zhang, Junlong; Tu, Weifeng; Dai, Jianqiang; Lv, Qing; Yang, Xiaoqi

    2011-01-01

    The pre- and post-operative cardiac autonomic nervous functions were compared in elderly, non-cardiac surgery patients with diabetes mellitus (DM) and without diabetes mellitus (NDM). A group of 30 unpremedicated elderly patients scheduled to undergo elective non-cardiac surgery were studied, including 15 DM patients and 15 NDM patients. Each component of heart rate variability (HRV) analysis in the frequency domain was monitored with Holter during the nights of the day before and on 1st and 2nd day after operation. After surgery, total power (TP), high frequency (HF), low frequency (LF) and very low frequency (VLF) significantly decreased as compared to the baseline values before operation in both groups (p<0.05). The LF/HF ratio was significantly changed in DM group but did not change in NDM group. On the 2nd postoperative day, TP, HF, LF and VLF in DM group were further decreased as compared to those on the 1st postoperative day and were significantly lower than those in NDM group (p<0.01 or 0.05), but these indices in NDM group did not show significant decreases. Surgery induced the cardiac autonomic nervous dysfunction in elderly patients not only with DM but also without diabetes. On the 2nd postoperative day, the disturbances of cardiac autonomic nervous activity were more sever in DM patients, compared to the 1st postoperative day, but was not significantly more sever than in the NDM patients.

  12. Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction.

    Science.gov (United States)

    Wysoczynski, Marcin; Solanki, Mitesh; Borkowska, Sylwia; van Hoose, Patrick; Brittian, Kenneth R; Prabhu, Sumanth D; Ratajczak, Mariusz Z; Rokosh, Gregg

    2014-09-01

    Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kit(pos) cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67(pos) CSPCs and decreased formation of new BrdU(pos) /α-sarcomeric actin(pos) myocytes, and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate that CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function.

  13. Predictors of in-hospital mortality after mitral valve surgery for post-myocardial infarction papillary muscle rupture

    NARCIS (Netherlands)

    Bouma, Wobbe; Hamer, Inez J. Wijdh-den; Koene, Bart M.; Kuijpers, Michiel; Natour, Ehsan; Erasmus, Michiel E.; van der Horst, Iwan C. C.; Gorman, Joseph H.; Gorman, Robert C.; Mariani, Massimo A.

    2014-01-01

    Background: Papillary muscle rupture (PMR) is a rare, but often life-threatening mechanical complication of myocardial infarction (MI). Immediate surgical intervention is considered the optimal and most rational treatment for acute PMR, but carries high risks. At this point it is not entirely clear

  14. Post-myocardial infarction quality of care among disabled Medicaid beneficiaries with and without serious mental illness

    Science.gov (United States)

    McGinty, Emma E.; Blasco-Colmenares, Elena; Zhang, Yiyi; dosReis, Susan C.; Ford, Daniel E.; Steinwachs, Donald M.; Guallar, Eliseo; Daumit, Gail

    2012-01-01

    Objective To examine the association between serious mental illness and quality of care for myocardial infarction among disabled Maryland Medicaid beneficiaries. Methods We conducted a retrospective cohort study disabled Maryland Medicaid beneficiaries with myocardial infarction from 1994 to 2004. Cardiac procedures and guideline-based medication use were compared for persons with and without serious mental illness. Results Of the 633 cohort members with myocardial infarction, 137 had serious mental illness. Serious mental illness was not associated with differences in receipt of cardiac procedures or guideline-based medications. Overall use of guideline-based medications was low; 30 days after the index hospitalization for myocardial infarction, 19%, 35%, and 11% of cohort members with serious mental illness and 22%, 37%, and 13% of cohort members without serious mental illness had any use of angiotensin converting enzyme inhibitors or angiotensin receptor blockers, beta-blockers and statins, respectively. Study participants with and without serious mental illness had similar rates of mortality. Overall, use of beta-blockers (hazard ratio 0.93, 95% CI 0.90-0.97) and statins (hazard ratio 0.93, 95% CI 0.89-0.98) were associated with reduced risk of mortality. Conclusions Quality improvement programs should consider how to increase adherence to medications of known benefit among disabled Medicaid beneficiaries with and without serious mental illness. PMID:22763001

  15. Prognostic Association of Anxiety Post Myocardial Infarction With Mortality and New Cardiac Events : A Meta-Analysis

    NARCIS (Netherlands)

    Roest, Annelieke M.; Martens, Elisabeth J.; Denollet, Johan; de Jonge, Peter; de, Jonge P.

    2010-01-01

    Objective: To assess the association of anxiety after myocardial infarction (MI) with cardiac prognosis. Methods: A meta-analysis of references derived from MEDLINE, EMBASE, and PSYCINFO (1975-March 2009) was performed without language restrictions. End point was cardiac outcome defined as all-cause

  16. The predictive value of CHADS₂ risk score in post myocardial infarction arrhythmias - a Cardiac Arrhythmias and RIsk Stratification after Myocardial infArction (CARISMA) substudy

    DEFF Research Database (Denmark)

    Ruwald, Anne-Christine Huth; Gang, Uffe; Thomsen, Poul Erik Bloch;

    2014-01-01

    of this study was to investigate if CHADS₂ score (congestive heart failure, hypertension, age ≥75 years, diabetes and previous stroke/TCI [doubled]) can be used as a risk tool for predicting cardiac arrhythmias after MI. METHODS: The study included 297 post-MI patients from the CARISMA study with left...

  17. The significance of post-stress decrease in left ventricular ejection fraction in patients undergoing regadenoson stress gated SPECT myocardial perfusion imaging.

    Science.gov (United States)

    Gomez, Javier; Golzar, Yasmeen; Fughhi, Ibtihaj; Olusanya, Adebayo; Doukky, Rami

    2017-02-08

    The significance of post-stress decrease in left ventricular ejection fraction (LVEF) with regadenoson stress gated SPECT (GSPECT) myocardial perfusion imaging (MPI) has not been studied. Consecutive patients who underwent rest/regadenoson stress GSPECT-MPI followed by coronary angiography within 6 months were analyzed. Change in LVEF by GSPECT-MPI was calculated as stress LVEF minus rest LVEF; a significant decrease was tested at 5% and 10% thresholds. In a diagnostic cohort of 793 subjects, LVEF change was not predictive of severe/extensive coronary artery disease (area under the curve, 0.50; 95% confidence interval, 0.44-0.57; P = 0.946). There was no significant difference in the rates of severe/extensive coronary artery disease in patients with or without a decrease in LVEF, irrespective of MPI findings. In an outcome cohort of the 929 subjects followed for 30 ± 16 months, post-regadenoson stress decrease in LVEF was not associated with increased risk of the composite endpoint of cardiac death or myocardial infarction or in the risk of coronary revascularization. In patients selected to undergo coronary angiography following regadenoson stress GSPECT-MPI, a decrease in LVEF after regadenoson stress is not predictive of severe/extensive CAD or adverse clinical outcomes, irrespective of MPI findings.

  18. Comparison of regional versus global assessment of left ventricular function in patients with left ventricular dysfunction, heart failure, or both after myocardial infarction: the valsartan in acute myocardial infarction echocardiographic study

    DEFF Research Database (Denmark)

    Thune, Jens Jakob; Køber, Lars; Pfeffer, Marc A

    2006-01-01

    BACKGROUND: Left ventricular (LV) ejection fraction (EF) and wall-motion index (WMI) have both been shown to be independent predictors of outcome after myocardial infarction (MI). OBJECTIVES: We sought to determine whether these two measurements of LV systolic function provide similar or compleme...

  19. Long-Term Outcome of Combined (Percutaneous Intramyocardial and Intracoronary) Application of Autologous Bone Marrow Mononuclear Cells Post Myocardial Infarction: The 5-Year MYSTAR Study

    Science.gov (United States)

    Syeda, Bonni; Charwat, Silvia; Marzluf, Beatrice; Mascherbauer, Julia; Jakab, Andras; Zimba, Abelina; Sárközy, Márta; Pavo, Noemi; Sochor, Heinz; Graf, Senta; Lang, Irene; Maurer, Gerald; Bergler-Klein, Jutta

    2016-01-01

    Objective The long-term (5-year) outcome of early (3–6 weeks after acute myocardial infarction [AMI], BM-MNC Early group) and late (3–4 months after AMI, BM-MNC Late group) combined (percutaneous intramyocardial and intracoronary) delivery of autologous bone marrow mononuclear cells (BM-MNCs) was evaluated in patients with ejection fractions (EF) between 30–45% post-AMI. Methods Major adverse cardiac and cerebrovascular events (MACCE) and hospitalization were recorded. Left (LV) and right (RV) ventricular function were measured by transthoracic echocardiography. Cardiac magnetic resonance imaging (MRI) and myocardial single photon emission computed tomography was performed in a subgroup of patients. Pre-cell therapy myocardial voltage values of treated areas (assessed by NOGA mapping) were correlated with clinical outcome. Results Five-year MACCE incidences (7.4%. vs 24.1%) and the composite of all adverse events (11.1% vs 27.6%) were not different between the Early and Late treatment groups. The significant LV-EF increase at 1-year follow-up was preserved at the 5-year control (from baseline to 5-year: 5.3%, 95% CI:0.5–10.1, and 5.7%, 95% CI:1.7–9.6, p<0.05 in the Early and Late groups, respectively), with no significant changes between 1- and 5-year follow-ups. Similarly, RVEF increased significantly from baseline to the 5-year follow-up (Early group: 5.4%, 95% CI:1.0–9.6; and Late group: 8.4%, 95% CI:4.5–12.3). Lower baseline levels of myocardial viability of the treated cardiac area (6.3±2.4 vs 8.2±3.0 mV, p<0.05) were associated with incidence of MACCE. Conclusions Percutaneous combined delivery of autologous BM-MNCs is feasible and safe after 5 years, and may result in sustained improvement of cardiac function at 5 years in patients with low EF post-AMI (Clinicaltrials.gov NCT01395212). PMID:27764157

  20. Systemic and Cardiac Depletion of M2 Macrophage through CSF-1R Signaling Inhibition Alters Cardiac Function Post Myocardial Infarction

    OpenAIRE

    Anne-Laure Leblond; Kerstin Klinkert; Kenneth Martin; Turner, Elizebeth C.; Arun H Kumar; Tara Browne; Caplice, Noel M.

    2015-01-01

    The heart hosts tissue resident macrophages which are capable of modulating cardiac inflammation and function by multiple mechanisms. At present, the consequences of phenotypic diversity in macrophages in the heart are incompletely understood. The contribution of cardiac M2-polarized macrophages to the resolution of inflammation and repair response following myocardial infarction remains to be fully defined. In this study, the role of M2 macrophages was investigated utilising a specific CSF-1...

  1. Crise de feocromocitoma simulando um infarto agudo do miocárdio em paciente com artérias coronárias normais Pheochromocytoma-induced segmental myocardial dysfunction mimicking an acute myocardial infarction in a patient with normal coronary arteries

    Directory of Open Access Journals (Sweden)

    Eduardo S. Darzé

    2004-02-01

    Full Text Available Relatamos o caso de um paciente com alterações eletrocardiográficas e disfunção miocárdica segmentar induzidas por feocromocitoma, simulando infarto agudo do miocárdio. A angiografia coronariana foi normal e houve normalização completa do eletrocardiograma e ecocardiograma, após terapia com um bloqueador alfa-adrenérgico e ressecção do tumor. Espasmo coronariano foi o provável mecanismo envolvido na produção dessas alterações, ilustrando a importância de manter um alto grau de suspeição clínica em pacientes com evento miocárdico inesperado em meio a uma crise hipertensiva.We report a case of pheochromocytoma-induced segmental myocardial dysfunction and electrocardiographic abnormalities mimicking an acute anterior myocardial infarction, probably due to coronary spasm. Coronary angiography showed normal coronaries, and the electrocardiographic and echocardiographic changes resolved completely after therapy with an alpha-adrenergic blocker and tumor removal. Our case illustrates the importance of maintaining a high index of suspicion in patients presenting with an unexpected myocardial event and a hypertensive crisis.

  2. Long-term outcomes of left bundle branch block in high-risk survivors of acute myocardial infarction: the VALIANT experience

    DEFF Research Database (Denmark)

    Stephenson, Kent; Skali, Hicham; McMurray, John J V;

    2006-01-01

    BACKGROUND: In survivors of myocardial infarction (MI), new left bundle branch block (LBBB) is associated with adverse outcomes, but its impact is not well described in post-MI patients with left ventricular (LV) systolic dysfunction and/or heart failure (HF). OBJECTIVES: The aim of this study wa...

  3. Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo study

    DEFF Research Database (Denmark)

    Meris, Alessandra; Amigoni, Maria; Uno, Hajime

    2009-01-01

    AIMS: To assess the relationship between left atrial (LA) size and outcome after high-risk myocardial infarction (MI) and to study dynamic changes in LA size during long-term follow-up. METHODS AND RESULTS: The VALIANT Echocardiography study prospectively enrolled 610 patients with left ventricul...

  4. Permanent ligation of the left anterior descending coronary artery in mice: a model of post-myocardial infarction remodelling and heart failure.

    Science.gov (United States)

    Muthuramu, Ilayaraja; Lox, Marleen; Jacobs, Frank; De Geest, Bart

    2014-12-02

    Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It is characterized by fluid retention, shortness of breath, and fatigue, in particular on exertion. Heart failure is a growing public health problem, the leading cause of hospitalization, and a major cause of mortality. Ischemic heart disease is the main cause of heart failure. Ventricular remodelling refers to changes in structure, size, and shape of the left ventricle. This architectural remodelling of the left ventricle is induced by injury (e.g., myocardial infarction), by pressure overload (e.g., systemic arterial hypertension or aortic stenosis), or by volume overload. Since ventricular remodelling affects wall stress, it has a profound impact on cardiac function and on the development of heart failure. A model of permanent ligation of the left anterior descending coronary artery in mice is used to investigate ventricular remodelling and cardiac function post-myocardial infarction. This model is fundamentally different in terms of objectives and pathophysiological relevance compared to the model of transient ligation of the left anterior descending coronary artery. In this latter model of ischemia/reperfusion injury, the initial extent of the infarct may be modulated by factors that affect myocardial salvage following reperfusion. In contrast, the infarct area at 24 hr after permanent ligation of the left anterior descending coronary artery is fixed. Cardiac function in this model will be affected by 1) the process of infarct expansion, infarct healing, and scar formation; and 2) the concomitant development of left ventricular dilatation, cardiac hypertrophy, and ventricular remodelling. Besides the model of permanent ligation of the left anterior descending coronary artery, the technique of invasive hemodynamic measurements in mice is presented in detail.

  5. Relationship between age/gender-induced survival changes and the magnitude of inflammatory activation and organ dysfunction in post-traumatic sepsis.

    Directory of Open Access Journals (Sweden)

    Susanne Drechsler

    Full Text Available Age/gender may likely influence the course of septic complications after trauma. We aimed to characterize the influence of age/gender on the response of circulating cytokines, cells and organ function in post-traumatic sepsis. We additionally tested whether post-traumatic responses alone can accurately predict outcomes in subsequent post-traumatic sepsis. A mouse 2-hit model of trauma/hemorrhage (TH, 1(st hit and cecal ligation and puncture (CLP, 2(nd hit was employed. 3, 15 and 20 month (m old female (♀ and male (♂ CD-1 mice underwent sublethal TH followed by CLP 2 days later. Blood was sampled daily until day 6 post-TH and survival was followed for 16 days. To compare general response patterns among groups, we calculated two scores: the inflammatory response (including KC, MIP-1α, TNFα, MCP-1, IFNγ, IL-1β,-5,-6,-10 and the organ dysfunction score (Urea, ALT, AST and LDH. Moreover, mice were retrospectively divided into survivors (SUR and dying (DIE based on post-CLP outcome. In general, females survived better than males and their survival did not correspond to any specific estrus cycle phase. Pre-CLP phase: the post-TH inflammatory score was weakest in 3 m♂ but there were no changes among remaining groups (similar lack of differences in the organ dysfunction score. TH induced a 40% increase of IFNγ, MIP-1α and IL-5 in 15 m♂ SUR (vs. DIE but predictive accuracy for post-CLP outcomes was moderate. Post-CLP phase: while stable in males, inflammatory response score in 15 m and 20 m females decreased with age at day 1 and 2 post-CLP. SUR vs. DIE differences in inflammatory and organ dysfunction score were evident but their magnitude was comparable across age/gender. Nearly identical activation of the humoral inflammatory and organ function compartments, both across groups and according to sepsis severity, suggests that they are not directly responsible for the age/gender-dependent disparity in TH-CLP survival in the studied young

  6. Relationship between myocardial extracellular space expansion estimated with post-contrast T1 mapping MRI and left ventricular remodeling and neurohormonal activation in patients with dilated cardiomyopathy

    Energy Technology Data Exchange (ETDEWEB)

    Yoon, Ji Hyun; Son, Jung Woo; Chung, Hye Moon [Cardiology Division, Dept. of Internal Medicine, Yonsei University College of Medicine, Seoul (Korea, Republic of); and others

    2015-10-15

    Post-contrast T1 values are closely related to the degree of myocardial extracellular space expansion. We determined the relationship between post-contrast T1 values and left ventricular (LV) diastolic function, LV remodeling, and neurohormonal activation in patients with dilated cardiomyopathy (DCM). Fifty-nine patients with DCM (mean age, 55 ± 15 years; 41 males and 18 females) who underwent both 1.5T magnetic resonance imaging and echocardiography were enrolled. The post-contrast 10-minute T1 value was generated from inversion time scout images obtained using the Look-Locker inversion recovery sequence and a curve-fitting algorithm. The T1 sample volume was obtained from three interventricular septal points, and the mean T1 value was used for analysis. The N-Terminal pro-B-type natriuretic peptide (NT-proBNP) level was measured in 40 patients. The mean LV ejection fraction was 24 ± 9% and the post-T1 value was 254.5 ± 46.4 ms. The post-contrast T1 value was significantly correlated with systolic longitudinal septal velocity (s'), peak late diastolic velocity of the mitral annulus (a'), the diastolic elastance index (Ed, [E/e']/stroke volume), LV mass/volume ratio, LV end-diastolic wall stress, and LV end-systolic wall stress. In a multivariate analysis without NT-proBNP, T1 values were independently correlated with Ed (β = -0.351, p = 0.016) and the LV mass/volume ratio (β = 0.495, p = 0.001). When NT-proBNP was used in the analysis, NT-proBNP was independently correlated with the T1 values (β = -0.339, p = 0.017). Post-contrast T1 is closely related to LV remodeling, diastolic function, and neurohormonal activation in patients with DCM.

  7. Is there a clinically significant gender bias in post-myocardial infarction pharmacological management in the older (>60 population of a primary care practice?

    Directory of Open Access Journals (Sweden)

    Upshur Ross EG

    2002-05-01

    Full Text Available Abstract Background Differences in the management of coronary artery disease between men and women have been reported in the literature. There are few studies of potential inequalities of treatment that arise from a primary care context. This study investigated the existence of such inequalities in the medical management of post myocardial infarction in older patients. Methods A comprehensive chart audit was conducted of 142 men and 81 women in an academic primary care practice. Variables were extracted on demographic variables, cardiovascular risk factors, medical and non-medical management of myocardial infarction. Results Women were older than men. The groups were comparable in terms of cardiac risk factors. A statistically significant difference (14.6%: 95% CI 0.048–28.7 p = 0.047 was found between men and women for the prescription of lipid lowering medications. 25.3% (p = 0.0005, CI 11.45, 39.65 more men than women had undergone angiography, and 14.4 % (p = 0.029, CI 2.2, 26.6 more men than women had undergone coronary artery bypass graft surgery. Conclusion Women are less likely than men to receive lipid-lowering medication which may indicate less aggressive secondary prevention in the primary care setting.

  8. Previous exercise training increases levels of PPAR-α in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response

    Directory of Open Access Journals (Sweden)

    Marília Harumi Higuchi Santos

    2016-03-01

    Full Text Available OBJECTIVE: Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-α is involved in the beneficial effects of previous exercise on myocardial infarction (MI and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome. METHODS AND RESULTS: Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1 or 4 weeks (EI4 or SI4 of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-α, TNF-α and NF-κB antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%, without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35% and a higher apoptosis/area rate (3.97±0.61 vs 1.90±1.82 in infarcted areas (both p=0.001. Immunohistochemistry also revealed higher TNF-α levels in SI1 than in EI1 (9.59 vs 4.09, p<0.001 in infarcted areas. In non-infarcted areas, EI4 showed higher levels of TNF-α and positive correlations between PPAR-α and NF-κB (r=0.75, p=0.02, in contrast to SI4 (r=0.05, p=0.87. CONCLUSION: Previously exercised animals had better long-term ventricular function post-MI, in addition to lower levels of local inflammatory markers and less myocardial apoptosis

  9. Potential demographic and baselines variables for risk stratification of high-risk post-myocardial infarction patients in the era of implantable cardioverter-defibrillator - a prognostic indicator

    DEFF Research Database (Denmark)

    Yap, Yee Guan; Duong, Trinh; Bland, Martin

    2008-01-01

    , sex, previous MI or angina, hypertension, diabetes, systolic blood pressure, heart rate, NYHA functional class and non-Q wave infarct on electrocardiogram. Distinct survival curves were obtained for 3 risk groups based on the median and inter-quartile range for the prognostic index. In the high-risk......BACKGROUND: Risk stratification after myocardial infarction (MI) remains expensive and disappointing. We designed a prognostic indicator using demographic information to select patients at risk of dying after MI. METHOD AND RESULTS: We combined individual patient data from the placebo arms of EMIAT......, CAMIAT, TRACE and DIAMOND-MI with LVEF 10 ventricular premature beats/hour or a run of ventricular tachycardia). Risk factors for mortality beginning at day 45 post-MI up to 2 years were examined using Cox regression analysis. Risk scores were derived from the equation of a Cox regression model...

  10. Longitudinal left ventricular myocardial dysfunction assessed by 2D colour tissue Doppler imaging in a dog with systemic hypertension and severe arteriosclerosis.

    Science.gov (United States)

    Nicolle, A P; Carlos Sampedrano, C; Fontaine, J J; Tessier-Vetzel, D; Goumi, V; Pelligand, L; Pouchelon, J-L; Chetboul, V

    2005-03-01

    A 12-year-old sexually intact male Vendee Griffon Basset was presented for acute pulmonary oedema. Severe systemic systolic arterial hypertension (SAH) was diagnosed (290 mmHg). Despite blood and abdominal ultrasound tests, the underlying cause of the systemic hypertension could not be determined, and primary SAH was therefore suspected. Conventional echocardiography showed eccentric left ventricular hypertrophy with normal fractional shortening. Despite this apparent normal systolic function, 2D colour tissue Doppler imaging (TDI) identified a marked longitudinal systolic left ventricular myocardial alteration, whereas radial function was still preserved. Three months later, the dog underwent euthanasia because of an acute episode of distal aortic thromboembolism. Necropsy revealed severe aortic and iliac arteriosclerosis. SAH related to arteriosclerosis is a common finding in humans, but has not been previously described in dogs. Moreover, its consequence on longitudinal myocardial function using TDI has never been documented before in this species.

  11. Global analysis of myocardial peptides containing cysteines with irreversible sulfinic and sulfonic Acid post-translational modifications

    DEFF Research Database (Denmark)

    Paulech, Jana; Liddy, Kiersten A; Engholm-Keller, Kasper;

    2015-01-01

    Cysteine (Cys) oxidation is a crucial post-translational modification (PTM) associated with redox signaling and oxidative stress. As Cys is highly reactive to oxidants it forms a range of post-translational modifications, some that are biologically reversible (e.g. disulfides, Cys sulfenic acid...

  12. 应用心肌造影超声心动图结合速度向量成像对糖尿病大鼠心肌微循环与收缩功能障碍的相关性研究%Relationship between myocardial perfusion impairment and dysfunction in diabetic rats using myocardial contrast echocardiography and velocity vector imaging

    Institute of Scientific and Technical Information of China (English)

    卫张蕊; 张军; 张海滨; 苏海砾; 施红; 朱霆; 朱永胜

    2012-01-01

    目的 应用心肌造影超声心动图(MCE)结合速度向量成像(VVI)技术研究糖尿病(DM)大鼠左室心肌微循环障碍与心肌收缩功能损伤之间的相关关系.方法 雄性SD大鼠23只,腹腔注射链脲菌素复制DM模型,另23只体质量匹配的雄性SD大鼠腹腔注射等量生理盐水作为对照.分别在静息状态和潘生丁负荷后,对两组大鼠(12周)乳头肌水平左室短轴行MCE和VVI检查,分别测定心肌血流量(MBF)、心肌血流储备(MFR)、收缩期最大圆周应变率(SRc)及其储备,分析MBF/MFR与SRc/SRc储备之间是否存在相关关系.结果 DM组大鼠的SRc、SRc储备、MBF及MFR均较对照组显著减低.DM组大鼠SRc与MBF之间没有明显相关性,而SR.储备与MFR之间呈现显著的负相关.结论 静息状态下,心肌血流量的降低并不是圆周应变率降低的主要决定因素,而潘生丁负荷后,心肌血流储备的降低可能是心肌圆周应变率储备降低的主要决定因素.%Objective To investigate whether myocardial dysfunction and perfusion impairment had happened in diabetes mellitus(DM)rats,and to assess the relationship between them by using myocardial contrast echocardiography(MCE)and velocity vector imaging(VVI).Methods MCE and VVI were performed from the short-axis views of the mid-left ventricular level both at rest and after dipyridamole stress in control rats and DM rafs(12 weeks after induction with streptozotocin).MCE-derived myocardial blood flow(MBF)and myocardial flow reserve(MFR)and VVI-derived circumferential strain rate(SRc)and SRc reserve were obtained.Results SRc(absolute value)and MBF in the DM group were significantly lower than those in the control group at rest(P =0.03 for SRc and P =0.005 for MBF).SRc reserve and MFR in the DM group were significantly lower than those in the control group after dipyridamole stress (P =0.000 for SRc reserve and P =0.014 for MFR).There was no significant correlation between SRc and MBF at rest in the

  13. Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure.

    Directory of Open Access Journals (Sweden)

    Anne Berit Johnsen

    Full Text Available BACKGROUND: There is limited knowledge about atrial myocyte Ca(2+ handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca(2+ handling in rats with post-infarction heart failure (HF and to examine whether aerobic interval training could reverse a potential dysfunction. METHODS AND RESULTS: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01 and time to relaxation was prolonged (p<0.01 in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca(2+ amplitude, decreased SR Ca(2+ content, and slower Ca(2+ transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca(2+ ATPase activity, increased Na(+/Ca(2+-exchanger activity and increased diastolic Ca(2+ leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca(2+ handling in HF. CONCLUSION: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca(2+ handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.

  14. Assessment of myocardial perfusion by myocardial contrast echocardiography combined with intravenous infusion of levovist in patients with post-myocardial infaction%利声显经静脉心肌声学造影评价心肌梗死后患者的心肌灌注

    Institute of Scientific and Technical Information of China (English)

    仲肇舒; 孔繁荣; 张新琳; 朱正明

    2001-01-01

    Objective To evaluate myocardial perfusion by myocardial contrast echocardiography (MCE) with intermittent harmonic power Doppler imaging combined with intravenous infusion levovist in post-myocardial infaction patients.Methods The study was performed with a HP Sonos 5500 during intravenous infusion levovist (300 mg/ml, 2 ml/min) using harmonic power Doppler mode twenty-five post-myocardial infaction patients [mean age (67±7) years, 21 males]. The imaging was acquired during end-systolic triggering at intervals of 1∶4 beats. Using a 16 segments model, myocardial perfusion both in gray and power Doppler was scored as 0(contrast deficit),0.5(partial and non-homogenous contrast), 1(complete and homogenous contrast).Results ①Compared with baseline, heart rate and blood pressure didn′t show significant changes after MCE.There were no signs and symptoms in all patients during MCE.②Myocardial perfusion was detectable in all the patients. ③Intravenous infusion Levovist(300 mg/ml, 2 ml/min) using intermittent harmonic power Doppler model resulted in 4~5 minites of left ventricular opacification and avoided the attenuation.Conclusions Myocardial perfusion was detectable by using intravenous infusion Levovist with intermittent harmonic power Doppler imaging. MCE thus may be a clinically useful technique for the detection and quantification of coronary artery disease at rest.%目的 心肌造影超声心动图(MCE)采用触发谐频能量多普勒显像模式并用静脉持续输注利声显,观察心肌梗死后患者的心肌灌注情况。方法 使用谐频频率 1.8~3.6 MHz的能量多普勒模式,于心电图T波终末处,按1∶4心动周期进行触发。利声显浓度为300 mg/ml,采用微量输液泵将所配心肌造影剂于患者左肘静脉内持续输注4 min(2 ml/min)。观察25例心肌梗死后患者的血压和心率变化并对心肌灌注情况进行半定量分析。结果 ①MCE前后,患者血压和心率

  15. Lycopene attenuates inflammation and apoptosis in post-myocardial infarction remodeling by inhibiting the nuclear factor-κB signaling pathway.

    Science.gov (United States)

    He, Qin; Zhou, Wei; Xiong, Caijin; Tan, Gang; Chen, Manhua

    2015-01-01

    Inflammatory response and cardiomyocyte apoptosis are important processes in ventricular remodeling post-myocardial infarction (MI) and may form the basic mechanisms in the development of chronic heart failure. The nuclear factor κB (NF-κB) signaling pathway could promote inflammation and apoptosis and it has been demonstrated that lycopene inhibits cigarette smoke extract-mediated NF-κB activation. Therefore, it was hypothesized that the NF-κB signaling pathway may be a key target of lycopene in the reversal of ventricular remodeling post MI. An MI model was established by left anterior descending coronary artery ligation in mice. Following ligation, the mice were administered with lycopene (10 mg/kg/day) or saline. The mice underwent echocardiography and were sacrificed after 4 weeks. The mRNA expression of fibrosis markers transforming growth factor-β1 (TGF-β1), collagen I and III and inflammatory markers tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were examined by quantitative polymerase chain reaction. The protein expression of apoptotic markers, including caspase-3, -8, -9 and activation of the NF-κB signaling pathway were analyzed by western blotting. Lycopene reduced the expression of TGF-β1, collagen I, collagen III, TNF-α, IL-1β, caspase-3, -8 and -9 and inhibited the activation of the NF-κB signaling pathway. The level of ventricular remodeling post-MI was also attenuated following treatment with lycopene. Lycopene may inhibit the NF-κB signaling pathway thereby reducing the inflammatory response and cardiomyocyte apoptosis post-MI, which could be a key mechanism of lycopene in attenuating ventricular remodeling.

  16. Successful reversal of propionic acidaemia associated cardiomyopathy: evidence for low myocardial coenzyme Q10 status and secondary mitochondrial dysfunction as an underlying pathophysiological mechanism.

    Science.gov (United States)

    Baruteau, J; Hargreaves, I; Krywawych, S; Chalasani, A; Land, J M; Davison, J E; Kwok, M K; Christov, G; Karimova, A; Ashworth, M; Anderson, G; Prunty, H; Rahman, S; Grünewald, S

    2014-07-01

    Dilated cardiomyopathy is a rare complication in propionic acidaemia (PA). Underlying pathophysiological mechanisms are poorly understood. We present a child of Pakistani consanguineous parents, diagnosed with late-onset PA at 18months of age. He presented a mild phenotype, showed no severe further decompensations, normal growth and psychomotor development on a low protein diet and carnitine supplementation. At 15years, a mildly dilated left ventricle was noticed. At 17years he presented after a 2-3month history of lethargy and weight loss with severe decompensated dilated cardiomyopathy. He was stabilised on inotropic support and continuous haemofiltration; a Berlin Heart biventricular assist device was implanted. He received d,l-hydroxybutyrate 200mg/kg/day, riboflavin and thiamine 200mg/day each and coenzyme Q10 (CoQ10). Myocardial biopsy showed endocardial fibrosis, enlarged mitochondria, with atypical cristae and slightly low respiratory chain (RC) complex IV activity relative to citrate synthase (0.012, reference range 0.014-0.034). Myocardial CoQ10 was markedly decreased (224pmol/mg, reference range 942-2738), with a marginally decreased white blood cell level (34pmol/mg reference range 37-133). The dose of CoQ10 was increased from 1.5 to 25mg/kg/day. Cardiomyopathy slowly improved allowing removal of the external mechanical cardiac support after 67days. We demonstrate for the first time low myocardial CoQ10 in cardiomyopathy in PA, highlighting secondary mitochondrial impairment as a relevant causative mechanism. According to these findings, a high-dose CoQ10 supplementation could be a potential adjuvant therapeutic to be considered in PA-related cardiomyopathy.

  17. Investigation of the relationship between regression of hypertensive cardiac hypertrophy and improvement of cardiac sympathetic nervous dysfunction using iodine-123 metaiodobenzylguanidine myocardial imaging

    Energy Technology Data Exchange (ETDEWEB)

    Morimoto, Satoshi [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Terada, Koji [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Keira, Natsuya [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Satoda, Masahiko [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Inoue, Keiji [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Tatsukawa, Hirotaka [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Katoh, Shuji [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Ida, Kazunori [Dept. of Internal Medicine, Murakami Memorial Hospital, Asahi Univ., Gifu (Japan); Sugihara, Hiroki [Dept. of Radiology, Kyoto Prefectural Univ. of Medicine (Japan); Takeda, Kazuo [Second Dept. of Medicine, Kyoto Prefectural Univ. of Medicine (Japan); Nakagawa, Masao [Second Dept. of Medicine, Kyoto Prefectural Univ. of Medicine (Japan)

    1996-07-01

    Although many theories exist on the subject, the mechanisms responsible for a reduction of hypertensive cardiac hypertrophy in response to antihypertensive therapy are still unclear. In order to investigate the relationship between regression of hypertensive cardiac hypertrophy and cardiac nervous function, we studied ten patients with untreated essential hypertension (six men and four women, 62{+-}12 years old). Both echocardiography and iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging were performed before and after antihypertensive therapy. Left ventricular mass (LVM) was significantly reduced in conjunction with the reduction of blood pressure following treatment. MIBG myocardial images showed that the heart-to-mediastinum activity ratio (H/M) was significantly increased while the washout ratio was significantly decreased. Patients were divided into two groups according to the ratio of the LVM values before and after therapy (LVM ratio). Patients with an LVM ratio of less than 0.75 were classified as group A and those with values higher than 0.75 as group B. Neither the change in blood pressure nor the length of treatment was significantly different between these two groups. On the other hand, both the increase in H/M and the decrease in the washout ratio were significantly greater in group A than in group B. These results indicate that an improvement in cardiac sympathetic nervous function may be related to the regression of hypertensive cardiac hypertrophy. Increasing the subject base in these studies and a more precise analysis of the relevance of the data obtained from MIBG myocardial images are recommended to clarify how changes in cardiac sympathetic nervous function relate to the regression of hypertensive cardiac hypertrophy. (orig.)

  18. Rat experimental model of myocardial ischemia/reperfusion injury: an ethical approach to set up the analgesic management of acute post-surgical pain.

    Directory of Open Access Journals (Sweden)

    Maria Chiara Ciuffreda

    Full Text Available RATIONALE: During the past 30 years, myocardial ischemia/reperfusion injury in rodents became one of the most commonly used model in cardiovascular research. Appropriate pain-prevention appears critical since it may influence the outcome and the results obtained with this model. However, there are no proper guidelines for pain management in rats undergoing thoracic surgery. Accordingly, we evaluated three analgesic regimens in cardiac ischemia/reperfusion injury. This study was strongly focused on 3R's ethic principles, in particular the principle of Reduction. METHODS: Rats undergoing surgery were treated with pre-surgical tramadol (45 mg/kg intra-peritoneal, or carprofen (5 mg/kg sub-cutaneous, or with pre-surgical administration of carprofen followed by 2 post-surgery tramadol injections (multi-modal group. We assessed behavioral signs of pain and made a subjective evaluation of stress and suffering one and two hours after surgery. RESULTS: Multi-modal treatment significantly reduced the number of signs of pain compared to carprofen alone at both the first hour (61±42 vs 123±47; p<0.05 and the second hour (43±21 vs 74±24; p<0.05 post-surgery. Tramadol alone appeared as effective as multi-modal treatment during the first hour, but signs of pain significantly increased one hour later (from 66±72 to 151±86, p<0.05. Carprofen alone was more effective at the second hour post-surgery when signs of pain reduced to 74±24 from 113±40 in the first hour (p<0.05. Stress behaviors during the second hour were observed in only 20% of rats in the multimodal group compared to 75% and 86% in the carprofen and tramadol groups, respectively (p<0.05. CONCLUSIONS: Multi-modal treatment with carprofen and tramadol was more effective in preventing pain during the second hour after surgery compared with both tramadol or carprofen. Our results suggest that the combination of carprofen and tramadol represent the best therapy to prevent animal pain after

  19. Rat experimental model of myocardial ischemia/reperfusion injury: an ethical approach to set up the analgesic management of acute post-surgical pain.

    Science.gov (United States)

    Ciuffreda, Maria Chiara; Tolva, Valerio; Casana, Renato; Gnecchi, Massimiliano; Vanoli, Emilio; Spazzolini, Carla; Roughan, John; Calvillo, Laura

    2014-01-01

    During the past 30 years, myocardial ischemia/reperfusion injury in rodents became one of the most commonly used model in cardiovascular research. Appropriate pain-prevention appears critical since it may influence the outcome and the results obtained with this model. However, there are no proper guidelines for pain management in rats undergoing thoracic surgery. Accordingly, we evaluated three analgesic regimens in cardiac ischemia/reperfusion injury. This study was strongly focused on 3R's ethic principles, in particular the principle of Reduction. Rats undergoing surgery were treated with pre-surgical tramadol (45 mg/kg intra-peritoneal), or carprofen (5 mg/kg sub-cutaneous), or with pre-surgical administration of carprofen followed by 2 post-surgery tramadol injections (multi-modal group). We assessed behavioral signs of pain and made a subjective evaluation of stress and suffering one and two hours after surgery. Multi-modal treatment significantly reduced the number of signs of pain compared to carprofen alone at both the first hour (61±42 vs 123±47; p<0.05) and the second hour (43±21 vs 74±24; p<0.05) post-surgery. Tramadol alone appeared as effective as multi-modal treatment during the first hour, but signs of pain significantly increased one hour later (from 66±72 to 151±86, p<0.05). Carprofen alone was more effective at the second hour post-surgery when signs of pain reduced to 74±24 from 113±40 in the first hour (p<0.05). Stress behaviors during the second hour were observed in only 20% of rats in the multimodal group compared to 75% and 86% in the carprofen and tramadol groups, respectively (p<0.05). Multi-modal treatment with carprofen and tramadol was more effective in preventing pain during the second hour after surgery compared with both tramadol or carprofen. Our results suggest that the combination of carprofen and tramadol represent the best therapy to prevent animal pain after myocardial ischemia/reperfusion. We obtained our results

  20. Protection against doxorubicin-induced myocardial dysfunction in mice by cardiac-specific expression of carboxyl terminus of hsp70-interacting protein

    OpenAIRE

    Lei Wang; Tian-Peng Zhang; Yuan Zhang; Hai-Lian Bi; Xu-Min Guan; Hong-Xia Wang; Xia Wang; Jie Du; Yun-Long Xia; Hui-Hua Li

    2016-01-01

    Carboxyl terminus of Hsp70-interacting protein (CHIP) is a critical ubiquitin ligase/cochaperone to reduce cardiac oxidative stress, inflammation, cardiomyocyte apoptosis and autophage etc. However, it is unclear whether overexpression of CHIP in the heart would exert protective effects against DOX-induced cardiomyopathy. Cardiac-specific CHIP transgenic (CHIP-TG) mice and the wild-type (WT) littermates were treated with DOX or saline. DOX-induced cardiac atrophy, dysfunction, inflammation, o...

  1. Nitrite Therapy Ameliorates Myocardial Dysfunction via H2S and Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2)-Dependent Signaling in Chronic Heart Failure.

    Science.gov (United States)

    Donnarumma, Erminia; Bhushan, Shashi; Bradley, Jessica M; Otsuka, Hiroyuki; Donnelly, Erinn L; Lefer, David J; Islam, Kazi N

    2016-07-29

    Bioavailability of nitric oxide (NO) and hydrogen sulfide (H2S) is reduced in heart failure (HF). Recent studies suggest cross-talk between NO and H2S signaling. We previously reported that sodium nitrite (NaNO2) ameliorates myocardial ischemia-reperfusion injury and HF. Nuclear factor-erythroid-2-related factor 2 (Nrf2) regulates the antioxidant proteins expression and is upregulated by H2S. We examined the NaNO2 effects on endogenous H2S bioavailability and Nrf2 activation in mice subjected to ischemia-induced chronic heart failure (CHF). Mice underwent 60 minutes of left coronary artery occlusion and 4 weeks of reperfusion. NaNO2 (165 μg/kgic) or vehicle was administered at reperfusion and then in drinking water (100 mg/L) for 4 weeks. Left ventricular (LV), ejection fraction (EF), LV end diastolic (LVEDD) and systolic dimensions (LVESD) were determined at baseline and at 4 weeks of reperfusion. Myocardial tissue was analyzed for oxidative stress and respective gene/protein-related assays. We found that NaNO2 therapy preserved LVEF, LVEDD and LVSD at 4 weeks during ischemia-induced HF. Myocardial malondialdehyde and protein carbonyl content were significantly reduced in NaNO2-treated mice as compared to vehicle, suggesting a reduction in oxidative stress. NaNO2 therapy markedly increased expression of Cu,Zn-superoxide dismutase, catalase, and glutathione peroxidase during 4 weeks of reperfusion. Furthermore, NaNO2 upregulated the activity of Nrf2, as well as H2S-producing enzymes, and ultimately increased H2S bioavailability in ischemia-induced CHF in mice as compared with vehicle. Our results demonstrate that NaNO2 therapy significantly improves LV function via increasing H2S bioavailability, Nrf2 activation, and antioxidant defenses. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  2. Characteristic findings of exercise ECG test, perfusion SPECT and coronary angiography in patients with exercise induced myocardial stunning

    Energy Technology Data Exchange (ETDEWEB)

    Ahn, Byeong Cheol; Seo, Ji Hyoung; Bae, Jin Ho; Jeong, Shin Young; Park, Hun Sik; Lee, Jae Tae; Chae, Shung Chull; Lee, Kyu Bo [School of Medicine, Kyungpook National Univ., Daegu (Korea, Republic of)

    2004-06-01

    Transient wall motion abnormality and contractile dysfunction of the left ventricle (LV) can be observed in patients with coronary artery disease due to post-stress myocardial stunning. To understand clinical characteristics of stress induced LV dysfunction, we have compared the findings of exercise stress test, myocardial perfusion SPECT and coronary angiography between subjects with and without post-stress LV dysfunction. Among subjects who underwent exercise stress test, myocardial perfusion SPECT and coronary angiography within a month of interval, we enrolled 36 patients with post-stress LV ejection fraction (LVEF) was {>=}5% lower than rest (stunning group) and 16 patients with difference of post-stress and rest LVEF was lesser than 1% (non-stunning group) for this study. Treadmill exercise stress gated myocardial perfusion SPECT was performed with dual head SPECT camera using 740 MBq Tc-99m MIBI and coronary angiography was also performed by conventional Judkins method. Stunning group had a significantly higher incidence of hypercholesterolemia than non-stunning group(45.5 vs 7.1%, p=0.01). Stunning group also had higher incidence of diabetes mellitus and lower incidence of hypertension, but these were not statistically significant. Stunning group had larger and more severe perfusion defect in stress perfusion myocardial SPECT than non-stunning group(extent 18.2 vs 9.2%, p=0.029; severity 13.5 vs 6.9, p=0.040). Stunning group also had higher degree of reversibility of perfusion defect, higher incidence of positive exercise stress test and higher incidence of having severe stenosis(80{approx}99%) in coronary angiography than non-stunning group, but these were not statistically significant. In stunning group, all of 4 patients without perfusion defect had significant coronary artery stenosis and had received revascularization treatment. Patients with post-stress LV dysfunction had larger and more severe perfusion defect and severe coronary artery stenosis than

  3. Intracoronary artery transplantation of cardiomyoblast-like cells from human adipose tissue-derived multi-lineage progenitor cells improve left ventricular dysfunction and survival in a swine model of chronic myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Okura, Hanayuki [The Center for Medical Engineering and Informatics, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0879 (Japan); Department of Somatic Stem Cell Therapy and Health Policy, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation, 2-2 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Saga, Ayami; Soeda, Mayumi [Department of Somatic Stem Cell Therapy and Health Policy, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation, 2-2 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Miyagawa, Shigeru; Sawa, Yoshiki [Department of Surgery, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0879 (Japan); Daimon, Takashi [Division of Biostatistics, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501 (Japan); Ichinose, Akihiro [Department of Plastic Surgery, Kobe University Hospital, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe, Hyogo (Japan); Matsuyama, Akifumi, E-mail: akifumi-matsuyama@umin.ac.jp [The Center for Medical Engineering and Informatics, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0879 (Japan); Department of Plastic Surgery, Kobe University Hospital, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe, Hyogo (Japan); RIKEN Program for Drug Discovery and Medical Technology Platforms, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045 (Japan)

    2012-09-07

    Highlights: Black-Right-Pointing-Pointer We administered human CLCs in a swine model of MI via intracoronary artery. Black-Right-Pointing-Pointer Histological studies demonstrated engraftment of hCLCs into the scarred myocardium. Black-Right-Pointing-Pointer Echocardiography showed rescue of cardiac function in the hCLCs transplanted swine. Black-Right-Pointing-Pointer Transplantation of hCLCs is an effective therapeutics for cardiac regeneration. -- Abstract: Transplantation of human cardiomyoblast-like cells (hCLCs) from human adipose tissue-derived multi-lineage progenitor cells improved left ventricular function and survival of rats with myocardial infarction. Here we examined the effect of intracoronary artery transplantation of human CLCs in a swine model of chronic heart failure. Twenty-four pigs underwent balloon-occlusion of the first diagonal branch followed by reperfusion, with a second balloon-occlusion of the left ascending coronary artery 1 week later followed by reperfusion. Four weeks after the second occlusion/reperfusion, 17 of the 18 surviving animals with severe chronic MI (ejection fraction <35% by echocardiography) were immunosuppressed then randomly assigned to receive either intracoronary artery transplantation of hCLCs hADMPCs or placebo lactic Ringer's solution with heparin. Intracoronary artery transplantation was followed by the distribution of DiI-stained hCLCs into the scarred myocardial milieu. Echocardiography at post-transplant days 4 and 8 weeks showed rescue and maintenance of cardiac function in the hCLCs transplanted group, but not in the control animals, indicating myocardial functional recovery by hCLCs intracoronary transplantation. At 8 week post-transplantation, 7 of 8 hCLCs transplanted animals were still alive compared with only 1 of the 5 control (p = 0.0147). Histological studies at week 12 post-transplantation demonstrated engraftment of the pre DiI-stained hCLCs into the scarred myocardium and their expression of

  4. Two-dimensional longitudinal strains and torsion analysis to assess the protective effects of ischemic postconditioning on myocardial function: a speckle tracking echocardiography study in rabbits.

    Science.gov (United States)

    Liu, Y J; Leng, X P; Du, G Q; Wang, X D; Tian, J W; Ren, M

    2015-02-01

    The reperfusion injury that occurs in the early reperfusion often results in myocardial dysfunction. This study evaluated global and regional left ventricular (LV) function using speckle tracking echocardiography (STE) in a rabbit ischemia-reperfusion (I/R) model with and without ischemic postconditioning (I-PostC). The aim is to investigate the potential benefit of I-PostC for myocardial function and validate whether regional longitudinal strain is an appropriate index to indicate myocardial dysfunction. Forty rabbits were divided into an ischemia-reperfusion group (group I) and an I-PostC group (group II). After the coronary arteries were ligated, LV systolic strain and twist parameters decreased, and absolute value of strain rate of isovolumetric relaxation period (SRivr) and post-systolic strain index (PSI) increased significantly in both groups (all pstrain rate (SRsys), systolic strain (Ssys), LV twist and untwisting rate increased, and SRivr and PSI decreased in group II. These changes were not seen in group I. All STE parameters were correlated with area of necrosis (AN)/area at risk (AR) (all p0.8 or 0.6. The sensitivities of GSRsys, GSsys, SRsys, Ssys, and LV twist to detect the myocardial infarction were 81.3%, 62.5%, 87.5%, 93.8% and 81.3%, respectively. And the specificities of those parameters were 75.0%, 81.2%, 75.0%, 87.5% and 68.7%. These results indicate that STE is useful for quantitative detection on myocardial function improvement induced by I-PostC in a rabbit I/R model. The regional index-Ssys is an appropriate parameter to indicate myocardial dysfunction because of its sensitivity, specificity, and repeatability.

  5. [Impact of renal dysfunction on clinical course of myocardial infarction complicated by acute heart failure in patients with preserved systolic function].

    Science.gov (United States)

    Parkhomenko, O M; Hur"ieva, O S; Kornatskyĭ, Iu V; Kozhukhov, S M; Sopko, O O

    2013-01-01

    Aiming to assess the relationships between renal function and ST-segment elevation myocardial infarction (MI) clinical course and remote outcomes in patients with preserved systolic left ventricular (LV) function (LV ejection fraction > 40%) estimated glomerular filtration rates (eGFR) were evaluated on 1st and 3rd -10th MI day (n = 491). On 3rd-10th day of MI in patients with acute heart failure (HF) symptoms on admission day (1st group, n = 153) eGFR infarction (Hazzard Ratio (HR) with 95% confidence intervals (95% CI) = 4,08 [1,72 -11,73], P acute HF (2nd group, n = 338) eGFR renal dysfucntion in patients with and without acute HF and preserved LV function.

  6. Left Ventricular Regional Myocardial Longitudinal Systolic Dysfunctions in HFNEF%射血分数正常时心力衰竭左室节段心肌长轴收缩运动的研究

    Institute of Scientific and Technical Information of China (English)

    胡敏; 江成璠; 王素霞; 孙晓霞; 张晓轩; 张胜; 冯芳芳

    2013-01-01

    目的 研究射血分数正常的心力衰竭(HFNEF)左室节段心肌长轴收缩运动.方法 使用基于组织多普勒(TDI)的应变技术对比分析44例HFNEF患者(A组)和33例条件匹配的健康对照者(B组)左室节段心肌长轴方向应变指标的差异.结果 A组较B组应变峰值绝对值降低,达峰时间延长,发生收缩后收缩及收缩期反常伸展的节段增多(均P<0.01);达峰时间标准差增大(P=0.02).结论 HFNEF左室节段心肌存在长轴收缩运动异常.%Objective To investigate left ventricular (LV) regional myocardial longitudinal contractile function in HFNEF by TDI derived strain. Methods There were 44 HFNEF patients (group A) and 33 matched health controls (group B) , the TDI derived strain was used to analyze the longitudinal contractile function of LV segments which were obtained from four chamber, two chamber and long axis apical view. Results The group A's peak strain was lower, the timing to peak strain was longer, the postsystolic shortening's segments and the paradoxic systolic expansion's segments increased, all P<0. 01; the timing to peak strain's standard deviation of LV 18 segments was larger (P = 0. 02), compared to the group B. Conclusions HFNEF existed LV regional myocardial longitudinal systolic dysfunctions.

  7. Newly diagnosed glucose intolerance and prognosis after acute myocardial infarction: comparison of post-challenge versus fasting glucose concentrations

    Science.gov (United States)

    Katayama, Minako; Takagi, Tsutomu; Yamamuro, Atsushi; Kaji, Shuichiro; Yoshikawa, Junichi; Furukawa, Yutaka

    2012-01-01

    Background Recent studies have demonstrated that newly diagnosed glucose intolerance is common among patients with acute myocardial infarction (AMI). The purpose of this study was to assess the long-term clinical cardiovascular outcomes in participants with AMI with abnormal fasting glucose compared with normal fasting glucose and an abnormal oral glucose tolerance test (OGTT) compared with a normal OGTT. Methods A prospective study was performed in 275 consecutive patients with AMI, 85 of whom had pre-diagnosed diabetes mellitus (DM). Those without DM were divided into two groups based on the 75 g OGTT at the time of discharge. Abnormal glucose tolerance (AGT) was defined as 2 h glucose ≥140 mg/dl; 78 patients had normal glucose tolerance (NGT) and 112 had AGT. The same patients were also reclassified into the normal fasting glucose group (NFG; n=168) or the impaired fasting glucose group (IFG; n=22). The association between the glucometabolic status and long-term major adverse cardiovascular event rates was evaluated. Results Kaplan–Meier survival curves showed that the AGT group had a worse prognosis than the NGT group and an equivalent prognosis to the DM group (p<0.0005). Cox proportional hazard model analysis showed that the HR of AGT to NGT for major adverse cardiovascular event rates was 2.65 (95% CI 1.37 to 5.15, p=0.004) while the HR of DM to NGT was 3.27 (1.68 to 6.38, p=0.0005). However, Cox HR of IFG to NFG for major adverse cardiovascular event rates was 1.83 (0.86 to 3.87), which was not significant. Conclusion In patients with AMI, an abnormal OGTT is a better risk factor for future adverse cardiovascular events than impaired fasting blood glucose. PMID:22581733

  8. PROTECTIVE EFFECT OF Ailanthus excelsa ROXB IN MYOCARDIAL INFARCTION POST MESENCHYMAL STEM CELL TRANSPLANTATION: STUDY IN CHRONIC ISCHEMIC RAT MODEL.

    Science.gov (United States)

    Gong, Xia

    2016-01-01

    Thia study evaluates the effects of Ailanthus excelsa Roxb methanolic extract (AER-ME) in rats induced with Myocardial Infarction (MI) followed by transplantation of MSCs. Rats were induced with MI by ligation technique of left coronary artery. The sham-operated the control and AER-ME treated group of rats received transplantation of PKH-26 and marked MSCs followed by normal saline and AER-ME treatment (200mg/kg/day of AER-ME extract) respectively for 30 days. Parameters such as cardiac function, inflammation, oxidative stress, apoptosis and differentiation of MSCs (angiogenesis) were evaluated. Histological studies of infracted myocardium reveled anti-inflammatory activity of AER-ME treatment. Oxidative stress parameters revealed decrease in levels of malondialdehyde (MDA) and increase in superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHpx) activity significantly indicating antioxidant activity of the extract. There was a reduction in cell death rate of treated rats due to the decrease in apoptotic index with prolongation of MI when compared to both control and sham-operated groups. The expression of Fas protein was parallel to apoptotic index. The vascular density increased significantly in extract treated group. The treatment showed improved cardiac activity with decreased left ventricular end diastolic (LVEDP) and arterial pressure while the left ventricular end systolic pressure (LVEP) and dp/dtmax increased significantly when compared to both control and sham-operated groups respectively showing the protective effect of the extract as necessitated by the transplantation of MSCs. The study marked the protective outcomes of AER-ME treatment for MSCs in microenvironment of infracted myocardium by improving their viability and increasing differentiation into cardiomyocytes.

  9. Klotho suppresses the inflammatory responses and ameliorates cardiac dysfunction in aging endotoxemic mice.

    Science.gov (United States)

    Hui, Haipeng; Zhai, Yufeng; Ao, Lihua; Cleveland, Joseph C; Liu, Hongbin; Fullerton, David A; Meng, Xianzhong

    2017-02-28

    Aging augments endotoxemic cardiac dysfunction, but the mechanism remains unclear. Anti-aging protein Klotho has been found to modulate tissue inflammatory responses. We tested the hypothesis that a reduced Klotho level in aging heart plays a role in the augmented endotoxemic cardiac dysfunction. Endotoxin (0.5 mg/kg, iv) was injected to adults (4-6 months) and aging (18-20 months) C57BL/6 mice. Recombinant Klotho (10 μg/kg, iv) was administered to a group of aging mice after endotoxin injection. Cardiac function was analyzed using a microcatheter at 24 and 48 h after endotoxin administration. Myocardial levels of Klotho and heat shock protein 70 (HSP70) were determined by immunoblotting, and plasma and myocardial cytokines were analyzed using ELISA. More severe cardiac dysfunction in aging mice were accompanied by greater cytokine levels in the plasma and myocardium. Klotho was detected in the myocardial tissue. Klotho levels were lower in aging hearts and were further reduced during endotoxemia. Myocardial HSP70 levels were correlated with Klotho levels. Recombinant Klotho increased myocardial HSP70, inhibited NF-κB activation, reduced cytokine levels, and improved cardiac function in aging endotoxemic mice. Delivery of HSP70 into cultured macrophages suppressed endotoxin-induced NF-κB activation. Aging-related augmentation of inflammatory responses and cardiac dysfunction is associated with relative Klotho deficiency. Post-treatment with recombinant Klotho suppresses the inflammatory responses and improves cardiac function in aging endotoxemic mice. Klotho modulates HSP70 levels and HSP70 appears to be involved in the anti-inflammatory mechanism of Klotho. Klotho may have therapeutic potential in amelioration of aging-related endotoxemic cardiac dysfunction.

  10. Influencing Factors of Cognitive Dysfunction in Patients with Acute Myocardial Infarction%急性心肌梗死患者发生认知功能障碍的影响因素研究

    Institute of Scientific and Technical Information of China (English)

    吴永辉; 史哲; 任凤学

    2015-01-01

    目的:研究急性心肌梗死患者发生认知功能障碍的影响因素。方法选择2010年2月—2014年1月航空总医院心血管内科收治的420例急性心肌梗死患者,收集患者一般临床资料并应用蒙特利尔认知评估量表(MoCA)评估患者认知功能及焦虑抑郁状态,采用多因素Logistic回归方法分析认知功能障碍的危险因素。结果认知功能障碍组和对照组在吸烟、年龄、空腹血糖受损、心房颤动、糖耐量受损、糖尿病、高密度脂蛋白胆固醇(HDL C)、收缩压及焦虑抑郁方面差异有统计学意义(P<0.05),行多因素Logistic回归分析,年龄、心房颤动、收缩压、糖尿病、HDL C及焦虑抑郁是急性心肌梗死患者发生认知功能障碍的独立危险因素(P<0.05)。广泛前壁和右室梗死与急性心肌梗死患者认知功能障碍密切相关(P<0.05)。结论急性心肌梗死患者发生认知功能障碍较高,对于重要部位梗死及合并心房颤动、高血压病、糖尿病的患者更应加强关注,重视其心理疏导和治疗,缓解抑郁状态,有助于对认知功能障碍早发现、早干预。%Objective To study the influencing factors of cognitive dysfunction in patients with acute myocardial infarction(AMI).Meth-ods Four hundreds and twenty patients with AMI were selected from February 2010 to January 2014 in Department of cardiovascu-lar medicine in Aviation General Hospital.The clinical data were col ected.The cognitive function in patients with depression was as-sessed by the Montreal Cognitive Assessment(MoCA).The risk factors of cognitive dysfunction were analysed by multivariate Logistic regression method.Results There was significant difference in age,smoking,atrial fibril ation,anemia,impaired fasting glucose,im-paired glucose tolerance,diabetes,systolic blood pressure between the cognitive dysfunction group and cognitive control group(P<0.05).The multivariate Logistic regression analysis

  11. Kidney function and specific mortality in 60-80 years old post-myocardial infarction patients: A 10-year follow-up study

    Science.gov (United States)

    Geleijnse, Johanna M.; Giltay, Erik J.; Soedamah-Muthu, Sabita S.; de Goede, Janette; Oude Griep, Linda M.; Stijnen, Theo; Kromhout, Daan

    2017-01-01

    Chronic kidney disease (CKD) is highly prevalent among older post-myocardial infarction (MI) patients. It is not known whether CKD is an independent risk factor for mortality in older post-MI patients with optimal cardiovascular drug-treatment. Therefore, we studied the relation between kidney function and all-cause and specific mortality among older post-MI patients, without severe heart failure, who are treated with state-of-the-art pharmacotherapy. From 2002–2006, 4,561 Dutch post-MI patients were enrolled and followed until death or January 2012. We estimated Glomerular Filtration Rate (eGFR) with cystatin C (cysC) and creatinine (cr) using the CKD-EPI equations and analyzed the relation with any and major causes of death using Cox models and restricted cubic splines. Mean (SD) for age was 69 years (5.6), 79% were men, 17% smoked, 21% had diabetes, 90% used antihypertensive drugs, 98% used antithrombotic drugs and 85% used statins. Patients were divided into four categories of baseline eGFRcysC: ≥90 (33%; reference), 60–89 (47%), 30–59 (18%), and cancer, and 194 (22%) from other causes. After adjustment for age, sex and classic cardiovascular risk factor, hazard ratios (95%-confidence intervals) for any death according to the four eGFRcysC categories were: 1 (reference), 1.4 (1.1–1.7), 2.9 (2.3–3.6) and 4.4 (3.0–6.4). The hazard ratios of all-cause and cause-specific mortality increased linearly below kidney functions of 80 ml/min/1.73 m2. Weaker results were obtained for eGFRcr. To conclude, we found in optimal cardiovascular drug-treated post-MI patients an inverse graded relation between kidney function and mortality for both cardiovascular as well as non-cardiovascular causes. Risk of mortality increased linearly below kidney function of about 80 ml/min/1.73 m2. PMID:28182761

  12. GAMMAGRAFÍA DE PERFUSIÓN MIOCÁRDICA EN MUJERES POSMENOPÁUSICAS CON ANGINA Y CORONARIAS EPICÁRDICAS ANGIOGRÁFICAMENTE NORMALES / Myocardial perfusion scintigraphy in postmenopausal women with angina and angiographically normal epicardial coronary

    Directory of Open Access Journals (Sweden)

    Sherien Sixto Fernández

    2011-03-01

    Full Text Available Introduction and Objectives: Microvascular angina is common in postmenopausal women. Myocardial ischemia was induced by stress testing, and reports have been published about the relationship between endothelial dysfunction and myocardial perfusion. The objective of this research was to determine whether myocardial ischemia can be evidenced by abnormalities in perfusion and function, as detected by myocardial scintigraphy in women with typical angina, normal coronary angiography and endothelial dysfunction. Methods: 59 women underwent lipid and endothelial function measurements by brachial artery ultrasound, in addition, a 24-hour ECG study (Holter. During the scintigraphy a stress-rest protocol was applied. Patients were divided into two groups according to presence (group I or absence (group II of myocardial perfusion defects. Results: 21 patients showed perfusion defects. 57 % of group I exhibited greater endothelial dysfunction. Only twelve patients showed reversible perfusion defects, and 75 % of the cases was associated with a reduction of post-stress left ventricular ejection fraction, greater than 5 %, and regional abnormalities of wall motion. Three patients in group I showed evidence of ischemia compared with four in Group II. Conclusions: The stress-induced ischemia was associated with a reduced post-stress ejection fraction and endothelial dysfunction in the studied women, and no ischemic changes in the Holter were found.

  13. Regional Coherence Alterations Revealed by Resting-State fMRI in Post-Stroke Patients with Cognitive Dysfunction

    National Research Council Canada - National Science Library

    Peng, Cheng-Yu; Chen, Yu-Chen; Cui, Ying; Zhao, Deng-Ling; Jiao, Yun; Tang, Tian-Yu; Ju, Shenghong; Teng, Gao-Jun

    2016-01-01

    ...) to investigate the alterations in regional coherence in patients after subcortical stroke. Resting-state fMRI measurements were acquired from 16 post-stroke patients with poor cognitive function (PSPC...

  14. The regional myocardial microvascular dysfunction differences in hypertrophic cardiomyopathy patients with or without left ventricular outflow tract obstruction: Assessment with first-pass perfusion imaging using 3.0-T cardiac magnetic resonance

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Hua-yan [Department of Radiology, National Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 37# Guo Xue Xiang, Chengdu, Sichuan 610041 (China); Yang, Zhi-gang, E-mail: yangzg666@163.com [Department of Radiology, National Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 37# Guo Xue Xiang, Chengdu, Sichuan 610041 (China); Sun, Jia-yu; Wen, Ling-yi; Zhang, Ge; Zhang, Shuai [Department of Radiology, National Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 37# Guo Xue Xiang, Chengdu, Sichuan 610041 (China); Guo, Ying-kun [Department of Radiology, West China Second University Hospital, Sichuan University (China)

    2014-04-15

    Purpose: To assess regional myocardial microvascular dysfunction differences in hypertrophic cardiomyopathy (HCM) patients with or without left ventricular outflow tract obstruction using 3.0-T cardiac magnetic resonance (CMR) first-pass perfusion imaging. Materials and methods: Forty-two HCM patients, including 25 HCM patients with left ventricular outflow tract obstruction (HOCM), 17 HCM patients without left ventricular outflow tract obstruction (NOHCM), and 14 healthy subjects underwent CMR. The left ventricular (LV) function, left ventricular end-diastolic wall thickness (EDTH), and diameter of left ventricular outflow tract (LVOT) were measured and calculated. Based on the signal–time curve of the first-pass myocardium perfusion imaging, perfusion parameters including upslope, time to peak, and peak intensity, were assessed and compared by using one-way analysis of variance and independent t tests. Results: On the first-pass perfusion imaging, lower upslope and peak intensity and longer time to peak were found in HCM patients compared with normal subjects (all p < 0.05). In contrast to the NOHCM group, the average time to peak of the HOCM group was increased (13.30 ± 4.82 s vs 16.28 ± 4.90 s, p < 0.05), but first-pass perfusion upslope was reduced (4.96 ± 2.55 vs 2.58 ± 0.77, p < 0.05). According to the bull's-eye model, the HOCM group's average thickness of basal segments was thicker than the NOHCM group, especially the anteroseptal, inferolateral, and anterior wall values, with a corresponding lower first-pass perfusion upslope than the NOHCM group (all p < 0.05). A significant correlation was observed between first-pass perfusion upslope and LV EDTH (r = −0.551, p < 0.001) and LVOT diameter (r = 0.472, p < 0.001). Conclusions: The regional myocardial microvascular dysfunction differences in hypertrophic cardiomyopathy (HCM) patients with or without left ventricular outflow tract obstruction can be detected with first-pass perfusion CMR

  15. Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure

    Directory of Open Access Journals (Sweden)

    van Gilst Wiek H

    2011-09-01

    Full Text Available Abstract Background Progressive remodeling after myocardial infarction (MI is a leading cause of morbidity and mortality. Recently, glucagon-like peptide (GLP-1 was shown to have cardioprotective effects, but treatment with GLP-1 is limited by its short half-life. It is rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4, an enzyme which inhibits GLP-1 activity. We hypothesized that the DPP-4 inhibitor vildagliptin will increase levels of GLP-1 and may exert protective effects on cardiac function after MI. Methods Sprague-Dawley rats were either subjected to coronary ligation to induce MI and left ventricular (LV remodeling, or sham operation. Parts of the rats with an MI were pre-treated for 2 days with the DPP-4 inhibitor vildagliptin (MI-Vildagliptin immediate, MI-VI, 15 mg/kg/day. The remainder of the rats was, three weeks after coronary artery ligation, subjected to treatment with DPP-4 inhibitor vildagliptin (MI-Vildagliptin Late, MI-VL or control (MI. At 12 weeks, echocardiography and invasive hemodynamics were measured and molecular analysis and immunohistochemistry were performed. Results Vildagliptin inhibited the DPP-4 enzymatic activity by almost 70% and increased active GLP-1 levels by about 3-fold in plasma in both treated groups (p Conclusion Vildagliptin increases the active GLP-1 level via inhibition of DPP-4, but it has no substantial protective effects on cardiac function in this well established long-term post-MI cardiac remodeling model.

  16. PET-measured heterogeneity in longitudinal myocardial blood flow in response to sympathetic and pharmacologic stress as a non-invasive probe of epicardial vasomotor dysfunction

    Energy Technology Data Exchange (ETDEWEB)

    Schindler, Thomas H.; Facta, Alvaro D.; Prior, John O.; Campisi, Roxana; Inubushi, Masayuki; Kreissl, Michael C.; Zhang, Xiao-Li; Sayre, James; Dahlbom, Magnus; Schelbert, Heinrich R. [University of California at Los Angeles, Department of Molecular and Medical Pharmacology, Los Angeles, CA (United States)

    2006-10-15

    We investigated whether a myocardial perfusion gradient during pharmacologically induced hyperemia also occurred during sympathetic stimulation with cold pressor testing (CPT), which commonly induces a paradoxical coronary vasoconstriction in individuals with coronary risk factors. Myocardial blood flow (MBF) was measured in absolute units (ml/g/min) with {sup 13}N-ammonia and PET at rest, during CPT, and during pharmacologic vasodilation in 59 participants with coronary risk factors (''at risk'') and in 43 healthy individuals (controls). MBF was assessed globally as mean MBF, and in the mid and mid-distal myocardium of the left ventricle (LV). A decrease in MBF from mid to mid-distal LV myocardium was defined as MBF difference indicative of a perfusion gradient. The change in mean MBF to CPT ({delta}MBF) in the at-risk group was significantly reduced compared with controls (0.05{+-}0.19 vs 0.31{+-}0.20 ml/g/min, p<0.0001), whereas mean MBF during pharmacologic vasodilation in the at-risk group tended to be lower than in controls (1.72{+-}0.71 vs 2.00{+-}0.64 ml/g/min, p=NS). Absolute MBFs during CPT and pharmacologic vasodilation were significantly lower in the mid-distal than in the mid LV myocardium, resulting in a significant MBF difference in the at-risk group (0.15{+-}0.06 and 0.27{+-}0.12 ml/g/min, p<0.0001) that was not observed in controls (0.007{+-}0.05 and 0.014{+-}0.10 ml/g/min, p=NS). In the at-risk group there was a significant correlation between the difference of mid to mid-distal MBF during CPT and that during pharmacologic vasodilation (r=0.43, p<0.004), suggesting functional alterations of epicardial vessels as the predominant cause for the observed MBF difference. The relative decrease in MBF from the mid to the mid-distal left-ventricular myocardium suggests an intracoronary pressure decline during CPT and pharmacologic vasodilation, which is likely to reflect an impairment of flow-mediated epicardial vasomotor function

  17. Hemostatic Status of Pre and Post Intracoronary Injection of Peripheral Blood Stem Cells in Patients with Recent Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Cosphiadi Irawan

    2014-01-01

    Full Text Available Aim: to investigate hemostatic parameter changes, such as platelet aggregation, blood and plasma viscosity, prothrombin time, APTT, CRP and fibrinogen, before and after administration of stem cell therapy. Methods: a total of 24 patients were enrolled. Peripheral blood stem cells (PBSCs were harvested and injected into the infarct-related artery after 5 consecutive days of G-CSF administration. Recombinant human erythropoietin was administered at the time of intracoronary PBSCs injection. Results: we were able to evaluate 11 from 24 of patients regarding hemostatic status pre–post stem cell injection. There were no significant difference between baseline vs 3 months in spontaneous aggregation (p=0.350, PT (p=0.793, aPTT (p=0.255 and TT (p=0.254. There were also no significant difference between baseline vs 3 months in plasma viscosity (p=0.442 and blood viscosity (p=0.843. Nevertheless the patient who had their blood and plasma viscosity above or below normal laboratory range return to normal level after the treatment. Both PT and APTT also show normalization value. Both Fibrinogen and CRP level show significant decrease between baseline and 3 months after treatment (p=0.009 and (p=0.04 respectively. Conclusion: combined G-CSF and EPO based-intracoronary infusion of PBSCs may open new perspective in the treatment of hypercoagulable state post AMI.

  18. Utility of peak creatine kinase-MB measurements in predicting myocardial infarct size, left ventricular dysfunction, and outcome after first anterior wall acute myocardial infarction (from the INFUSE-AMI trial).

    Science.gov (United States)

    Dohi, Tomotaka; Maehara, Akiko; Brener, Sorin J; Généreux, Philippe; Gershlick, Anthony H; Mehran, Roxana; Gibson, C Michael; Mintz, Gary S; Stone, Gregg W

    2015-03-01

    Infarct size after ST-segment elevation myocardial infarction (STEMI) is associated with long-term clinical outcomes. However, there is insufficient information correlating creatine kinase-MB (CK-MB) or troponin levels to infarct size and infarct location in first-time occurrence of STEMI. We, therefore, assessed the utility of CK-MB measurements after primary percutaneous coronary intervention of a first anterior STEMI using bivalirudin anticoagulation in patients who were randomized to intralesion abciximab versus no abciximab and to manual thrombus aspiration versus no aspiration. Infarct size (as a percentage of total left ventricular [LV] mass) and LV ejection fraction (LVEF) were evaluated by cardiac magnetic resonance imaging at 30 days and correlated to peak CK-MB. Peak CK-MB (median 240 IU/L; interquartile range 126 to 414) was significantly associated with infarct size and with LVEF (r = 0.67, p MB tertile group than in the other tertiles (87.6% vs 49.5% vs 9.1%, p MB of at least 300 IU/L predicted with moderate accuracy both a large infarct size (area under the curve 0.88) and an LVEF ≤40% (area under the curve 0.78). Furthermore, CK-MB was an independent predictor of 1-year major adverse cardiac events (hazard ratio 1.42 per each additional 100 IU/L [1.20 to 1.67], p MB measurement is useful in estimating infarct size and LVEF and in predicting 1-year clinical outcomes after primary percutaneous coronary intervention for first anterior STEMI. Copyright © 2015 Elsevier Inc. All rights reserved.

  19. Heart rate variability density analysis (Dyx) for identification of appropriate implantable cardioverter defibrillator recipients among elderly patients with acute myocardial infarction and left ventricular systolic dysfunction

    DEFF Research Database (Denmark)

    Jørgensen, Rikke Mørch; Levitan, Jacob; Halevi, Zohar

    2015-01-01

    AIMS: Dyx is a new heart rate variability (HRV) density analysis specifically designed to identify patients at high risk for malignant ventricular arrhythmias. The aim of this study was to test if Dyx can improve risk stratification for malignant ventricular tachyarrhythmias and to test if the pr......AIMS: Dyx is a new heart rate variability (HRV) density analysis specifically designed to identify patients at high risk for malignant ventricular arrhythmias. The aim of this study was to test if Dyx can improve risk stratification for malignant ventricular tachyarrhythmias and to test...... if the previously identified cut-off can be reproduced. METHODS AND RESULTS: This study included 248 patients from the CARISMA study with ejection fraction ≤40% after an acute myocardial infarction and an analysable 24 h Holter recording. All patients received an implantable cardiac monitor, which was used...... to diagnose the primary endpoint of near-fatal or fatal ventricular tachyarrhythmias likely preventable by an implantable cardioverter defibrillator (ICD), during a period of 2 years. A Dyx ≤ 1.96 was considered abnormal. The secondary endpoint was cardiovascular death. At enrolment 59 patients (24%) had...

  20. AB094. High-throughput sequencing of small RNA component of penile in a post-radical prostatectomy model of erectile dysfunction

    Science.gov (United States)

    Ruan, Yajun; Luan, Yang; Zhang, Yan; Li, Hao; Li, Rui; Cui, Kai; Jiang, Hongyang; Li, Mingchao; Wang, Tao; Liu, Jihong

    2016-01-01

    Objective The introduction of nerve-sparing radical prostatectomy represents a milestone in the treatment of prostate cancer. However, a certain percentage of cancer survivors still suffer from erectile dysfunction. Recent research has stated that using PDE 5-inhibitors after radical prostatectomy may lead to biochemical recurrence. This study was performed to identify the expression profile of small RNA in rats with neurogenic erectile dysfunction, and to investigate possible genes and signaling pathways involving in the disease. Methods Neurogenic erectile dysfunction (ED) was induced in male rats by bilateral cavernous nerve crushing injury (BCNI). After 28 days, erectile function was evaluated by cavernous nerve electrostimulation. Masson’s trichrome staining was performed to assess histologic changes. RNA was isolated from the corpus cavernosum (CC) of both control rats and neurogenic ED rats. Small RNA sequencing was conducted using an Illumina Hiseq 2,500/2,000 platform. Candidate small RNAs were validated by real-time polymerase chain reaction. Results Intracavernous pressure (ICP) was significantly decreased in BCNI group compared with SHAM group. Corporal tissue in the neurogenic ED rats showed a significantly lower smooth muscle/collagen ratio compared with tissue in the SHAM controls. Real time PCR validated that miR-9a-5p, miR-203a-5p, miR-378a-3p and miR-3557-5p were upregulated, and meanwhile miR-3084a-3p was downregulated. Conclusions Small RNA, including microRNA, may play an important role in the regulation of genes in CC and some certain miRs may participate in post-prostatectomy ED. Further studies will be designed to investigate the specific mechanisms of these changes.

  1. Inhaled nitric oxide plus iloprost in the setting of post-left assist device right heart dysfunction.

    Science.gov (United States)

    Antoniou, Theofani; Prokakis, Christos; Athanasopoulos, Georgios; Thanopoulos, Apostolos; Rellia, Panagiota; Zarkalis, Dimitrios; Kogerakis, Nektarios; Koletsis, Efstratios N; Bairaktaris, Andreas

    2012-09-01

    Pulmonary hypertension and right ventricular (RV) dysfunction may complicate the implantation of a left ventricular assist device (LVAD). We examined whether inhaled vasodilators can sufficiently reduce RV afterload, avoiding the need for temporary RV mechanical support. The study includes 7 patients with RV dysfunction after LVAD insertion. Treatment consisted of inotropes, inhaled nitric oxide (10 ppm), and iloprost (10 μg) in repeated doses. Full hemodynamic profile was obtained before inhalation, during administration of inhaled NO alone (before and after iloprost), as well as after the first two doses of inhaled iloprost. Tricuspid annular velocity was estimated at baseline and before and after adding iloprost. There was a statistically significant reduction in pulmonary vascular resistance (PVR), mean pulmonary artery pressure (MPAP), RV systolic pressure, and pulmonary capillary wedge pressure, and a considerable increase in LVAD flow, LV flow rate index, and tricuspid annular velocity at all points of evaluation versus baseline. By the end of the protocol, MPAP/mean systemic arterial pressure, and PVR/systemic vascular resistance ratios were reduced by 0.17±0.03 (95% confidence interval, 0.10 to 0.25, p=0.001) and 0.12±0.025 (95% confidence interval, 0.06 to 0.18; p=0.003), respectively. The tricuspid annular velocity increased by 2.3±0.18 cm/s (95% confidence interval, 1.83 to 2.73 cm/s; piloprost showed an important decrease in PVR (p=0.022), MPAP (p=0.001), pulmonary capillary wedge pressure (p=0.002), and RV systolic pressure (piloprost sufficiently decreased PVR and MPAP on the basis of an additive effect, improved RV function, and avoided the need for RV assist device. Copyright © 2012 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

  2. Identification of viable myocardium early after acute myocardial infarction under beta-blockade by enoximone echocardiography.

    Science.gov (United States)

    Natale, E; Minardi, G; Wang, F; Tubaro, M; Giovannini, E; Vajola, S F; Milazzotto, F

    1997-04-01

    The influence of the beta-blocker metoprolol on the capacity either of low-dose dobutamine echocardiography or the recently introduced enoximone echocardiography to detect viable dysfunctioning myocardium after myocardial infarction was investigated. Initial clinical experience would suggest that the phosphodiesterase III inhibitor enoximona could be an alternative pharmacological stimulation, inducing an increase in contractility in the presence or absence of beta-receptor stimulation. Ten patients with a baseline low-dose dobutamine-echocardiographic test (up to 10 micrograms/kg/min) positive for myocardial viability in > or = 1 segment(s), performed 4-5 days after a first acute myocardial infarction treated with rtPA, were randomized after the administration of intravenous metoprolol (15 mg in three 5-mg boluses) either to dobutamine (up to 15 micrograms/kg/min) or to an enoximone intravenous bolus (1 mg/kg over 5 min) under echocardiographic monitoring, in a crossover sequence, with a 24-h interval. The infarct related artery was patent (TIMI grade 2 o 3) in all the patients. Follow-up echocardiograms were performed 5-7 weeks later. Resting asynergy was found in 40 segments; of these, 17 were viable. All the viable segments remained unresponsive during the post-metoprolol dobutamine infusion, while improved their contractility during enoximone echocardiography. Two patients suffering from early post-infarction angina underwent coronary angioplasty successfully. Eight out of ten patients (2 revascularized and 6 not) showed contractile recovery in a total of 14 segments at the follow-up echocardiogram. Sensitivity, specificity and overall accuracy in predicting reversible dysfunction after acute myocardial infarction for enoximone echocardiography were 93, 85, and 88%, respectively. Our results support the value of enoximone echocardiography in the identification of myocardial viability after myocardial infarction, in patients treated with beta-blockers, which

  3. Predictors of ventricular remodelling in patients with reperfused acute myocardial infarction and left ventricular dysfunction candidates for bone marrow cell therapy: insights from the BONAMI trial

    Energy Technology Data Exchange (ETDEWEB)

    Manrique, Alain [Nuclear Medicine, CHU de Caen, Caen (France); Universite de Caen Normandie, EA 4650, Caen (France); CHU de Caen et GIP Cyceron, Caen cedex 6 (France); Lemarchand, Patricia; Delasalle, Beatrice; Lamirault, Guillaume; Trochu, Jean-Noel; Le Tourneau, Thierry [L' Institut du thorax, INSERM, UMR1087, Nantes (France); CNRS, UMR 6291, Nantes (France); Universite de Nantes, Nantes (France); CHU de Nantes, Nantes (France); Lairez, Olivier; Roncalli, Jerome [Institut CARDIOMET-Toulouse, Cardiac Imaging Center, CIC Biotherapies, CHU de Toulouse, Toulouse (France); Sportouch-Duckan, Catherine; Piot, Christophe [Universite Montpellier, Institut de Genomique Fonctionnelle, INSERM U661, CNRS UMR 5203, Montpellier (France); Clinique du Millenaire, Montpellier (France); Le Corvoisier, Philippe [Hopital Henri Mondor, INSERM, Centre d' Investigation Clinique 1430 et U955 equipe 3, Creteil (France); Neuder, Yannick [CHU de Grenoble, Pole Thorax et Vaisseaux, Grenoble (France); Richardson, Marjorie [CHRU Lille, Service d' Explorations Fonctionnelles Cardiovasculaires, Hopital Cardiologique, Lille (France); Lebon, Alain [CHU de Caen, Service de Cardiologie, Caen (France); Teiger, Emmanuel [Hopital Henri Mondor, AP-HP, Unite de Cardiologie Interventionnelle et Federation de Cardiologie, Creteil (France); Hossein-Foucher, Claude [Hopital Salengro CHRU de Lille, Service de Medecine Nucleaire, Lille (France); Universite de Lille 2, UFR de Medecine, Lille (France)

    2016-04-15

    Few data are available regarding the relation of left ventricular (LV) mechanical dyssynchrony to remodelling after acute myocardial infarction (MI) and stem cell therapy. We evaluated the 1-year time course of both LV mechanical dyssynchrony and remodelling in patients enrolled in the BONAMI trial, a randomized, multicenter controlled trial assessing cell therapy in patients with reperfused MI. Patients with acute MI and ejection fraction (EF) ≤ 45 % were randomized to cell therapy or to control and underwent thallium single-photon emission computed tomography (SPECT), radionuclide angiography, and echocardiography at baseline, 3 months, and 1 year. Eighty-three patients with a comprehensive 1-year follow-up were included. LV dyssynchrony was assessed by the standard deviation (SD) of the LV phase histogram using radionuclide angiography. Remodelling was defined as a 20 % increase in LV end-systolic volume index (LVESVI) at 1 year. At baseline, LVEF, wall motion score index, and perfusion defect size were significantly impaired in the 43 patients (52 %) with LV remodelling (all p < 0.001), without significant increase in LV mechanical dyssynchrony. During follow-up, there was a progressive increase in LV SD (p = 0.01). Baseline independent predictors of LV remodelling were perfusion SPECT defect size (p = 0.001), LVEF (p = 0.01) and a history of hypertension (p = 0.043). Bone marrow cell therapy did not affect the time-course of LV remodelling and dyssynchrony. LV remodelling 1 year after reperfused MI is associated with progressive LV dyssynchrony and is related to baseline infarct size and ejection fraction, without impact of cell therapy on this process. (orig.)

  4. Alcohol Dehydrogenase Protects against Endoplasmic Reticulum Stress-Induced Myocardial Contractile Dysfunction via Attenuation of Oxidative Stress and Autophagy: Role of PTEN-Akt-mTOR Signaling.

    Directory of Open Access Journals (Sweden)

    Jiaojiao Pang

    Full Text Available The endoplasmic reticulum (ER plays an essential role in ensuring proper folding of the newly synthesized proteins. Aberrant ER homeostasis triggers ER stress and development of cardiovascular diseases. ADH is involved in catalyzing ethanol to acetaldehyde although its role in cardiovascular diseases other than ethanol metabolism still remains elusive. This study was designed to examine the impact of ADH on ER stress-induced cardiac anomalies and underlying mechanisms involved using cardiac-specific overexpression of alcohol dehydrogenase (ADH.ADH and wild-type FVB mice were subjected to the ER stress inducer tunicamycin (1 mg/kg, i.p., for 48 hrs. Myocardial mechanical and intracellular Ca(2+ properties, ER stress, autophagy and associated cell signaling molecules were evaluated.ER stress compromised cardiac contractile function (evidenced as reduced fractional shortening, peak shortening, maximal velocity of shortening/relengthening, prolonged relengthening duration and impaired intracellular Ca(2+ homeostasis, oxidative stress and upregulated autophagy (increased LC3B, Atg5, Atg7 and p62, along with dephosphorylation of PTEN, Akt and mTOR, all of which were attenuated by ADH. In vitro study revealed that ER stress-induced cardiomyocyte anomaly was abrogated by ADH overexpression or autophagy inhibition using 3-MA. Interestingly, the beneficial effect of ADH was obliterated by autophagy induction, inhibition of Akt and mTOR. ER stress also promoted phosphorylation of the stress signaling ERK and JNK, the effect of which was unaffected by ADH transgene.Taken together, these findings suggested that ADH protects against ER stress-induced cardiac anomalies possibly via attenuation of oxidative stress and PTEN/Akt/mTOR pathway-regulated autophagy.

  5. Cell delivery and tracking in post-myocardial infarction cardiac stem cell therapy: an introduction for clinical researchers.

    Science.gov (United States)

    Wei, Heming; Ooi, Ting Huay; Tan, Genevieve; Lim, Sze Yun; Qian, Ling; Wong, Philip; Shim, Winston

    2010-01-01

    Stem cell-based therapy for patients with post-infarct heart failure is a relatively new and revolutionary concept in cardiology. Despite the encouraging results from pre-clinical studies, outcomes from most clinical trials remain moderately positive while the clinical benefits are largely attributed to transplanted cell-associated paracrine effects in stimulating angiogenesis and protecting endogenous cardiomyocytes. This scenario indicates that there may be a considerably protracted iterative process of conceptual and procedural refinement before true clinical benefits can be fully materialized. At present, many pressing questions regarding cell therapy remain unanswered. In addition to the primary interest in determining the ideal type of stem cells with best cardiogenic potential in vitro and in vivo, there are growing concerns on the impact of the host cardiac milieu on the transplanted cells, including their survival, migration, engraftment, and trans-differentiation as well as contribution to left ventricular function. Effective cell delivery and tracking methods are central to the unraveling of these questions. To date, cell-delivery modalities are yet to be optimized and strategies for safe and effective assessment of cells transplanted in the recipients are to be established. In this review, we discuss cell delivery and tracking modalities that are adopted in the current pre-clinical and clinical studies. We further discussed emerging technologies that are poised to impact the success of cell therapy.

  6. Augmented cardiac formation of oxidatively-induced carbonylated proteins accompanies the increased functional severity of post-myocardial infarction heart failure in the setting of type 1 diabetes mellitus.

    Science.gov (United States)

    Dennis, Kathleen E; Hill, Salisha; Rose, Kristie L; Sampson, Uchechukwu K A; Hill, Michael F

    2013-01-01

    Heart failure (HF) is a dominant cause for the higher mortality of diabetics after myocardial infarction (MI). In the present investigation, we have discovered that higher levels of oxidative stress (OS)-induced carbonylated proteins accompany worsening post-MI HF in the presence of type 1 diabetes. These findings provide a mechanistic link between amplified OS and exacerbation of post-infarction HF in diabetes. Type 1 diabetes mellitus (DM) patients surviving myocardial infarction (MI) manifest an increased incidence of subsequent heart failure (HF). We have previously shown that after MI, type 1 DM is associated with accentuated myocardial oxidative stress (OS) and concomitant worsening of left ventricular (LV) function. However, the precise mechanisms whereby type 1 DM-enhanced OS adversely affects HF after MI remain obscure. As carbonylation of proteins is an irreversible post-translational modification induced only by OS that often leads to the loss of function, we analyzed protein-bound carbonyls in the surviving LV myocardium of MI and DM+MI rats in relation to residual LV function. Type 1 DM was induced in rats via administration of streptozotocin. Two weeks after induction of type 1 DM, MI was produced in DM and non-DM rats by coronary artery ligation. Residual LV function and remodeling was assessed at 4 weeks post-MI by echocardiography. Myocardial carbonylated proteins were detected through OxyBlot analysis, and identified by mass spectrometry. Compared with MI rats, DM+MI rats exhibited significantly poorer residual LV systolic function and elevated wet to dry weight ratios of the lungs. Protein carbonyl content in cardiac tissue and isolated heart mitochondria of DM+MI rats was 20% and 48% higher, respectively, versus MI rats. Anti-oxidative enzymes and fatty acid utilization proteins were among the carbonylated protein candidates identified. These findings implicate myocardial protein carbonylation as part of the molecular pathophysiology of

  7. Dysfunction of affective network in post ischemic stroke depression: a resting-state functional magnetic resonance imaging study.

    Science.gov (United States)

    Zhang, Peiyao; Xu, Qin; Dai, Jianping; Wang, Jun; Zhang, Ning; Luo, Yuejia

    2014-01-01

    Previous studies have demonstrated that stroke characteristics and social and psychological factors jointly contribute to the development of poststroke depression (PSD). The purpose of this study was to identify altered functional connectivity (FC) of the affective network (AN) in patients with PSD and to explore the correlation between FC and the severity of PSD. 26 PSD patients, 24 stroke patients without depression, and 24 age-matched normal controls underwent the resting-state functional MRI (fMRI) scanning. The bilateral anterior cingulated cortices (ACCs) were selected as regions of interest (ROIs). FC was calculated and compared among the three groups. The association between FC and Hamilton Depression Rate Scale (HDRS) scores of PSD group was investigated. The FC of the AN was disrupted in PSD patients compared to stroke patients without depression and normal controls. Moreover, the left orbital part of inferior frontal gyrus which indicated altered FC was significantly correlated with HDRS scores in PSD patients. Dysfunction of the affective network may be one of the reasons of the development of PSD.

  8. Dysfunction of Affective Network in Post Ischemic Stroke Depression: A Resting-State Functional Magnetic Resonance Imaging Study

    Directory of Open Access Journals (Sweden)

    Peiyao Zhang

    2014-01-01

    Full Text Available Objective. Previous studies have demonstrated that stroke characteristics and social and psychological factors jointly contribute to the development of poststroke depression (PSD. The purpose of this study was to identify altered functional connectivity (FC of the affective network (AN in patients with PSD and to explore the correlation between FC and the severity of PSD. Materials and Methods. 26 PSD patients, 24 stroke patients without depression, and 24 age-matched normal controls underwent the resting-state functional MRI (fMRI scanning. The bilateral anterior cingulated cortices (ACCs were selected as regions of interest (ROIs. FC was calculated and compared among the three groups. The association between FC and Hamilton Depression Rate Scale (HDRS scores of PSD group was investigated. Results. The FC of the AN was disrupted in PSD patients compared to stroke patients without depression and normal controls. Moreover, the left orbital part of inferior frontal gyrus which indicated altered FC was significantly correlated with HDRS scores in PSD patients. Conclusions. Dysfunction of the affective network may be one of the reasons of the development of PSD.

  9. Scintigraphic Assessment of Myocardial Viability

    Energy Technology Data Exchange (ETDEWEB)

    Bom, Hee Seung [Chonnam University Hospital, Kwangju (Korea, Republic of)

    1993-07-15

    The identification of viable myocardium in patients with coronary artery disease and left ventricular dysfunction is an issue of increasing clinical relevance in the current era of myocardial revascularization. There are at least two forms of reversible myocardial dysfunction. Early reperfusion does not always lead to immediate functional improvement; rather, the return of contractility in tissue salvaged by reperfusion is delayed for hours, days or even weeks, a phenomenon that has been termed {sup s}tunned myocardium{sup .} Some patients with coronary artery disease show myocardial dysfunction ar rest which are associated with reduced perfusion, and which disappear after revascularization; this phenomenon has been termed {sup h}ibernating myocardium{sup .} Recently, cardiac imaging techniques that evaluate myocardial viability on the basis of perfusion contraction mismatch and inotropic reserve have gained substantial popularity and clinical success. This review focus on the application of {sup 201}T1 and {sup 99m}Tc-MIBI to address myocardial viability in patients with hibernating and stunned myocardium. It is clear that 4-hour redistribution images of {sup 201}T1 underestimate ischemia and overestimate scar. Delayed imaging and reinjection imaging have been developed for the assessment of viability. Among many protocols suggested, stress-redistribution-reinjection imaging gained most popularity. Although {sup 99m}Tc- MIBI could identify myocardial viability, {sup 201}T1 reinjection technique was regarded as superior to it. In conclusion, {sup 201}T1 stress, 4-hr rest redistribution, and reinjection imaging technique may be the most preferable method for evaluation of myocardial viability.

  10. Flow Mediated Dilatation, Carotid Intima Media Thickness, Ankle Brachial Pressure Index and Pulse Pressure in Young Male Post Myocardial Infarction Patients in India.

    Science.gov (United States)

    Gupta, Nikhil; Giri, Subhash; Rathi, Vinita; Ranga, Gajender Singh

    2016-10-01

    Due to increase in Coronary Artery Disease (CAD) at a younger age, we should try to diagnose atherosclerotic process and population at risk, at the earliest. Flow Mediated Dilatation (FMD), Carotid Intima-Media Thickness (CIMT) and Ankle-Brachial Pressure Index (ABI) are probable markers for early atherosclerosis and may be useful in coronary risk stratification. To compare and correlate the FMD, CIMT, ABI and Pulse Pressure (PP) in young male patients of Myocardial Infarction (MI) with age and sex matched healthy controls. Eighty male patients of MI aged ≤45 years, who presented to the Cardiac Care Unit and Department of Medicine of Guru Teg Bahadur Hospital, Delhi, India, from November 2010 to April 2012 were recruited consecutively for this case control study and same number of age and sex matched healthy controls were also analyzed. Six weeks after MI, FMD of the brachial artery, intima media thickness of carotid artery, ABPI and PP were measured in the cases and compared with healthy controls. The FMD was lower among young patients of MI than controls (p<0.001). CIMT was higher among cases than controls (p=0.001). ABI was lower among cases than controls (p<0.001). Compared to controls, PP was higher among cases (p=0.001). In all subjects, a negative correlation between FMD and CIMT (r=-0.220, p=0.005) and a positive correlation between FMD and ABPI (r=0.304, p<0.001) was found. A statistically significant negative correlation was found between endothelial dependent FMD and PP among cases and control groups (r=-0.209, p=0.007). Biophysical parameters were deranged in young post MI patients. Majority of our young male patients fell in low risk Framingham risk score but still they manifested with CAD. Despite six weeks of treatment among young male patients of MI, various biophysical parameters were still deranged.

  11. Myocardial Bridging

    Directory of Open Access Journals (Sweden)

    Shi-Min Yuan

    2016-02-01

    Full Text Available Abstract Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results.

  12. Evaluation of Myocardial Systolic Function by Strain and Strain Rate Imaging in Post-Myocardial inFarction Rats%心梗后大鼠应变、应变率成像及心室重塑研究

    Institute of Scientific and Technical Information of China (English)

    赵永锋; 朱文晖; 唐水娟; 段星星; 刘稳刚

    2011-01-01

    目的 应用应变及应变率成像评价心肌梗死后心力衰竭大鼠局部心肌收缩功能,探讨心肌收缩功能与心室重塑的关系.方法 雄性SD大鼠70只随机分为手术4周组(25)、4周对照组(10)、手术8周组(25)、8周对照组(10).结扎大鼠左冠脉前降支造模成功后,分别于4周末、8周末行应变及应变率成像,胶原容积分数(CVF)测定.结果 各手术组前壁基底段、中间段,侧壁基底段的收缩期峰值应变(Ssys)、收缩期峰值应变率(SRsys)较相应对照组显著降低(P<0.01).手术8周组较手术4周组显著下降(P<0.01).手术4周组CVF与平均收缩期峰值应变(mSsys)(r=0.76,P<0.01)及平均收缩期峰值应变率(mSRsys)(r=0.60,P<0.05)密切相关,手术8周组CVF与mSsys(r=0.74,P<0.01)、mSRsys(r=0.73,P<0.01)密切相关.结论 SI及SRI可定量评价心肌梗死后心力衰竭大鼠局部收缩功能改变,其收缩功能下降程度与心室重塑程度密切相关.%Objective To evaluate left ventricular segmental systolic function in post-myocardial infarction rats by strain imaging (SI) and strain rate imaging (SRI). Explore the relationship between systolic function and ventricular remodeling. Methods 70 male Sprague-Dawley rats were randomly divided into 4 groups: 4 weeks operation group (25), 4 weeks sham operation group ( 10), 8 weeks operation group (25), 8 weeks sham operation group (10). Postinfarction rat model was induced by left anterior descending ligature. SI and SRI were applied at 4 weeks and 8 weeks after operation. Measurement of collagen volume fraction (CVF) was carried out afterward. Results Compared with corresponding sham operation groups, peak systolic strain (Ssys) and peak systolic strain rate (SRsys) in middle anterior wall, basal anterior wall and basal lateral wall were significantly decreased in two operation groups(P<0. 01).Compared with 4 weeks operation group, Ssys and SRsys in these segments in 8 weeks operation group were significantly

  13. Thrombospondins in the transition from myocardial infarction to heart failure.

    Science.gov (United States)

    Kirk, Jonathan A; Cingolani, Oscar H

    2016-01-01

    The heart's reaction to ischemic injury from a myocardial infarction involves complex cross-talk between the extra-cellular matrix (ECM) and different cell types within the myocardium. The ECM functions not only as a scaffold where myocytes beat synchronously, but an active signaling environment that regulates the important post-MI responses. The thrombospondins are matricellular proteins that modulate cell--ECM interactions, functioning as "sensors" that mediate outside-in and inside-out signaling. Thrombospondins are highly expressed during embryonic stages, and although their levels decrease during adult life, can be re-expressed in high quantities in response to cardiac stress including myocardial infarction and heart failure. Like a Swiss-army knife, the thrombospondins possess many tools: numerous binding domains that allow them to interact with other elements of the ECM, cell surface receptors, and signaling molecules. It is through these that the thrombospondins function. In the present review, we provide basic as well as clinical evidence linking the thrombospondin proteins with the post myocardial infarction response, including inflammation, fibrotic matrix remodeling, angiogenesis, as well as myocyte hypertrophy, apoptosis, and contractile dysfunction in heart failure. We will describe what is known regarding the intracellular signaling pathways that are involved with these responses, paving the road for future studies identifying these proteins as therapeutic targets for cardiac disease.

  14. Depression after myocardial infarction.

    Science.gov (United States)

    Ziegelstein, R C

    2001-01-01

    Depression is an independent risk factor for increased postmyocardial infarction morbidity and mortality, even after controlling for the extent of coronary artery disease, infarct size, and the severity of left ventricular dysfunction. This risk factor takes on added significance when one considers that almost half of patients recovering from a myocardial infarction have major or minor depression and that major depression alone occurs in about one in five of these individuals. Despite the well-documented risk of depression, questions remain about the mechanism of the relationship between mood disturbance and adverse outcome. The link may be explained by an association with lower levels of social support, poor adherence to recommended medical therapy and lifestyle changes intended to reduce the risk of subsequent cardiac events, disturbances in autonomic tone, enhanced platelet activation and aggregation, and systemic immune activation. Unfortunately, questions about the pathophysiologic mechanism of depression in this setting are paralleled by uncertainties about the optimal treatment of depression for patients recovering from a myocardial infarction and by a lack of knowledge about whether treating depression lowers the associated increased mortality risk. Ongoing research studies will help to determine the benefits of psychosocial interventions and of antidepressant therapy for patients soon after myocardial infarction. Although the identification of depression as a risk factor may by itself be a reason to incorporate a comprehensive psychological evaluation into the routine care of patients with myocardial infarction, this practice should certainly become standard if studies show that treating depression reduces the increased mortality risk of these patients.

  15. Penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) responds to low-power laser irradiation : a case study and hypothesis about the role of transient receptor potential (TRP) ion channels

    NARCIS (Netherlands)

    Waldinger, Marcel D|info:eu-repo/dai/nl/163958564; van Coevorden, Ruben S; Schweitzer, Dave H; Georgiadis, Janniko

    2015-01-01

    Treatment of paroxetine-induced penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) by Low-power Laser Irradiation (LPLI) is unknown in medical literature. The aim of the current article is to report partial efficacy of LPLI for paroxetine-induced persistent penile anesthesia. We report on a ma

  16. Myocardial disease

    Institute of Scientific and Technical Information of China (English)

    1997-01-01

    970309 Myocardial injury of Keshan disease andapoptosis. ZHONG Xuekuan(钟学宽), et al. KeshanDis Instit, Harbin Med Univ, Harbin, 150086. Chin JEndemiol 1997, 16(2): 81-82. Objective: To discuss the relationship between my-ocardial injury Of Keshan disease and apoptosis. Meth-

  17. Invasive measurement of coronary microvascular resistance in patients with acute myocardial infarction treated by primary PCI.

    Science.gov (United States)

    Amier, Raquel P; Teunissen, Paul F A; Marques, Koen M; Knaapen, Paul; van Royen, Niels

    2014-01-01

    Up to 40% of patients with acute myocardial infarction develop microvascular obstruction (MVO) despite successful treatment with primary percutaneous coronary intervention (PCI). The presence of MVO is linked to negative remodelling and left ventricular dysfunction, leading to decreased long-term survival, increased morbidity and reduced quality of life. The acute obstruction and dysfunction of the microvasculature can potentially be reversed by pharmacological treatment in addition to the standard PCI treatment. Identifying patients with post-PCI occurrence of MVO is essential in assessing which patients could benefit from additional treatment. However, at present there is no validated method to identify these patients. Angiographic parameters like myocardial blush grade or corrected Thrombolysis In Myocardial Infarction (TIMI) flow do not accurately predict the occurrence of MVO as visualised by MRI in the days after the acute event. Theoretically, acute MVO can be detected by intracoronary measurements of flow and resistance directly following the PCI procedure. In MVO the microvasculature is obstructed or destructed and will therefore display a higher coronary microvascular resistance (CMVR). The methods for intracoronary assessment of CMVR are based on either thermodilution or Doppler-flow measurements. The aim of this review is to present an overview of the currently available methods and parameters for assessing CMVR, with special attention given to their use in clinical practice and information provided by clinical studies performed in patients with acute myocardial infarction.

  18. Effects of Ivabradine and Metoprolol on Cardiac Angiogenesis and Endothelial Dysfunction in Rats With Heart Failure

    NARCIS (Netherlands)

    Ulu, Nadir; Henning, Rob H.; Goris, Maaike; Schoeinaker, Regien G.; van Gilst, Wiek H.

    2009-01-01

    Myocardial infarction (MI)-induced remodeling is associated with disturbed myocardial perfusion through vascular changes, such as reduced capillary density and endothelial dysfunction. Heart rate reduction (HRR) initiated immediately after MI stimulates angiogenesis and attenuates left ventricular d

  19. Idade e distúrbios psicológicos: variáveis associadas à disfunção sexual no período pós-infarto Age and psychologic disorders: variables associated to post-infarction sexual dysfunction

    Directory of Open Access Journals (Sweden)

    Luciano Janussi Vacanti

    2005-08-01

    interference of classic risk factors was analysed for atherosclerosis, for PD and for the use of medications when SD was present up to month 6 after MI. RESULTS: After MI, 91% of patients resumed sexual activity. Twenty-six patients (60% reported sexual dysfunction up to month 6 from hospital discharge (9 with precocious ejaculation (PE, 15 with erectile dysfunction (ED, and 20 with hypoactive sexual desire disorder (HSDD. PD patients reported sexual dysfunction at higher frequency as compared to those who did not report PD (100%x47%, p=0.001. The sexual dysfunction group was significantly older than the group not reporting sexual dysfunction: 53±8.9 years of age versus 47±8.7 years of age (p=0.04. CONCLUSION: Patients reported significant reduction of sexual activity frequency and high incidence of SD after acute myocardial infarction (AMI. PD and older age were shown to be associated to higher incidence of post-infarction SD.

  20. Assessment of right ventricular function by myocardial performance index in diabetic patients

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    Ayman Ahmed Abdelaziz

    2011-09-01

    Conclusion: Myocardial performance index is a useful noninvasive tool for the detection of early right ventricular systolic and diastolic dysfunction in diabetic patients, regardless of coexisting hypertension.

  1. Structural and functional changes in the heart and clinical features of heart failure with preserved left ventricular ejection fraction in patients after myocardial infarction, comorbided with arterial hypertension

    Directory of Open Access Journals (Sweden)

    V. D. Syvolap

    2013-12-01

    Full Text Available Recently, much attention was paid to left ventricular diastolic dysfunction and its role in the occurrence of chronic heart failure. In patients after myocardial infarction, diastolic dysfunction often precedes systolic dysfunction and predicts prognosis. In patients after myocardial infarction, diastolic dysfunction is caused by a violation of early diastolic relaxation in the area of increasing stiffness. Diastolic dysfunction is formed by hypertrophy, fibrosis, myocardial ischemia and arterial hypertension. Given the important role of diastolic dysfunction in the formation of heart failure in postinfarction patients with concomitant arterial hypertension, the mechanisms of its impact on clinical features and structural-functional changes of the heart is an actual problem. Objective: To determine the structural and functional changes in the heart and clinical features of heart failure with preserved left ventricular ejection fraction in patients after myocardial infarction with concomitant arterial hypertension. Materials and methods: In 91 patients with post-infarction cardiosclerosis and preserved left ventricular ejection fraction (EF > 45 % with arterial hypertension were investigated structural and functional changes in the heart and clinical features of heart failure by assessing clinical status and ultrasound of the heart. Prescription myocardial infarction ranged from 2 months to 3 years. Patients were divided into 3 groups. The first group included 50 patients with diastolic dysfunction and symptoms of heart failure (mean age 64,1 ± 1,2 years. In the second group were 31 patients with diastolic dysfunction without heart failure symptoms (mean age 59,5 ± 1,6 years. The third group consisted of 10 patients without diastolic dysfunction and manifestations of heart failure (mean age 57 ± 2,8 years. Results and discussion: 10% patients with postinfarction cardiosclerosis and concomitant hypertension with diastolic heart failure had NYHA

  2. The prognostic importance of creatinine clearance after acute myocardial infarction

    DEFF Research Database (Denmark)

    Sørensen, C R; Brendorp, B; Rask-Madsen, C

    2002-01-01

    AIMS: The purpose of this study was to assess renal dysfunction as an independent predictor of mortality after acute myocardial infarction. METHODS: The study population was 6252 patients with a myocardial infarction admitted alive from 1990 to 1992. The mortality status was obtained after at least.......9-1.3) respectively. CONCLUSION: Renal dysfunction is an important risk factor after acute myocardial infarction. When the risk is adjusted for available competing risk factors only severely reduced renal function is associated with an important and independent risk of mortality after acute myocardial infarction...

  3. Antiarrhythmic effect of carvedilol after acute myocardial infarction: results of the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial

    DEFF Research Database (Denmark)

    McMurray, John; Køber, Lars; Robertson, Michele;

    2005-01-01

    ratio (HR) of 0.41 (95% confidence interval [CI] 0.25 to 0.68; p = 0.0003). The corresponding rates of ventricular tachycardia/flutter/fibrillation were 38 to 984 (3.9%) and 9 to 975 (0.9%) (HR 0.24, 95% CI 0.11 to 0.49; p

  4. Non-invasive imaging in detecting myocardial viability: Myocardial function versus perfusion

    Directory of Open Access Journals (Sweden)

    Iqbal A. Elfigih

    2014-12-01

    Full Text Available Coronary artery disease (CAD is the most prevalent and single most common cause of morbidity and mortality [1] with the resulting left ventricular (LV dysfunction an important complication. The distinction between viable and non-viable myocardium in patients with LV dysfunction is a clinically important issue among possible candidates for myocardial revascularization. Several available non-invasive techniques are used to detect and assess ischemia and myocardial viability. These techniques include echocardiography, radionuclide images, cardiac magnetic resonance imaging and recently myocardial computed tomography perfusion imaging. This review aims to distinguish between the available non-invasive imaging techniques in detecting signs of functional and perfusion viability and identify those which have the most clinical relevance in detecting myocardial viability in patients with CAD and chronic ischemic LV dysfunction. The most current available studies showed that both myocardial perfusion and function based on non-invasive imaging have high sensitivity with however wide range of specificity for detecting myocardial viability. Both perfusion and function imaging modalities provide complementary information about myocardial viability and no optimum single imaging technique exists that can provide very accurate diagnostic and prognostic viability assessment. The weight of the body of evidence suggested that non-invasive imaging can help in guiding therapeutic decision making in patients with LV dysfunction.

  5. Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling.

    Science.gov (United States)

    Erikson, John M; Valente, Anthony J; Mummidi, Srinivas; Kandikattu, Hemanth Kumar; DeMarco, Vincent G; Bender, Shawn B; Fay, William P; Siebenlist, Ulrich; Chandrasekar, Bysani

    2017-02-10

    Re-establishing blood supply is the primary goal for reducing myocardial injury in subjects with ischemic heart disease. Paradoxically, reperfusion results in nitroxidative stress and a marked inflammatory response in the heart. TRAF3IP2 (TRAF3 Interacting Protein 2; previously known as CIKS or Act1) is an oxidative stress-responsive cytoplasmic adapter molecule that is an upstream regulator of both IκB kinase (IKK) and c-Jun N-terminal kinase (JNK), and an important mediator of autoimmune and inflammatory responses. Here we investigated the role of TRAF3IP2 in ischemia/reperfusion (I/R)-induced nitroxidative stress, inflammation, myocardial dysfunction, injury, and adverse remodeling. Our data show that I/R up-regulates TRAF3IP2 expression in the heart, and its gene deletion, in a conditional cardiomyocyte-specific manner, significantly attenuates I/R-induced nitroxidative stress, IKK/NF-κB and JNK/AP-1 activation, inflammatory cytokine, chemokine, and adhesion molecule expression, immune cell infiltration, myocardial injury, and contractile dysfunction. Furthermore, Traf3ip2 gene deletion blunts adverse remodeling 12 weeks post-I/R, as evidenced by reduced hypertrophy, fibrosis, and contractile dysfunction. Supporting the genetic approach, an interventional approach using ultrasound-targeted microbubble destruction-mediated delivery of phosphorothioated TRAF3IP2 antisense oligonucleotides into the LV in a clinically relevant time frame significantly inhibits TRAF3IP2 expression and myocardial injury in wild type mice post-I/R. Furthermore, ameliorating myocardial damage by targeting TRAF3IP2 appears to be more effective to inhibiting its downstream signaling intermediates NF-κB and JNK. Therefore, TRAF3IP2 could be a potential therapeutic target in ischemic heart disease.

  6. Experiences with ACE inhibitors early after acute myocardial infarction. Rationale and design of the German Multicenter Study on the Effects of Captopril on Cardiopulmonary Exercise parameters post myocardial infarction (ECCE).

    Science.gov (United States)

    Kleber, F X; Reindl, I; Wenzel, M; Rodewyk, P; Beil, S; Kosloswki, B; Doering, W; Sabin, G V; Hinzmann, S; Winter, U J

    1993-12-01

    Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

  7. Assessment of myocardial viability using multidetector computed tomography in patients with reperfused acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kim, T. [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Choi, B.J. [Department of Cardiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Kang, D.K., E-mail: kdklsm@ajou.ac.kr [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Sun, J.S. [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of)

    2012-08-15

    Aim: To assess the prognostic value of 64-section multidetector computed tomography (MDCT) to predict follow-up myocardial dysfunction and functional recovery after reperfusion therapy in patients with acute myocardial infarction (MI) as defined by echocardiography. Materials and methods: After reperfusion therapy for acute MI, 71 patients underwent two-phase contrast-enhanced MDCT and follow-up echocardiography. MDCT findings were compared with echocardiographic findings using kappa statistics. The areas under the receiver operating characteristic curves (AUCs) and the odds ratios (ORs) of early perfusion defects (EPD), delayed enhancement (DE), and residual perfusion defects (RPD) for predicting follow-up myocardial dysfunction and functional recovery were calculated on a segmental basis. Results: The presence of transmural EPD (EPD{sub TM}) or RPD showed good agreement (k = 0.611 and 0.658, respectively) with follow-up myocardial dysfunction, while subendocardial EPD (EPD{sub sub}) or subendocardial DE (DE{sub sub}) showed fair agreement with follow-up myocardial dysfunction (k = 0.235 and 0.234, respectively). The AUC of RPD (0.796) was superior (p < 0.001 and 0.031, respectively) to those of EPD{sub TM} (0.761) and DE{sub TM} (0.771). The presence of EPD{sub TM}, DE{sub TM}, and RPD were significant, independent positive predictors of follow-up myocardial dysfunction (OR = 6.4, 1.9, and 9.8, respectively). EPD{sub TM} was a significant, independent negative predictor of myocardial functional recovery (OR = 0.13). Conclusion: Abnormal myocardial attenuation on two-phase MDCT after reperfusion therapy may provide promising information regarding myocardial viability in patients with acute MI.

  8. Pre-event quality of life and its influence on the post-event quality of life among patients with ST elevation and non-ST elevation myocardial infarctions of a premier province of Sri Lanka.

    Science.gov (United States)

    Mahesh, P K B; Gunathunga, M W; Jayasinghe, Saroj; Arnold, S M; Haniffa, R; De Silva, A P

    2017-08-01

    Pre-event Quality of Life (QOL) reflects the true social circumstances in which people live prior to the onset of myocardial infarctions. It is believed to be a predictor of the post-event QOL. The aim of this study was to describe the pre-event QOL and its influence on the post-event Quality of Life among patients with ST elevation (STEMI) and Non-ST elevation myocardial infarctions (NSTEMI) using Short Form-36 (SF-36), a generic QOL tool with 8 domains. Documented literature is rare in this regard in Sri Lanka, which is a lower-middle-income country. A cross-sectional study with a 28-day post-discharge follow-up was carried out in 13 hospitals. Three hundred and forty-four patients who were diagnosed with STEMI or NSTEMI were recruited during the hospital stay. The pre-event QOL was measured using an interviewer-administered questionnaire which included the SF-36 QOL tool and medical details. Follow-up QOL was gathered using a questionnaire that was filled and posted back by participants. Of the recruited sample, 235 responded for the follow-up component. Analysis was conducted for associations between pre- and post-discharge QOL. Furthermore, comparisons were made between the STEMI and NSTEMI groups. Mann Whiney U test, Wilcoxon signed rank test and chi square test were used in the analysis. The post-event QOL was lower in seven out of eight domains than the pre-event QOL (p event QOL for seven domains (p  0.05) between the STEMI and NSTEMI groups. Post-discharge general-health QOL domain score was higher than the pre-MI score (p = 0.028) and was higher in the STEMI group compared to the NSTEMI group (p = 0.042). Regression analysis showed a significant beta coefficient between pre- and post-QOL for five domains in STEMI and for all domains in NSTEMI groups when adjusted for the disease severity. The R square values ranged from 12.3 to 62.3% for STEMI and 7.3 to 64.8% for NSTEMI. Pre-event QOL is lower in the NSTEMI group compared to the STEMI group

  9. Successful treatment of post-exertion acute myocardial infarction by primary angioplasty and stenting in a patient with antiphospholipid antibody syndrome.

    Science.gov (United States)

    Musuraca, Gerardo; Imperadore, Ferdinando; Terraneo, Clotilde; De Girolamo, Piergiuseppe; Cemin, Claudio; Bonmassari, Roberto; Vergara, Giuseppe

    2004-01-01

    Antiphospholipid syndrome is a disorder characterized by arterial and venous thromboses, thrombocytopaenia and stroke. Acute myocardial infarction is rarely associated with this syndrome. The treatment of these patients is a clinical challenge. This report is about a patient with antiphospholipid syndrome presenting with an acute myocardial infarction after an exercise test. The infarct-related coronary artery was successfully revascularized by primary angioplasty and stenting without any major bleeding complications. We think that the physical exertion could have favoured acute coronary thrombosis in this particular setting.

  10. Myocardial dysfunction in patients with chronic kidney disease evaluated by global 2-dimensional strain imaging%二维超声应变评价慢性肾病心肌损害的价值

    Institute of Scientific and Technical Information of China (English)

    王泓; 曹铁生; 杨斌; 傅宁华; 李娟; 孙晖

    2011-01-01

    Objective To evaluate whether global 2-dimensional strain imaging can offer additional benefit over conventional echocardiography to detect subclinical myocardial damage in patients with chronic kidney disease(CKD). Methods Conventional echocardiography and global 2-dimension strain imaging were performed in 39 patients with CKD [23 men and 16 women,mean age (45.6± 14.6) years] and 29 control subjects. Twenty patients had CKD stage 2 or 3(group 1 ) and nineteen patients had CKD stage 4 or 5(group 2). Left ventricular structure and function were evaluated by conventional echocardiography. Global longitudinal and circumferential strain and strain rate were analyzed. Results There were no differences in ejection fraction and fraction shortening between CKD patients and controls. Compared with controls, CKD groups had significantly decreased value of global longitudinal strain and strain rate. Global longitudinal strain decreased from - (23.8 ± 3.1 ) % in controls to - ( 18. 5 ± 2.4) % in group 1 and to - (15.2 ± 3.2) % in group 2 ( P <0. 001 ). Compared with controls, there was no difference in global circumferential strain and strain rate between group 1 and controls, but global circumferential strain and strain rate of group 2 was reduced [ - (17.1± 3. 0) % vs -(21.2±2.8)%, P<0.05;-(1.0±0.2)% vs -(1.3±0.3)%, P<0.05]. In correlation analyses, global longitudinal strain was positively related to eGFR( r =0. 376, P <0. 001 ) and inversely related to left ventricular mass index( r = - 0. 473, P <0.01). Conclusions Global 2-dimensional strain imaging may represent a useful tool for the assessment of subclinical myocardial dysfunction in patients with CKD.%目的 探讨整体二维超声应变成像评价慢性肾病(CKD)心肌损害的价值.方法 39例CKD患者,其中20例为2~3期CKD患者(组1),19例为4~5期CKD患者(组2),设29例正常对照.使用常规超声心动图评价左室结构和功能,使用二维超声应变成像评价心肌整

  11. 脑卒中执行功能障碍康复技术的研究进展①%Advance in Rehabilitation for Post-stroke Executive Dysfunction (review)

    Institute of Scientific and Technical Information of China (English)

    2013-01-01

    Executive dysfunction is one of the cognitive impairment in patients with stroke. This paper reviewed the assessment tools and rehabilitation approaches for post-stroke executive dysfunction, and the interactive game such as Xbox Kinect may be prospective reha-bilitation for executive dysfunction.%  执行功能障碍是脑卒中患者常见的认知功能障碍之一。本文综述脑卒中执行功能障碍的常见评测工具及康复技术,指出体感游戏Xbox360 Kinect可能成为执行功能障碍康复技术有希望的方法。

  12. Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure

    NARCIS (Netherlands)

    Yin, Meimei; Sillje, Herman H. W.; Meissner, Maxi; van Gilst, Wiek H.; de Boer, Rudolf A.

    2011-01-01

    Background: Progressive remodeling after myocardial infarction (MI) is a leading cause of morbidity and mortality. Recently, glucagon-like peptide (GLP)-1 was shown to have cardioprotective effects, but treatment with GLP-1 is limited by its short half-life. It is rapidly degraded by the enzyme dipe

  13. Relation between renal dysfunction and the prognosis of patients withacute myocardial infarction%肾功能不全与急性心肌梗死患者预后的关系

    Institute of Scientific and Technical Information of China (English)

    徐琼; 刘进军; 宣玲

    2015-01-01

    目的 探讨肾功能不全(renal dysfunction)与急性心肌梗死(acute myocardial infarction,AMI)患者预后的关系.方法 搜集蚌埠医学院第一附属医院108例因急性心肌梗死入院患者的资料,将入院首次测得血肌酐值代入改良的MDRD方程计算出肾小球滤过率(c-aGFR),据其值将患者分为4组,GFR≥90 ml/(min·1.73 m2)为A组,60 ml/(min· 1.73 m2)≤GFR≤89 ml/(min· 1.73 m2)为B组,30 ml/(min· 1.73 m2)≤GFR≤59 ml/(min·1.73 m2)为C组,GFR≤29 ml/(min·1.73 m2)为D组,随访期为住院期间及出院后1年内,观察各组患者随访期内心绞痛、心力衰竭、再次心肌梗死、心源性死亡的发生情况,即主要心血管不良事件.结果 在随访期内发生主要心血管不良事件的患者为45例,包括15例心绞痛、15例心力衰竭、8例再次心肌梗死、7例心源性死亡,发生主要心血管不良事件患者中肾功能不全组较肾功能正常组明显增多,差异有统计学意义.结论 GFR值对评估AMI患者预后有一定价值,GFR是衡量肾功能的指标,肾功能不全患者其住院期间及出院1年内预后较差.

  14. Tei index in evaluation on left ventricular dysfunction in early phase acute myocardial infarction in rats%Tei指数评价大鼠超急性期心肌梗死左心功能

    Institute of Scientific and Technical Information of China (English)

    林蔚; 白旭东; 刘美佳

    2012-01-01

    目的 探讨Tei指数对评价大鼠超急性期心肌梗死后左心功能的作用.方法 将健康雄性Wistar大鼠23只随机分为两组:13只予垂体后叶素腹腔注射(实验组),10只予等量生理盐水腹腔注射(对照组).建模后分别记录两组大鼠心电图,用超声心动图检测获取左心室射血分数(EF)、等容收缩时间(ICT)、射血时间(ET)及等容舒张时间(IRT),然后取心肌组织行病理检查.结果 实验组ICT、Tei指数较对照组显著增加(P<0.01).Pearson相关分析显示,ICT及Tei指数与心电图ST段抬高程度、EF相关性良好(P<0.01).结论 Tei指数及其相关参数能客观评价大鼠超急性期心肌梗死的左心功能,可作为基础研究中判断该期心功能异常的良好指标.%Objective To observe the value of Tei index in evaluation on left ventricular dysfunction in early stage of acute myocardial infarction (AMI) in rat. Methods A total of 23 healthy male Wistar rats were randomly classified into experimental group (n=13) and control group (n=10) , and intraperitoneal injecting of Pituitrin or saline was performed, respectively. Parameters were measured with electrocardiography, and left ventricular ejection fraction (EF) , isovolumetric contraction time (ICT) , ejection time (ET) and isovolumic relaxation time (IRT) were obtained with echocardiography after modeling. Then pathological examination was performed in myocardium tissue sections. Results Compared with control group, ICT and Tei index of experimental group significantly increased (P<0. 01). Pearson correlation analysis showed ICT and Tei index were well correlated with ST segment elevation and EF (P<0. 01). Conclusion Tei index and the related parameters are efficient enough to evaluate left ventricular function after rat AMI in super early period, which can be used for basic research in evaluation of cardiac function.

  15. Changes in myocardial lactate, pyruvate and lactate-pyruvate ratio during cardiopulmonary bypass for elective adult cardiac surgery: Early indicator of morbidity

    Directory of Open Access Journals (Sweden)

    P M Kapoor

    2011-01-01

    Full Text Available Background: Myocardial lactate assays have been established as a standard method to compare various myocardial protection strategies. This study was designed to test whether coronary sinus (CS lactates, pyruvate and lactate-pyruvate (LP ratio correlates with myocardial dysfunction and predict postoperative outcomes. Materials and Methods: This prospective observational study was conducted on 40 adult patients undergoing elective cardiac surgery with the aid of cardiopulmonary bypass (CPB. CS blood sampling was done for estimation of myocardial lactate (ML, pyruvate (MP and lactate-pyruvate ratio (MLPR namely: pre-CPB (T 1 , after removal of aortic cross clamp (T 2 and 30 minutes post-CPB (T 3 . Results: Baseline myocardial LPR strongly correlated with Troponin-I at T1 (s: 0.6. Patients were sub grouped according to the median value of myocardial lactate (2.9 at baseline T1 into low myocardial lactate (LML group, mean (2.39±0.4 mmol/l, n=19 and a high myocardial lactate (HML group, mean (3.65±0.9 mmol/l, n=21. A significant increase in PL, ML, MLPR and TropI occurred in both groups as compared to baseline. Patients in HML group had significant longer period of ICU stay. Patients with higher inotrope score had significantly higher ML (T2, T3. ML with a baseline value of 2.9 mmol/l had 70.83% sensitivity and 62.5% specificity (ROC area: 0.7109 Std error: 0.09 while myocardial pyruvate with a baseline value of 0.07 mmol/l has 79.17% sensitivity and 68.75% specificity (ROC area: 0.7852, Std error: 0.0765 for predicting inotrope requirement after CPB. Conclusion: CS lactate, pyruvate and LP ratio correlate with myocardial function and can predict postoperative outcome.

  16. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in patients with chronic renal failure

    Directory of Open Access Journals (Sweden)

    Randa Aly Soliman

    2014-04-01

    Conclusions: Patients with CKD and regular hemodialysis who experience moderate or severe intradialytic hypotension have significantly higher prevalence of myocardial ischemia and stress induced myocardial dysfunction, than those who experience no or mild intradialytic hypotension.

  17. Atorvastatin reduces myocardial fibrosis in a rat model with post-myocardial infarction heart failure by increasing the matrix metaHoproteinase-2/tissue matrix metalloproteinase inhibitor-2 ratio

    Institute of Scientific and Technical Information of China (English)

    AN Zhe; YANG Guang; HE Yu-quan; DONG Ning; GE Li-li; LI Shu-mei; ZHANG Wen-qi

    2013-01-01

    Background The cholesterol-lowering statin drugs have some non-lipid-lowering effects,such as inhibiting myocardial remodeling.However,the underlying mechanism is still unclear.Methods The left anterior descending coronary artery was ligated to establish a rat model of heart failure,and the rats were divided into a sham operation (SO) group,myocardial infarction model (MI) group,and MI-atorvastatin group.Changes in hemodynamic parameters were recorded after the final drug administration.Histological diagnosis was made by reviewing hematoxylin and eosin (HE) stained tissue.Real-time quantitative polymerase chain reaction (PCR)was performed to determine the expressions of type Ⅰ and type Ⅲ collagen,matrix metalloproteinase-2 (MMP-2),and tissue matrix metalloproteinase inhibitor-2 (TIMP-2).Further,primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation.Results The model of heart failure was established and the results of HE staining and Masson's trichrome staining revealed that the rats in the heart failure group showed obvious hyperplasia of fibrotic tissue,which was significantly reduced in the atorvastatin group.Real-time quantitative PCR showed that the MI group showed a significantly increased expression of type Ⅰ and type Ⅲ collagen,MMP-2,and TIMP-2,but a significantly reduced MMP-2/TIMP-2 ratio.Compared with the MI group,the atorvastatin group showed significantly reduced expression of type Ⅰ and Ⅲcollagen,unchanged expression of MMP-2,significantly reduced expression of TIMP-2,and an increased MMP-2/TIMP-2 ratio.We further found that atorvastatin significantly inhibited the Ang Ⅱ-induced flbroblast proliferation and the expression of type Ⅰ and type Ⅲ collagen in cardiac flbroblasts while increasing the MMP-2/TIMP-2 ratio.Conclusions These data suggest that atorvastatin can inhibit cardiac fibroblast proliferation and enhance collagen degradation

  18. Evaluation on myocardial perfusion of coronary heart disease percutaneous coronary intervention pre and post by the transvenous myocardial contrast echocardiography%实时心肌声学造影评价冠心病介入治疗前后心肌灌注

    Institute of Scientific and Technical Information of China (English)

    吴向军

    2011-01-01

    Objective To evaluate myocardial perfusion of coronary heart disease percutaneous coronary intervention ( PCI ) pre and post. Methods 42 cases were selected by doctors in department of cardiology who are confirmed coronary artery normal subjects and have coronary artery stenosis subjects by the coronary angiography, transvenous myocardial contrast echocardiography were conducted pre and post PCI in patients with coronary artery stenosis and coronary artery normal, quantitative diagnosis of coronary microcir-culation perfusion through the extent of myocardial development and record images, will be comparative analysis pre and post treatment and coronary artery normal subjects, evaluate surgical efficacy, estimate prognosis of patients. Results After PCI treatment to 23 cases, the correlation-myocardial segments to the partial cross sectional area of all the capillaries( A ), blood flow velocity( β ), myocardial blood flow volume correlation-myocardial segments group compared to the coronary artery normal subjects of the correlationmyocardial segments group, the partial cross sectional area of all the capillaries( A ), blood flow velocity ( β ), myocatrlial blood flow volume( A·β )still all decreased, correlation analysis showed, follow-up period EF values and wall motion score index incwased significantly compared with those of preoperative and after treatment with PCI in A, β, A · β good correlation. Conclusion Transvenous myocardial contrast echocardiography examination for the diagnosis and treatment of coronary heart disease areas provide an accurate, noninvasive evaluation of myocardial microcirculation and clinical test; further evaluate the treatment of percutaneous coronary intervention in patients with myocardial infarction to improve myocardial perfusion effectively. Those patients without reperfusion therapy and angina pectofis or myocardial infarction should be treated with delayed PCI as early as possible, to save the ischemic myocardial

  19. A rare case of peripartum cardiomyopathy posted for caesarean section

    Directory of Open Access Journals (Sweden)

    Nalini Kotekar

    2007-01-01

    Full Text Available Post Partum Cardiomyopathy (PPCM is a relatively rare form of heart failure associated with pregnancy. It was recognized first in the 19th century by Ritchie and is defined as the onset of acute heart failure in the last trimester or early post partum period in the absence of infections, metabolic, toxic, ischaemic or valvular causes of myocardial dysfunction. Prognosis depends on the degree of cardiomegaly at presentation and in the following 6 months. Initial high risk period carries a mortality of 25 to 50%. Keeping in mind the reduced contractility and ejection fraction with ventricular dilatation proceeding to cardiac failure, the anesthesiologist managing a case of PPCM faces the challenge of avoiding myocardial depression, hypovolemia and increased SVR, all of which may be hazardous

  20. Risperidone Attenuates Modified Stress-Re-stress Paradigm-Induced Mitochondrial Dysfunction and Apoptosis in Rats Exhibiting Post-traumatic Stress Disorder-Like Symptoms.

    Science.gov (United States)

    Garabadu, Debapriya; Ahmad, Ausaf; Krishnamurthy, Sairam

    2015-06-01

    Mitochondria play a significant role in the pathophysiology of post-traumatic stress disorder (PTSD). Risperidone and paroxetine were evaluated for their effect on mitochondrial dysfunction and mitochondria-dependent apoptosis in discrete brain regions in modified stress re-stress (SRS) animal model of PTSD. Male rats were subjected to stress protocol of 2 h restraint and 20 min forced swim followed by halothane anesthesia on day 2 (D-2). Thereafter, rats were exposed to re-stress (forced swim) on D-8 and at 6-day intervals on D-14, D-20, D-26, and D-32. The rats were treated with risperidone (0.01, 0.1, and 1.0 mg/kg p.o.) and paroxetine (10.0 mg/kg p.o.) from D-8 to D-32. Risperidone at median dose and paroxetine ameliorated modified SRS-induced depressive-like symptom (increase in immobility period) in forced swim, anxiety-like behavior (decrease in percentage of open arm entries and time spent) in elevated plus maze and cognitive deficits (loss in spatial recognition memory) in Y-maze tests on D-32. Risperidone, but not paroxetine, attenuated modified SRS-induced decreases in plasma corticosterone levels. Risperidone ameliorated increase in the activity of mitochondrial respiratory complex (I, II, IV, and V), decreases in the levels of mitochondrial membrane potential, cytochrome-C and caspase-9 in the hippocampus, hypothalamus, pre-frontal cortex, and amygdala. However, both drugs attenuated modified SRS-induced increase in the number of apoptotic cells and caspase-3 levels in all the brain regions indicating anti-apoptotic activity of these drugs. Hence, these results suggest that anti-apoptotic activity could be a common mechanism for anti-PTSD-like effect irrespective of the pathways of apoptosis in the modified SRS model.

  1. Genetic deletion of NOS3 increases lethal cardiac dysfunction following mouse cardiac arrest.

    Science.gov (United States)

    Beiser, David G; Orbelyan, Gerasim A; Inouye, Brendan T; Costakis, James G; Hamann, Kimm J; McNally, Elizabeth M; Vanden Hoek, Terry L

    2011-01-01

    Cardiac arrest mortality is significantly affected by failure to obtain return of spontaneous circulation (ROSC) despite cardiopulmonary resuscitation (CPR). Severe myocardial dysfunction and cardiovascular collapse further affects mortality within hours of initial ROSC. Recent work suggests that enhancement of nitric oxide (NO) signaling within minutes of CPR can improve myocardial function and survival. We studied the role of NO signaling on cardiovascular outcomes following cardiac arrest and resuscitation using endothelial NO synthase knockout (NOS3(-/-)) mice. Adult female wild-type (WT) and NOS3(-/-) mice were anesthetized, intubated, and instrumented with left-ventricular pressure-volume catheters. Cardiac arrest was induced with intravenous potassium chloride. CPR was performed after 8min of untreated arrest. ROSC rate, cardiac function, whole-blood nitrosylhemoglobin (HbNO) concentrations, heart NOS3 content and phosphorylation (p-NOS3), cyclic guanosine monophosphate (cGMP), and phospho-troponin I (p-TnI) were measured. Despite equal quality CPR, NOS3(-/-) mice displayed lower rates of ROSC compared to WT (47.6% [10/21] vs. 82.4% [14/17], pNOS3(-/-) vs. WT mice exhibited increased left-ventricular dysfunction and 120min mortality. Prior to ROSC, myocardial effectors of NO signaling including cGMP and p-TnI were decreased in NOS3(-/-) vs. WT mice (pNOS3-dependent increases in circulating HbNO were seen by 120min. Significant increases in cardiac p-NOS3 occurred between end-arrest and 15min post-ROSC, while total NOS3 content was increased by 120min post-ROSC (pNOS3 decreases ROSC rate and worsens post-ROSC left-ventricular function. Poor cardiovascular outcomes are associated with differences in NOS3-dependent myocardial cGMP signaling and circulating NO metabolites. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

  2. Severe myocardial injury and extracorporeal membrane oxygenation following perinatal asphyxia

    Directory of Open Access Journals (Sweden)

    P. Benson Ham

    2015-05-01

    Full Text Available Perinatal asphyxia is a common cause of morbidity and mortality in the newborn and is associated with myocardial injury in a significant proportion of cases. Biomarkers, echocardiography, and rhythm disturbances are sensitive indicators of myocardial ischemia and may predict mortality. We present a case of severe myocardial dysfunction immediately after delivery managed with extracorporeal membrane oxygenation (ECMO and discuss the role of cardiac biomarkers, echocardiography, electrocardiography, and ECMO in the asphyxiated newborn.

  3. Serum profiles of circulating granulocyte-macrophage colony-stimulating factor in acute myocardial infarction and relation with post-infarction left ventricular function

    Institute of Scientific and Technical Information of China (English)

    MA Yi-tong; FU Zhen-yan

    2005-01-01

    @@ Accumulating evidence indicates that inflammation plays an important role in cardiac repairing and remodeling after acute myocardial infarction (AMI), process of which is mediated by a cytokine reaction cascade.1 Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine, which belongs to the family of haemopoietic cell colony-stimulating factor and regulates the proliferation and differentiation of myeloid progenitor cells.

  4. Use of myocardial imaging in the evaluation of patients with cardiovascular disease

    Energy Technology Data Exchange (ETDEWEB)

    Pitt, B.; Strauss, H.W.; Trhall, J.H.

    1980-01-01

    The role of radioisotope tracer techniques in the evaluation of patients with congenital heart disease, valvular heart disease, suspected myocardial infarction, ischemia or suspected ventricular dysfunction is reviewed. Thallium-201 myocardial imaging and exercise blood pool imaging and Technetium-88m pyrophosphate imaging of myocardial infarction are most commonly used.

  5. Role of Exercise Training on Autonomic Changes and Inflammatory Profile Induced by Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Bruno Rodrigues

    2014-01-01

    Full Text Available The cardiovascular autonomic imbalance in patients after myocardial infarction (MI provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.

  6. Evaluation of regional left ventricular systolic dysfunction in patients with infarct and ischemia myocardial by speckle tracking imaging%斑点追踪成像技术评价梗死心肌和缺血心肌对左心室局部收缩功能的影响

    Institute of Scientific and Technical Information of China (English)

    覃琴; 周青; 邓倾; 朱丽敏; 郭瑞强

    2011-01-01

    Objective To assess the longitudinal, radial and circumferential systolic strain ( LS , RS , CS ) and strain rate ( LSR, RSR, CSR ) from regional myocardial in patients with myocardial infarction and ischemia by speckle tracking imaging STI ) and to evaluate regional left ventricular systolic dysfunction. Methods The high frame rate two-dimensional echocardiography were performed in the 30 patients of the myocardial infarction and 25 patients of the ischemia myocardial group and 25healthy subjects. The longitudinal and radial and circumferential systolic strain ( LS,RS , CS ) and strain rate ( LSR , RSR , CSR ) from 18 regional myocardial were measured in the apical 2-chamber view.apical 4-chamber view and three level of short-axis views mitral valve, papillary muscle and cardial apex ) by STI. Results Compared with normal segments , the LS , RS, CS and LSR, RSR, CSR of ischemia segments were decreased. LS and LSR were significantly decreased from control group ( P<0.05 ),while there were no significant differences in CS, CSR and RS, RSR ( P> 0.05 ).Compared with normal segments , LS , RS, CS and LSR, RSR, CSR of infarct segments were significantly decreased ( P<0.01 ). Conclusions Regional left ventricular systolic dysfunction could be accurately analyzed by LS, RS, CS and LSR , RSR, CSR from regional myocardial in patients with infarction and ischemia myocardial by STI. LS and LSR are more sensitive than other indices in myocardial ischemia.%目的 应用超声斑点追踪成像(STI)技术分析梗死心肌及缺血心肌节段心肌纵向、径向及周向的收缩期峰值应变及应变率,评价其对左心室局部心肌收缩功能的影响.方法 35例心肌梗死患者(梗死组)、25例心肌缺血患者(缺血组)和25例正常体检者(正常组),接受超声检查,采集左心室长轴观、心尖四腔观,心尖二腔观及左心室短轴观(二尖瓣环水平、乳头肌水平和心尖水平)二维灰阶图像,按左心室18节段划分法,

  7. Post treatment thyroid dysfunction and obesity in children with acute lymphoblastic leukemia and non-Hodgkin’s lymphoma: a brief report

    Directory of Open Access Journals (Sweden)

    Ali Ghasemi

    2014-04-01

    Conclusion: Regarding to effects of thyroid dysfunction on short stature and obesity in adolescent with ALL and NHL, we suggest to have more attention about growth, thy-roid test to avoid late side effect of malignancy treatment.

  8. Clinical outcomes with the STENTYS self-apposing coronary stent in patients presenting with ST-segment elevation myocardial infarction: two-year insights from the APPOSITION III (A Post-Market registry to assess the STENTYS self-exPanding COronary Stent In AcuTe MyocardIal InfarctiON) registry.

    Science.gov (United States)

    Lu, Huangling; Grundeken, Maik J; Vos, Nicola S; IJsselmuiden, Alexander J J; van Geuns, Robert-Jan; Wessely, Rainer; Dengler, Thomas; La Manna, Alessio; Silvain, Johanne; Montalescot, Gilles; Spaargaren, René; Tijssen, Jan G P; Amoroso, Giovanni; de Winter, Robbert J; Koch, Karel T

    2017-08-04

    The APPOSITION III registry evaluated the feasibility and performance of the STENTYS self-apposing stent in an ST-segment elevation myocardial infarction (STEMI) population. This novel self-apposing stent device lowers stent strut malapposition rates and therefore carries the potential to prevent stent undersizing during primary percutaneous coronary intervention (PCI) in STEMI patients. To date, no long-term data are available using this device in the setting of STEMI. We aimed to evaluate the long-term clinical outcomes of the APPOSITION III registry. This was an international, prospective, multicentre post-marketing registry. The study population consisted of 965 STEMI patients. The primary endpoint, major adverse cardiac events (MACE), was defined as the composite of cardiac death, recurrent target vessel myocardial infarction (TV-MI), and clinically driven target lesion revascularisation (CD-TLR). At two years, MACE occurred in 11.2%, cardiac death occurred in 2.3%, TV-MI occurred in 2.3% and CD-TLR in 9.2% of patients. The two-year definite stent thrombosis (ST) rate was 3.3%. Incremental event rates between one- and two-year follow-up were 1.0% for TV-MI, 1.8% for CD-TLR, and 0.5% for definite ST. Post-dilation resulted in significantly reduced CD-TLR and ST rates at 30-day landmark analyses. Results were equivalent between the BMS and PES STENTYS subgroups. This registry revealed low rates of adverse events at two-year follow-up, with an incremental ST rate as low as 0.5% in the second year, demonstrating that the self-apposing technique is feasible in STEMI patients on long-term follow-up while using post-dilatation.

  9. Myocardial disease

    Institute of Scientific and Technical Information of China (English)

    1992-01-01

    920666 Immunocytochemical study ofCuZn superoxide dismutase in the myocardi-um of normal subjects and patients ofrheumatic heart disease.ZHENG Yi(郑毅),et al. Dept Intern Med, Navy General Hosp,PLA, Beijing. 100037. Natl Med J China 1992;72(4): 225-227. By using the methods of immunocytochemistry

  10. Depression following myocardial infarction

    DEFF Research Database (Denmark)

    Larsen, Karen Kjær

    2013-01-01

    Myocardial infarction (MI) is a severe life event that is accompanied by an increased risk of depression. Mounting evidence suggests that post-MI depression is associated with adverse outcomes, but the underlying mechanisms of this association remain unclear, and no previous studies have examined...... whether the mental burden of MI is so heavy that it increases the risk of suicide. Although post-MI depression is common and burdensome, the condition remains under-recognised and under-treated. The development of new strategies to improve the quality of care for people with post-MI depression requires...... thorough understanding of the mechanisms that influence the prognosis as well as knowledge of the present care provided. The purpose of this PhD thesis is accordingly subdivided into four specific aims: 1. To estimate the prevalence of depression in people with MI after three months, and to estimate...

  11. Diastolic Dysfunction

    Science.gov (United States)

    ... Kawasaki Disease Long Q-T Syndrome Marfan Syndrome Metabolic Syndrome Mitral Valve Prolapse Myocardial Bridge Myocarditis Obstructive Sleep Apnea Pericarditis Peripheral Vascular Disease Rheumatic Fever Sick Sinus Syndrome Silent Ischemia Stroke Sudden ...

  12. [Anti-arrhythmic effect of acupuncture pretreatment in the rat of myocardial ischemia the post-receptor signaling pathway of beta-adrenergic receptor].

    Science.gov (United States)

    Gao, Jun-hong; Fu, Wei-xing; Jin, Zhi-gao; Yu, Xiao-chun

    2006-06-01

    To observe anti-arrhythmic effect of acupuncture pretreatment in the rat of myocardial ischemia and reperfusion (MIR) and to explore the role of cAMP and Gsa protein in beta-adrenergic receptor signaling. MIR was produced by ligation and reperfusion of the left anterior descending coronary artery in the rat. Arrhythmic score, content of cAMP and Gsalpha protein in ischemic myocardium were compared among the normal control (NC), ischemia and reperfusion (IR), electroacupuncture (EA) and EA plus propranolol (EAP) groups. The arrhythmic score in the IR group at 10 min after reperfusion was higher than the NC group (P signaling pathway of beta-adrenergic receptor.

  13. The impact of renal dysfunction on outcomes in the ExTRACT-TIMI 25 trial.

    NARCIS (Netherlands)

    Fox, K.A.; Antman, E.M.; Montalescot, G.; Agewall, S.; SomaRaju, B.; Verheugt, F.W.A.; Lopez-Sendon, J.; Hod, H.; Murphy, S.A.; Braunwald, E.

    2007-01-01

    OBJECTIVES: The ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment-Thrombolysis In Myocardial Infarction 25) trial provided the opportunity to evaluate the impact of renal dysfunction on outcomes in patients with ST-segment elevation myocardial infarct

  14. Insulin-like growth factor 1 treatment of MSCs attenuates inflammation and cardiac dysfunction following MI.

    Science.gov (United States)

    Guo, Jun; Zheng, Dong; Li, Wen-feng; Li, Hai-rui; Zhang, Ai-dong; Li, Zi-cheng

    2014-12-01

    It has been reported that insulin-like growth factor 1 (IGF-1) promoted migration of endothelial cells and cardiac resident progenitor cells. In the previous study, we found the time-dependent and dose-dependent effects of IGF-1 treatment on the CXCR4 expression in MSCs in vitro, but it is still not clear whether IGF-1 pretreatment of MSCs may play anti-apoptotic and anti-inflammation role in myocardial infarction. In this study, we demonstrated that IGF-1-treated MSCs' transplantation attenuate cardiac dysfunction, increase the survival of engrafted cells in the ischemic heart, decrease myocardium cells apoptosis, and inhibit protein production and gene expression of inflammation cytokines tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6. IGF-1 pretreatment of MSCs may play anti-apoptotic and anti-inflammation roles in post-myocardial infarction.

  15. Myocardial overexpression of TIMP3 after myocardial infarction exerts beneficial effects by promoting angiogenesis and suppressing early proteolysis.

    Science.gov (United States)

    Takawale, Abhijit; Zhang, Pu; Azad, Abul; Wang, Wang; Wang, Xiuhua; Murray, Allan G; Kassiri, Zamaneh

    2017-08-01

    Myocardial infarction (MI) results in loss of cardiomyocytes, adverse extracellular matrix (ECM) and structural remodeling, and left ventricular (LV) dilation and dysfunction. Tissue inhibitors of metalloproteinase (TIMPs) inhibit matrix metalloproteinases (MMPs), the main regulators of ECM turnover. TIMPs also have MMP-independent functions. TIMP3 levels are reduced in the heart within 24 h of MI in mice. We investigated if overexpression of TIMP3 post-MI limits adverse remodeling and LV dilation and dysfunction. MI was induced by left anterior descending coronary artery ligation in 10- to 12-wk-old male C57BL/6J mice, and adenoviral constructs expressing human (h)TIMP3 (Ad-hTIMP3) or no TIMP (Ad-Null) were injected in the peri-infarct zone (5.4 × 10(7) plaque-forming units/heart, 5 injections/heart). Cardiac function assessed by echocardiography showed improved LV physiology and reduced LV dilation after TIMP3 overexpression compared with the Ad-Null-MI group. Post-MI adverse remodeling was attenuated in the Ad-hTIMP3-MI group, as assessed by greater cardiomyocyte density, less infarct expansion, and ECM disruption. TIMP3 overexpression blunted the early rise in proteolytic activities post-MI. A higher density of coronary arteries and a greater number of proliferating endothelial cells were detected in the infarct and peri-infarct regions in the Ad-hTIMP3-MI group compared with the Ad-Null-MI group. In vitro three-dimensional angiogenesis assay confirmed that recombinant TIMP3 promotes angiogenesis in human endothelial cells, although biphasically and in a dose-dependent manner. Intriguingly, overexpression of Ad-hTIMP3 at 10-fold higher concentration had no beneficial effects, consistent with antiangiogenic effects of TIMP3 at higher doses. In conclusion, optimal overexpression of TIMP3 can be a promising therapeutic approach to limit adverse post-MI remodeling by dually inhibiting early proteolysis and promoting angiogenesis.NEW & NOTEWORTHY Here, we report

  16. Alcohol consumption negates estrogen-mediated myocardial repair in ovariectomized mice by inhibiting endothelial progenitor cell mobilization and function.

    Science.gov (United States)

    Mackie, Alexander R; Krishnamurthy, Prasanna; Verma, Suresh K; Thorne, Tina; Ramirez, Veronica; Qin, Gangjian; Abramova, Tatiana; Hamada, Hiromichi; Losordo, Douglas W; Kishore, Raj

    2013-06-21

    We have shown previously that estrogen (estradiol, E2) supplementation enhances voluntary alcohol consumption in ovariectomized female rodents and that increased alcohol consumption impairs ischemic hind limb vascular repair. However, the effect of E2-induced alcohol consumption on post-infarct myocardial repair and on the phenotypic/functional properties of endothelial progenitor cells (EPCs) is not known. Additionally, the molecular signaling of alcohol-estrogen interactions remains to be elucidated. This study examined the effect of E2-induced increases in ethanol consumption on post-infarct myocardial function/repair. Ovariectomized female mice, implanted with 17β-E2 or placebo pellets were given access to alcohol for 6 weeks and subjected to acute myocardial infarction. Left ventricular functions were consistently depressed in mice consuming ethanol compared with those receiving only E2. Alcohol-consuming mice also displayed significantly increased infarct size and reduced capillary density. Ethanol consumption also reduced E2-induced mobilization and homing of EPCs to injured myocardium compared with the E2-alone group. In vitro, exposure of EPCs to ethanol suppressed E2-induced proliferation, survival, and migration and markedly altered E2-induced estrogen receptor-dependent cell survival signaling and gene expression. Furthermore, ethanol-mediated suppression of EPC biology was endothelial nitric oxide synthase-dependent because endothelial nitric oxide synthase-null mice displayed an exaggerated response to post-acute myocardial infarction left ventricular functions. These data suggest that E2 modulation of alcohol consumption, and the ensuing EPC dysfunction, may negatively compete with the beneficial effects of estrogen on post-infarct myocardial repair.

  17. Assessment of Regional Myocardial Function in Patients with Hypertrophic Cardiomyopathy by Tissue Strain Imaging

    Institute of Scientific and Technical Information of China (English)

    XIONG Runqing; XIE Mingxing; WANG Xinfang; L(U) Qing

    2006-01-01

    The value of tissue strain imaging (SI) in regional myocardial systolic anddiastolic function assessment was studied. In 18 patients with nonobstructive hypertrophic cardiomyopathy (HCM) and 20 age-matched healthy subjects, regional myocardial longitudinal peak systolic strain in eject time (represented by εet) was measured at basal, mid and apical segments of septal, lateral and posterior walls of the left ventricle (LV) and compared between groups. εet had no significant difference between segments in control group (P>0.05), which displayed a decreasing trend from basal segments to apical ones. εet in the HCM group was significantly decreased (P<0. 05) as compared with that in the healthy group. In the HCM group, εet in the midseptum was significantly less than at the basal and apical septum, and was also less than at the rest LV walls in the same group (P<0.01). The systolic reversed εet was noticed in 35 % of the hypertrophic segments in HCM group. Significantly negative correlation existed between the absolute value of εet and wall thickness in the midseptum (r=- 0.83). The post-systolic strain(PSS) segment number the and amplitudes in healthy group were significantly less than those in HCM group (P<0.05). Both regional myocardial systolic and diastolic functions were impaired in hypertrophic or non-hypertrophic segments in patients with the HCM, especially in hypertrophic segments. Strain imaging technique is a sensitive and accura tool in myocardial dysfunction assessment.

  18. PET and MRI for the evaluation of regional myocardial perfusion and wall thickening after myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Slart, Riemer H.J.A.; Golestani, Reza; Glaudemans, Andor W.J.M. [University Medical Center Groningen, University of Groningen, Department of Nuclear Medicine and Molecular Imaging, Hanzeplein 1, P.O. Box 30001, Groningen (Netherlands); Glauche, Julius; Jansen, Jan W. [University Medical Center Groningen, University of Groningen, Department of Nuclear Medicine and Molecular Imaging, Hanzeplein 1, P.O. Box 30001, Groningen (Netherlands); University Medical Center Groningen, University of Groningen, Department of Cardiology, Groningen (Netherlands); Zeebregts, Clark J. [University Medical Center Groningen, University of Groningen, Department of Surgery, Division of Vascular Surgery, Groningen (Netherlands); Dierckx, Rudi A.J.O. [University Medical Center Groningen, University of Groningen, Department of Nuclear Medicine and Molecular Imaging, Hanzeplein 1, P.O. Box 30001, Groningen (Netherlands); Ghent University Hospital, Department of Nuclear Medicine, Ghent (Belgium); Oudkerk, Matthijs; Willems, Tineke P. [University Medical Center Groningen, University of Groningen, Department of Radiology, Groningen (Netherlands); Boersma, Hendrikus H. [University Medical Center Groningen, University of Groningen, Department of Nuclear Medicine and Molecular Imaging, Hanzeplein 1, P.O. Box 30001, Groningen (Netherlands); University Medical Center Groningen, University of Groningen, Clinical and Hospital Pharmacy, Groningen (Netherlands); Tio, Rene A. [University Medical Center Groningen, University of Groningen, Department of Cardiology, Groningen (Netherlands)

    2012-06-15

    Deterioration of left ventricular (LV) function after myocardial infarction (MI) is a major cause of heart failure. Myocardial perfusion performance may play an important role in deterioration or improvement in LV function after MI. The aim of this study was to evaluate the myocardial perfusion reserve (MPR) and stress perfusion in deteriorating and non-deteriorating LV segments in patients after MI by PET and MRI, respectively. Regional wall thickening of 352 segments in 22 patients was assessed at 4 and 24 months after MI by cardiac MRI. PET was performed to evaluate MPR and adenosine stress {sup 13}N-ammonia perfusion 24 months after MI. Segments were divided into four groups according to deterioration or improvement in wall thickening. Normal functional segments at 4 months after MI that remained stable had a significantly higher mean MPR and mean stress perfusion PET value than deteriorated segments (p < 0.001). Furthermore, dysfunctional segments that improved had a significantly higher mean stress perfusion PET value than dysfunctional segments that remained dysfunctional (p < 0.001). This study demonstrated the additional value of myocardial perfusion assessment in relation to the functional integrity of the injured myocardium. Segmental functional LV improvement after MI was associated with better regional myocardial perfusion characteristics. Furthermore, the amount of wall thickening reduction was associated with regional myocardial perfusion abnormalities in patients after MI. (orig.)

  19. Delivery of an engineered HGF fragment in an extracellular matrix-derived hydrogel prevents negative LV remodeling post-myocardial infarction.

    Science.gov (United States)

    Sonnenberg, Sonya B; Rane, Aboli A; Liu, Cassie J; Rao, Nikhil; Agmon, Gillie; Suarez, Sophia; Wang, Raymond; Munoz, Adam; Bajaj, Vaibhav; Zhang, Shirley; Braden, Rebecca; Schup-Magoffin, Pamela J; Kwan, Oi Ling; DeMaria, Anthony N; Cochran, Jennifer R; Christman, Karen L

    2015-03-01

    Hepatocyte growth factor (HGF) has been shown to have anti-fibrotic, pro-angiogenic, and cardioprotective effects; however, it is highly unstable and expensive to manufacture, hindering its clinical translation. Recently, a HGF fragment (HGF-f), an alternative c-MET agonist, was engineered to possess increased stability and recombinant expression yields. In this study, we assessed the potential of HGF-f, delivered in an extracellular matrix (ECM)-derived hydrogel, as a potential treatment for myocardial infarction (MI). HGF-f protected cardiomyocytes from serum-starvation and induced down-regulation of fibrotic markers in whole cardiac cell isolate compared to the untreated control. The ECM hydrogel prolonged release of HGF-f compared to collagen gels, and in vivo delivery of HGF-f from ECM hydrogels mitigated negative left ventricular (LV) remodeling, improved fractional area change (FAC), and increased arteriole density in a rat myocardial infarction model. These results indicate that HGF-f may be a viable alternative to using recombinant HGF, and that an ECM hydrogel can be employed to increase growth factor retention and efficacy.

  20. Pseudoinfarto agudo do miocárdio devido à síndrome da disfunção ventricular apical transitória (síndrome de Takotsubo Pseudo-acute myocardial infarction due to transient apical ventricular dysfunction syndrome (Takotsubo syndrome

    Directory of Open Access Journals (Sweden)

    Bruno Araújo Maciel

    2013-03-01

    Full Text Available A síndrome de Takotsubo caracteriza-se por disfunção ventricular esquerda transitória, predominantemente medioapical, desencadeada caracteristicamente por estresse físico ou emocional. Relata-se aqui o caso de uma paciente de 61 anos de idade, admitida com tontura, sudorese profusa e mal-estar súbito, após intenso estresse emocional. Exame físico e eletrocardiograma inicial foram normais, porém havia elevação de troponina I e CKMB massa. Suspeitou-se de infarto agudo do miocárdio sem supradesnivelamento do segmento ST, indicando cineangiocoronariografia de urgência. Foram evidenciados ventrículo esquerdo com hipocinesia difusa grave, balonamento sistólico medioapical e coronárias sem lesões significativas. A paciente foi encaminhada aos cuidados intensivos, evoluindo satisfatoriamente com terapia de suporte. Conforme visto, a cardiomiopatia de Takotsubo pode simular infarto agudo do miocárdio, sendo a cineangiocoronariografia importante para distinção na fase aguda. Neste caso, a paciente evoluiu com resolução espontânea da disfunção ventricular, sem sequelas.Takotsubo syndrome is characterized by predominantly medial-apical transient left ventricular dysfunction, which is typically triggered by physical or emotional stress. The present article reports the case of a 61-year-old female patient presenting with dizziness, excessive sweating, and sudden state of ill feeling following an episode involving intense emotional stress. The physical examination and electrocardiogram were normal upon admission, but the troponin I and creatine kinase-MB concentrations were increased. Acute myocardial infarction without ST segment elevation was suspected, and coronary angiography was immediately performed, which showed severe diffuse left ventricular hypokinesia, medial-apical systolic ballooning, and a lack of significant coronary injury. The patient was referred to the intensive care unit and was successfully treated with supportive

  1. Influence of preinfarction angina and coronary collateral blood flow on the efficacy of remote ischaemic conditioning in patients with ST segment elevation myocardial infarction: post hoc subgroup analysis of a randomised controlled trial

    Science.gov (United States)

    Pryds, Kasper; Bøttcher, Morten; Sloth, Astrid Drivsholm; Munk, Kim; Rahbek Schmidt, Michael; Bøtker, Hans Erik

    2016-01-01

    Objectives Remote ischaemic conditioning (RIC) confers cardioprotection in patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). We investigated whether preinfarction angina and coronary collateral blood flow (CCBF) to the infarct-related artery modify the efficacy of RIC. Design Post hoc subgroup analysis of a randomised controlled trial. Participants A total of 139 patients with STEMI randomised to treatment with pPCI or RIC+pPCI. Interventions RIC was performed prior to pPCI as four cycles of 5 min upper arm ischaemia and reperfusion with a blood pressure cuff. Primary outcome measure Myocardial salvage index (MSI) assessed by single-photon emission computerised tomography. We evaluated the efficacy of RIC in subgroups of patients with or without preinfarction angina or CCBF. Results Of 139 patients included in the study, 109 had available data for preinfarction angina status and 54 had preinfarction angina. Among 83 patients with Thrombolysis In Myocardial Infarction flow 0/1 on arrival, 43 had CCBF. Overall, RIC+pPCI increased median MSI compared with pPCI alone (0.75 vs 0.56, p=0.045). Mean MSI did not differ between patients with and without preinfarction angina in either the pPCI alone (0.58 and 0.57; 95% CI −0.17 to 0.19, p=0.94) or the RIC+pPCI group (0.66 and 0.69; 95% CI −0.18 to 0.10, p=0.58). Mean MSI did not differ between patients with and without CCBF in the pPCI alone group (0.51 and 0.55; 95% CI −0.20 to 0.13, p=0.64), but was increased in patients with CCBF versus without CCBF in the RIC+pPCI group (0.75 vs 0.58; 95% CI 0.03 to 0.31, p=0.02; effect modification from CCBF on the effect of RIC on MSI, p=0.06). Conclusions Preinfarction angina did not modify the efficacy of RIC in patients with STEMI undergoing pPCI. CCBF to the infarct-related artery seems to be of importance for the cardioprotective efficacy of RIC. Trial registration number NCT00435266, Post

  2. Hypothalamic dysfunction

    Science.gov (United States)

    ... common causes of hypothalamic dysfunction are surgery, traumatic brain injury, tumors, and radiation. Other causes include: Anorexia nervosa or bulimia Bleeding Genetic disorders that cause iron ...

  3. Impaired coronary flow reserve is the most important marker of viable myocardium in the myocardial segment-based analysis of dual-isotope gated myocardial perfusion single-photon emission computed tomography

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Won Woo [Dept. of Nuclear Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam (Korea, Republic of); So, Young [Dept. of Nuclear Medicine, Konkuk University School of Medicine, Seoul (Korea, Republic of); Kim, Ki Bong; Lee, Dong Soo [Seoul National University Hospital, Seoul National University College of Medicine, Seoul (Korea, Republic of)

    2014-04-15

    The aim of this study was to investigate the most robust predictor of myocardial viability among stress/rest reversibility (coronary flow reserve [CFR] impairment), {sup 201}Tl perfusion status at rest, {sup 201}Tl 24 hours redistribution and systolic wall thickening of {sup 99m}Tc-methoxyisobutylisonitrile using a dual isotope gated myocardial perfusion single-photon emission computed tomography (SPECT) in patients with coronary artery disease (CAD) who were re-vascularized with a coronary artery bypass graft (CABG) surgery. A total of 39 patients with CAD was enrolled (34 men and 5 women), aged between 36 and 72 years (mean 58 ± 8 standard in years) who underwent both pre- and 3 months post-CABG myocardial SPECT. We analyzed 17 myocardial segments per patient. Perfusion status and wall motion were semi-quantitatively evaluated using a 4-point grading system. Viable myocardium was defined as dysfunctional myocardium which showed wall motion improvement after CABG. The left ventricular ejection fraction (LVEF) significantly increased from 37.8 ± 9.0% to 45.5 ± 12.3% (p < 0.001) in 22 patients who had a pre-CABG LVEF lower than 50%. Among 590 myocardial segments in the re-vascularized area, 115 showed abnormal wall motion before CABG and 73.9% (85 of 115) had wall motion improvement after CABG. In the univariate analysis (n = 115 segments), stress/rest reversibility (p < 0.001) and {sup 201}Tl rest perfusion status (p = 0.024) were significant predictors of wall motion improvement. However, in multiple logistic regression analysis, stress/rest reversibility alone was a significant predictor for post-CABG wall motion improvement (p < 0.001). Stress/rest reversibility (impaired CFR) during dual-isotope gated myocardial perfusion SPECT was the single most important predictor of wall motion improvement after CABG.

  4. Predictors of the first heart failure hospitalization in patients who are stable survivors of myocardial infarction complicated by pulmonary congestion and/or left ventricular dysfunction: a VALIANT study

    DEFF Research Database (Denmark)

    Lewis, Eldrin F; Velazquez, Eric J; Solomon, Scott D

    2008-01-01

    AIMS: We sought to assess the incidence of and prognostic factors for heart failure (HF) hospitalization among survivors of high-risk acute myocardial infarction (MI). METHODS AND RESULTS: We assessed the risk of an initial hospitalization for HF in 11 040 stable MI patients (no major non-fatal c...

  5. Cardiac tamponade and para-aortic hematoma post elective surgical myocardial revascularization on a beating heart - a possible complication of the Lima-stitch and sequential venous anastomosis.

    Science.gov (United States)

    Marcinkiewicz, Anna; Jaszewski, Ryszard; Piestrzeniewicz, Katarzyna; Zwoliński, Radosław

    2014-06-04

    Off-pump coronary artery bypass (OPCAB) surgery can be associated with some intrinsic, but relatively rare complications. A pericardial effusion is a common finding after cardiac surgeries, but the prevalence of a cardiac tamponade does not exceed 2% and is less frequent after myocardial revascularization.Authors believe that in our patient an injury of a nutritional pericardial or descending aorta vessel caused by the Lima stitch resulted in oozing bleeding, which gradually leaded to cardiac tamponade. The bleeding increased after introduction of double antiplatelet therapy and caused life-threatening hemodynamic destabilization. According to our knowledge it is the first report of such a complication after OPCAB. We present a case of a 61-year old man, who underwent elective surgical myocardial revascularization on a beating heart. On the 11th postoperative day the patient was readmitted emergently to the intensive care unit for severe chest pain, dyspnoea and hypotension. Coronary angiographic control showed a patency of the bypass grafts and significant narrowing of circumflex artery, treated with angioplasty and stenting. The symptoms and hemodynamic instability exacerbated. A suspicion of dissection of the ascending aorta and para-aortic hematoma was stated on 16-slice cardiac computed tomography. The patient was referred to the Cardiovascular Surgery Clinic. Transthoracic echocardiography revealed cardiac tamponade. On transesophageal echocardiography there were no signs of the ascending aorta dissection, but a possible lesion of the descending aorta with para-aortic hematoma was visualized. Emergent rethoracotomy and cardiac tamponade decompression were performed. 12 days after intervention the control 64-slice computed tomography showed no lesions of the ascending or descending aorta. On one-year follow-up patient is in a good condition, the left ventricular function is preserved and there is no pathology in thoracic aorta on echocardiography. Mechanical

  6. Testosterone replacement attenuates mitochondrial damage in a rat model of myocardial infarction.

    Science.gov (United States)

    Wang, Fengyue; Yang, Jing; Sun, Junfeng; Dong, Yanli; Zhao, Hong; Shi, Hui; Fu, Lu

    2015-05-01

    Testosterone can affect cardiovascular disease, but its effects on mitochondrial dynamics in the post-infarct myocardium remain unclear. To observe the effects of testosterone replacement, a rat model of castration-myocardial infarction (MI) was established by ligating the left anterior descending coronary artery 2 weeks after castration with or without testosterone treatment. Expression of mitochondrial fission and fusion proteins was detected by western blot and immunofluorescence 14 days after MI. Cardiac function, myocardial inflammatory infiltration and fibrosis, cardiomyocyte apoptosis, mitochondrial microstructure, and ATP levels were also assessed. Compared with MI rats, castrated rats showed aggravated mitochondrial and myocardial insults, including mitochondrial swelling and disordered arrangement; loss of cristae, reduced mitochondrial length; decreased ATP levels; cardiomyocyte apoptosis; and impaired cardiac function. Results of western blotting analyses indicated that castration downregulated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1A) and mitofusin 2, but upregulated dynamin-related protein 1. The results were also supported by results obtained using immunofluorescence. However, these detrimental effects were reversed by testosterone supplementation, which also elevated the upstream AMP-activated protein kinase (AMPK) activation of PGC1A. Thus, testosterone can protect mitochondria in the post-infarct myocardium, partly via the AMPK-PGC1A pathway, thereby decreasing mitochondrial dysfunction and cardiomyocyte apoptosis. The effects of testosterone were confirmed by the results of ELISA analyses.

  7. Role of toll-like receptor 2 and toll-like receptor 4 in post-ischemic coronary endothelial dysfunction in mice

    Institute of Scientific and Technical Information of China (English)

    J.FAVRE; P.MUSETTE; JPHENRY; C.THUILLEZ; V.RICHARD

    2004-01-01

    AIM: A growing body of evidence suggests a role of the toll-like receptors (TLR) in inflammatory processes. In addition to LPS,TLR are activated by many endogenous ligands such as heat shock proteins and oxygeil-derived free radicals which are both produced during cardiac ischemia-reperfusion (I/R). Among TLR,TLR-2 and TLR-4 are expressed in endothelial and myocardial cells and appear to regulate neutrophil-endothelial interactions.Since neutrophil adhesion is a critical event in endothelial injury

  8. Myocardial Infarction Type 2 and Myocardial Injury

    DEFF Research Database (Denmark)

    Sandoval, Yader; Thygesen, Kristian

    2017-01-01

    BACKGROUND: The development and implementation of sensitive and high-sensitivity cardiac troponin assays has not only expedited the early ruling in and ruling out of acute myocardial infarction, but has also contributed to the identification of patients at risk for myocardial injury with necrosis......, as confirmed by the presence of cardiac troponin concentrations above the 99th percentile. Myocardial injury with necrosis may occur either in the presence of overt ischemia from myocardial infarction, or in the absence of overt ischemia from myocardial injury accompanying other conditions. Myocardial...... infarction type 2 (T2MI) has been a focus of attention; conceptually T2MI occurs in a clinical setting with overt myocardial ischemia where a condition other than an acute atherothrombotic event is the major contributor to a significant imbalance between myocardial oxygen supply and/or demand. Much debate...

  9. Soluble TNF-related apoptosis induced ligand (sTRAIL) is augmented by Post-Conditioning and correlates to infarct size and left ventricle dysfunction in STEMI patients: a substudy from a randomized clinical trial.

    Science.gov (United States)

    Luz, André; Santos, Mário; Magalhães, Rui; Oliveira, José Carlos; Pacheco, Ana; Silveira, João; Cabral, Sofia; Torres, Severo; Leite-Moreira, Adelino F; Carvalho, Henrique

    2017-02-01

    Low levels of Soluble TNF-related apoptosis induced ligand (sTRAIL) seem to be related to worse prognosis after an acute coronary syndrome. PostConditioning (PostCond) may protect the heart from reperfusion injury. We sought to evaluate the impact of PostCond on sTRAIL in relationship to infarct size (area under the curve of Troponin T, AUCTnT) and left ventricle ejection fraction (LVEF) in a series of patients undergoing primary coronary intervention for ST-segment elevation myocardial infarction (STEMI). In a substudy of a randomized trial that tested the effects of PostCond in STEMI-patients, sTRAIL was measured 24 h after reperfusion (PostCond n = 39, Control n = 39). Correlations between sTRAIL and both AUCTnT and LVEF were studied for each study arm. At 24 h, sTRAIL was higher for PostCond vs Controls (46.4 ± 30.6 vs 32.9 ± 23.4, p = 0.031), was negatively related to AUCTnT [B = -0.09, 95 % CI (-0.15 to -0.30), p = 0.005] and was positively related to both in-hospital [B = 0.10, 95 % CI (0.02-0.17), p = 0.018], and follow-up LVEF [B = 0.21, 95 % (0.10-0.32), p = 0.001]. No significant relationship was found for Controls. On multivariate analysis, PostCond was an independent predictor for sTRAIL [B = 12.13 95 % CI (0.40-23.87), p = 0.043]. In conclusion, PostCond positively influenced sTRAIL, which was related to reduced infarct size and better LVEF. Further studies are needed to understand potential mechanisms elicited by PostCond in infarct size reduction.

  10. Intra-myocardial injection of both growth factors and heart derived Sca-1+/CD31- cells attenuates post-MI LV remodeling more than does cell transplantation alone: neither intervention enhances functionally significant cardiomyocyte regeneration.

    Directory of Open Access Journals (Sweden)

    Xiaohong Wang

    Full Text Available Insulin-like growth factor 1 (IGF-1 and hepatocyte growth factor (HGF are two potent cell survival and regenerative factors in response to myocardial injury (MI. We hypothesized that simultaneous delivery of IGF+HGF combined with Sca-1+/CD31- cells would improve the outcome of transplantation therapy in response to the altered hostile microenvironment post MI. One million adenovirus nuclear LacZ-labeled Sca-1+/CD31- cells were injected into the peri-infarction area after left anterior descending coronary artery (LAD ligation in mice. Recombinant mouse IGF-1+HGF was added to the cell suspension prior to the injection. The left ventricular (LV function was assessed by echocardiography 4 weeks after the transplantation. The cell engraftment, differentiation and cardiomyocyte regeneration were evaluated by histological analysis. Sca-1+/CD31- cells formed viable grafts and improved LV ejection fraction (EF (Control, 54.5+/-2.4; MI, 17.6+/-3.1; Cell, 28.2+/-4.2, n = 9, P<0.01. IGF+HGF significantly enhanced the benefits of cell transplantation as evidenced by increased EF (38.8+/-2.2; n = 9, P<0.01 and attenuated adverse structural remodeling. Furthermore, IGF+HGF supplementation increased the cell engraftment rate, promoted the transplanted cell survival, enhanced angiogenesis, and minimally stimulated endogenous cardiomyocyte regeneration in vivo. The in vitro experiments showed that IGF+HGF treatment stimulated Sca-1+/CD31- cell proliferation and inhibited serum free medium induced apoptosis. Supperarray profiling of Sca-1+/CD31- cells revealed that Sca-1+/CD31- cells highly expressed various trophic factor mRNAs and IGF+HGF treatment altered the mRNAs expression patterns of these cells. These data indicate that IGF-1+HGF could serve as an adjuvant to cell transplantation for myocardial repair by stimulating donor cell and endogenous cardiac stem cell survival, regeneration and promoting angiogenesis.

  11. Effect on treadmill exercise capacity, myocardial ischemia, and left ventricular function as a result of repeated whole-body periodic acceleration with heparin pretreatment in patients with angina pectoris and mild left ventricular dysfunction.

    Science.gov (United States)

    Miyamoto, Shoichi; Fujita, Masatoshi; Inoko, Moriaki; Oba, Muneo; Hosokawa, Ryohei; Haruna, Tetsuya; Izumi, Toshiaki; Saji, Yoshiaki; Nakane, Eisaku; Abe, Tomomi; Ueyama, Koji; Nohara, Ryuji

    2011-01-15

    Whole-body periodic acceleration (WBPA) has been developed as a passive exercise device capable of improving endothelial function by applying pulsatile shear stress to vascular endothelium. We hypothesized that treatment with WBPA improves exercise capacity, myocardial ischemia, and left ventricular (LV) function because of increased coronary and peripheral vasodilatory reserves in patients with angina. Twenty-six patients with angina who were not indicated for percutaneous coronary intervention and/or coronary artery bypass grafting were randomly assigned to remain sedentary (sedentary group) or undergo 20 sessions of WBPA with the motion platform for 4 weeks (WBPA group) in addition to conventional medical treatment. WBPA was applied at 2 to 3 Hz and approximately ±2.2 m/s² for 45 minutes. We repeated the symptom-limited treadmill exercise test and adenosine sestamibi myocardial scintigraphy. In the WBPA group, the exercise time until 0.1-mV ST-segment depression increased by 53% (p images at rest, LV end-diastolic volume index decreased by 18% (p exercise capacity, myocardial ischemia, and LV function.

  12. Renal function estimation and Cockroft-Gault formulas for predicting cardiovascular mortality in population-based, cardiovascular risk, heart failure and post-myocardial infarction cohorts: The Heart 'OMics' in AGEing (HOMAGE) and the high-risk myocardial infarction database initiatives.

    Science.gov (United States)

    Ferreira, João Pedro; Girerd, Nicolas; Pellicori, Pierpaolo; Duarte, Kevin; Girerd, Sophie; Pfeffer, Marc A; McMurray, John J V; Pitt, Bertram; Dickstein, Kenneth; Jacobs, Lotte; Staessen, Jan A; Butler, Javed; Latini, Roberto; Masson, Serge; Mebazaa, Alexandre; Rocca, Hans Peter Brunner-La; Delles, Christian; Heymans, Stephane; Sattar, Naveed; Jukema, J Wouter; Cleland, John G; Zannad, Faiez; Rossignol, Patrick

    2016-11-10

    Renal impairment is a major risk factor for mortality in various populations. Three formulas are frequently used to assess both glomerular filtration rate (eGFR) or creatinine clearance (CrCl) and mortality prediction: body surface area adjusted-Cockcroft-Gault (CG-BSA), Modification of Diet in Renal Disease Study (MDRD4), and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. The CKD-EPI is the most accurate eGFR estimator as compared to a "gold-standard"; however, which of the latter is the best formula to assess prognosis remains to be clarified. This study aimed to compare the prognostic value of these formulas in predicting the risk of cardiovascular mortality (CVM) in population-based, cardiovascular risk, heart failure (HF) and post-myocardial infarction (MI) cohorts. Two previously published cohorts of pooled patient data derived from the partners involved in the HOMAGE-consortium and from four clinical trials - CAPRICORN, EPHESUS, OPTIMAAL and VALIANT - the high risk MI initiative, were used. A total of 54,111 patients were included in the present analysis: 2644 from population-based cohorts; 20,895 from cardiovascular risk cohorts; 1801 from heart failure cohorts; and 28,771 from post-myocardial infarction cohorts. Participants were patients enrolled in the respective cohorts and trials. The primary outcome was CVM. All formulas were strongly and independently associated with CVM. Lower eGFR/CrCl was associated with increasing CVM rates for values below 60 mL/min/m(2). Categorical renal function stages diverged in a more pronounced manner with the CG-BSA formula in all populations (higher χ(2) values), with lower stages showing stronger associations. The discriminative improvement driven by the CG-BSA formula was superior to that of MDRD4 and CKD-EPI, but remained low overall (increase in C-index ranging from 0.5 to 2 %) while not statistically significant in population-based cohorts. The integrated discrimination improvement and

  13. A cross-sectional survey and cross-sectional clinical trial to determine the prevalence and management of eye movement disorders and vestibular dysfunction in post-stroke patients in the sub-acute phase: protocol

    Directory of Open Access Journals (Sweden)

    Andoret Van Wyk

    2016-09-01

    Full Text Available Introduction: Visual impairment, specifically eye movement disorders and vestibular dysfunction may have a negative influence on the functional recovery in post stroke patients. This type of sensory dysfunction may further be associated with poor functional outcome in patients post stroke.Methods: In phase 1 a cross-sectional survey (n = 100 will be conducted to determine the prevalence of eye movement disorders and vestibular dysfunction in patients that sustained a stroke. A cross-sectional clinical trial (n = 60 will be conducted during phase 2 of the study to determine the effect of the combination of vestibular rehabilitation therapy (VRT and visual scanning exercises (VSE (experimental group integrated with task-specific activities compared to the effect of task-specific activities as an intervention (control group on patients that present with eye movement impairment and central vestibular dysfunction post-stroke. An audiologist will assess; (a visual acuity (static and dynamic; (b nystagmus; (c; saccadic eye movements; (d smooth pursuit eye movements; (e vestibulo-ocular reflex; and (f saccular, utricular and vestibular nerve function. An independent physiotherapist will assess; (1 cognitive function; (2 residual oculomotor visual performance; (3 visual-perceptual system; (4 functional balance; (5 a patient’s ability to modify gait in response to changing task demands; (6 functional ability; and (7 presence of anxiety and/or depression and (8 level of participation in physical activity. Ethics and dissemination: Ethics approval has been obtained from the Ethics Committee of the Faculty of Health Sciences at the University of Pretoria (UP (374/2015. The study will be submitted as fulfilment for the PhD degree at UP. Dissemination will include submission to peer-reviewed professional journals and presentation at congresses. Training of rehabilitation team members on the integration of VSE and VRT into task-specific activities in

  14. Intracoronary Cardiosphere-Derived Cells After Myocardial Infarction

    Science.gov (United States)

    Malliaras, Konstantinos; Makkar, Raj R.; Smith, Rachel R.; Cheng, Ke; Wu, Edwin; Bonow, Robert O.; Marbán, Linda; Mendizabal, Adam; Cingolani, Eugenio; Johnston, Peter V.; Gerstenblith, Gary; Schuleri, Karl H.; Lardo, Albert C.; Marbán, Eduardo

    2013-01-01

    Objectives This study sought to report full 1-year results, detailed magnetic resonance imaging analysis, and determinants of efficacy in the prospective, randomized, controlled CADUCEUS (CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction) trial. Background Cardiosphere-derived cells (CDCs) exerted regenerative effects at 6 months in the CADUCEUS trial. Complete results at the final 1-year endpoint are unknown. Methods Autologous CDCs (12.5 to 25 × 106) grown from endomyocardial biopsy specimens were infused via the intracoronary route in 17 patients with left ventricular dysfunction 1.5 to 3 months after myocardial infarction (MI) (plus 1 infused off-protocol 14 months post-MI). Eight patients were followed as routine-care control patients. Results In 13.4 months of follow-up, safety endpoints were equivalent between groups. At 1 year, magnetic resonance imaging revealed that CDC-treated patients had smaller scar size compared with control patients. Scar mass decreased and viable mass increased in CDC-treated patients but not in control patients. The single patient infused 14 months post-MI responded similarly. CDC therapy led to improved regional function of infarcted segments compared with control patients. Scar shrinkage correlated with an increase in viability and with improvement in regional function. Scar reduction correlated with baseline scar size but not with a history of temporally remote MI or time from MI to infusion. The changes in left ventricular ejection fraction in CDC-treated subjects were consistent with the natural relationship between scar size and ejection fraction post-MI. Conclusions Intracoronary administration of autologous CDCs did not raise significant safety concerns. Preliminary indications of bioactivity include decreased scar size, increased viable myocardium, and improved regional function of infarcted myocardium at 1 year post-treatment. These results, which are consistent with therapeutic regeneration

  15. A post hoc analysis of long-term prognosis after exenatide treatment in patients with ST-segment elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kyhl, Kasper; Lønborg, Jacob; Vejlstrup, Niels

    2016-01-01

    AIMS: We aimed to assess the effect of exenatide treatment as an adjunct to primary percutaneous coronary intervention (PCI) on long-term clinical outcome. METHODS AND RESULTS: We performed a post hoc analysis in 334 patients with a first STEMI included in a previous study randomised to exenatide......% in the exenatide group versus 9% in the placebo group (HR 1.45, p=0.20). CONCLUSIONS: In this post hoc analysis of patients with a STEMI, treatment with exenatide at the time of primary PCI did not reduce the primary composite endpoint or the secondary endpoint of all-cause -mortality. However, exenatide treatment...

  16. Post-procedural hemodiafiltration in acute coronary syndrome patients with associated renal and cardiac dysfunction undergoing urgent and emergency coronary angiography.

    Science.gov (United States)

    Marenzi, Giancarlo; Mazzotta, Gianfranco; Londrino, Francesco; Gistri, Roberto; Moltrasio, Marco; Cabiati, Angelo; Assanelli, Emilio; Veglia, Fabrizio; Rombolà, Giuseppe

    2015-02-15

    We investigated the use of a 3-hr treatment with hemodiafiltration, initiated soon after emergency or urgent coronary angiography in acute coronary syndrome (ACS) patients with associated severe renal and cardiac dysfunction. Patients with ACS and severe combined renal and cardiac dysfunction have a particularly high mortality risk. In them, the ideal strategy to both optimize treatment of coronary disease and minimize renal injury risk is currently unknown. This was an interventional study. ACS patients (STEMI and NSTEMI) with associated severe renal (eGFR ≤30 ml/min/1.73 m(2) ) and cardiac (LVEF ≤40%) dysfunction, admitted at La Spezia Hospital emergency coronary procedure. Controls were patients matched for age, gender, Mehran's risk score, and kind of ACS, admitted at the Centro Cardiologico Monzino Milan. In-hospital and 1-year outcomes were evaluated. Sixty patients (30% STEMI), 30 hemodiafiltration-treated patients and 30 controls, with similar baseline characteristics, were included. In-hospital and cumulative 1-year mortality rates were significantly lower in hemodiafiltration-treated patients than in controls (3% vs. 23%; P = 0.05, and 10% vs. 53%; P emergency coronary angiography seems to be associated with a relevant improvement in survival. © 2014 Wiley Periodicals, Inc.

  17. Alteração tireoidiana: um fator de risco associado à depressão pós-parto? Thyroid dysfunction: a risk factor associated with post-partum depression?

    Directory of Open Access Journals (Sweden)

    Gustavo Enrico Cabral Ruschi

    2009-06-01

    Full Text Available OBJETIVOS: estudar prevalência de depressão pósparto e sua correlação com alterações tireoidianas maternas. MÉTODOS: estudo observacional descritivo transversal realizado com 292 mulheres entre 31 e 180 dias após o parto, atendidas em unidades de saúde pública da Região Metroplitana de Vitória, Espírito Santo, Brasil. Analisou-se a amostra segundo características sociodemográficas e clínico-obstétricas. Definiu-se transtorno depressivo pelo escore igual ou superior a 12 na Escala de Depressão Pós-Parto de Edimburgo (EPDS. A avaliação tireoidiana foi realizada por dosagens séricas de hormônio tireo-estimulante (TSH, tiroxina livre (T4 livre e dos anticorpos anti-peroxidase (TPO. Para avaliação dos resultados utilizamos técnicas de análise descritiva e teste do χ2, adotando nível de significância de 5%. RESULTADOS: 115 mulheres (39,4% apresentaram escores iguais ou superiores a 12 na EPDS, sendo consideradas deprimidas; 117 (60,6%, com escores inferiores a 12, foram consideradas não deprimidas. A prevalência de depressão pós-parto no grupo com alterações tireoidianas foi de 36% e no grupo sem alterações tireoidianas foi de 40%. Não houve diferença estatisticamente significante na frequência de depressão entre as pacientes com e sem alterações tireoidianas (χ2=0,131;p=0,717. CONCLUSÕES: a frequência de DPP foi elevada, não sendo observada associação entre depressão pós-parto e alterações tireoidianas.OBJECTIVES: to investigate the prevalence of post partum depression and its correlation with thyroid dysfunction in mothers. METHODS: a descriptive, cross-cutting observational study carried out among 292 women between the 31st and 180th days post partum, attending public health units in the Metropolitan Region of Vitória, in the State of Espírito Santo, Brazil. The sample was analyzed for socio-demographic and clinical-obstetric characteristics. A depressive disorder was defined by a score

  18. Treating cardiac arrhythmias detected with an implantable cardiac monitor in patients after an acute myocardial infarction

    DEFF Research Database (Denmark)

    Jøns, Christian; Thomsen, Poul Erik Bloch

    2012-01-01

    OPINION STATEMENT: Using an implantable cardiac monitor (ICM) in patients with acute myocardial infarction (MI) allows continuous electrocardiogram monitoring and provides a much more detailed picture of the incidence of brady- and tachyarrhythmias than conventional follow-up. The CARISMA study...... was the first to use the ICM in post-MI patients with moderate to severe left ventricular systolic dysfunction. Atrial fibrillation (AF) events lasting longer than 30 s were associated with an almost threefold increase in the risk of major cardiac events. This confirms the current definition of clinically...... significant AF episodes, as patients with episodes of shorter duration were not at increased risk. The association of AF to progressive heart failure, reinfarction, and cardiovascular death underlines the need for an intensive follow-up of post-MI patients with new-onset AF in order to reveal underlying...

  19. Endothelial NOS (NOS3) impairs myocardial function in developing sepsis.

    Science.gov (United States)

    van de Sandt, Annette M; Windler, Rainer; Gödecke, Axel; Ohlig, Jan; Zander, Simone; Reinartz, Michael; Graf, Jürgen; van Faassen, Ernst E; Rassaf, Tienush; Schrader, Jürgen; Kelm, Malte; Merx, Marc W

    2013-03-01

    Endothelial nitric oxide synthase (NOS)3-derived nitric oxide (NO) modulates inotropic response and diastolic interval for optimal cardiac performance under non-inflammatory conditions. In sepsis, excessive NO production plays a key role in severe hypotension and myocardial dysfunction. We aimed to determine the role of NOS3 on myocardial performance, NO production, and time course of sepsis development. NOS3(-/-) and C57BL/6 wildtype mice were rendered septic by cecum ligation and puncture (CLP). Cardiac function was analyzed by serial echocardiography, in vivo pressure and isolated heart measurements. Cardiac output (CO) increased to 160 % of baseline at 10 h after sepsis induction followed by a decline to 63 % of baseline after 18 h in wildtype mice. CO was unaltered in septic NOS3(-/-) mice. Despite the hyperdynamic state, cardiac function and mean arterial pressure were impaired in septic wildtype as early as 6 h post CLP. At 12 h, cardiac function in septic wildtype was refractory to catecholamines in vivo and respective isolated hearts showed impaired pressure development and limited coronary flow reserve. Hemodynamics remained stable in NOS3(-/-) mice leading to significant survival benefit. Unselective NOS inhibition in septic NOS3(-/-) mice diminished this survival benefit. Plasma NO( x )- and local myocardial NO( x )- and NO levels (via NO spin trapping) demonstrated enhanced NO( x )- and bioactive NO levels in septic wildtype as compared to NOS3(-/-) mice. Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility.

  20. Early Hepatic Dysfunction Is Associated with a Worse Outcome in Patients Presenting with Acute Respiratory Distress Syndrome: A Post-Hoc Analysis of the ACURASYS and PROSEVA Studies

    Science.gov (United States)

    Dizier, Stéphanie; Forel, Jean-Marie; Ayzac, Louis; Richard, Jean-Christophe; Hraiech, Sami; Lehingue, Samuel; Loundou, Anderson; Roch, Antoine; Guerin, Claude; Papazian, Laurent

    2015-01-01

    Introduction Bilirubin is well-recognized marker of hepatic dysfunction in intensive care unit (ICU) patients. Multiple organ failure often complicates acute respiratory distress syndrome (ARDS) evolution and is associated with high mortality. The effect of early hepatic dysfunction on ARDS mortality has been poorly investigated. We evaluated the incidence and the prognostic significance of increased serum bilirubin levels in the initial phase of ARDS. Methods The data of 805 patients with ARDS were retrospectively analysed. This population was extracted from two recent multicenter, prospective and randomised trials. Patients presenting with ARDS with a ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen < 150 mmHg measured with a PEEP ≥ 5 cm of water were included. The total serum bilirubin was measured at inclusion and at days 2, 4, 7 and 14. The primary objective was to analyse the bilirubin at inclusion according to the 90-day mortality rate. Results The 90-day mortality rate was 33.8% (n = 272). The non-survivors were older, had higher Sepsis-related Organ Failure Assessment (SOFA) score and were more likely to have a medical diagnosis on admission than the survivors. At inclusion, the SOFA score without the liver score (10.3±2.9 vs. 9.0±3.0, p<0.0001) and the serum bilirubin levels (36.1±57.0 vs. 20.5±31.5 μmol/L, p<0.0001) were significantly higher in the non-survivors than in the survivors. Age, the hepatic SOFA score, the coagulation SOFA score, the arterial pH level, and the plateau pressure were independently associated with 90-day mortality in patients with ARDS. Conclusion Bilirubin used as a surrogate marker of hepatic dysfunction and measured early in the course of ARDS was associated with the 90-day mortality rate. PMID:26636318

  1. Diastolic dysfunction in the critically ill patient.

    Science.gov (United States)

    Suárez, J C; López, P; Mancebo, J; Zapata, L

    2016-11-01

    Left ventricular diastolic dysfunction is a common finding in critically ill patients. It is characterized by a progressive deterioration of the relaxation and the compliance of the left ventricle. Two-dimensional and Doppler echocardiography is a cornerstone in its diagnosis. Acute pulmonary edema associated with hypertensive crisis is the most frequent presentation of diastolic dysfunction critically ill patients. Myocardial ischemia, sepsis and weaning failure from mechanical ventilation also may be associated with diastolic dysfunction. The treatment is based on the reduction of pulmonary congestion and left ventricular filling pressures. Some studies have found a prognostic role of diastolic dysfunction in some diseases such as sepsis. The present review aims to analyze thoroughly the echocardiographic diagnosis and the most frequent scenarios in critically ill patients in whom diastolic dysfunction plays a key role. Copyright © 2016 Elsevier España, S.L.U. y SEMICYUC. All rights reserved.

  2. Early and six-month outcome in patients with angina pectoris early after acute myocardial infarction (the GISSI-3 APPI [angina precoce post-infarto] study).

    Science.gov (United States)

    1996-12-01

    There is conflicting evidence whether or not early postinfarction angina implies an unfavorable prognosis. This prospective study assessed the significance and natural history of early angina in a broad population of patients conservatively managed after acute myocardial infarction (AMI) and enrolled in the third Gruppo Italiano per lo Studio della Sopravvivenza nel Infarto Miocardico (GISSI-3) trial. Out of 2,363 consecutive patients (age 63 +/- 11; first AMI in 86%; thrombolysis in 74%) admitted in 31 centers lacking on-site revascularization facilities, early angina associated with transient electrocardiographic (ECG) changes was documented in 332 (14%). At multivariate analysis, preinfarction angina, age > or = 70 years, female gender, and history of infarct were significant predictors of early angina. Though the in-hospital course was free from major cardiac events in 78% of patients after the first anginal episode, reinfarction was more common after early angina (7% vs 2% in patients without, RR 3.1, 95% confidence interval [CI] 1.9 to 5.6; p <0.001), and death occurred in 7% of patients with early angina (vs 5% of patients without, RR 1.4, CI 0.9 to 2.4, p = NS). No demographic or clinical characteristics identified patients who suffered nonfatal reinfarction after angina, and neither the ECG location (infarct zone or remote) nor patterns of ECG changes during angina proved significant predictors of in-hospital reinfarction or death. Early angina emerged as the sole independent predictor of 6-month cumulative reinfarction (12% vs 5% of patients without, RR 2.9, CI 2.0 to 4.4; p <0.0001) and an independent predictor of death (13% vs 7% of patients without early angina, RR 2.3, CI 1.6 to 3.3; p <0.0001). Early postinfarction angina is a powerful prognostic marker. Patients with early postinfarction angina had an unfavourable in-hospital outcome, but the prospective identification of patients at greater risk of major events after angina remains elusive

  3. Coronary microvascular dysfunction: an update

    Science.gov (United States)

    Crea, Filippo; Camici, Paolo G.; Bairey Merz, Cathleen Noel

    2014-01-01

    Many patients undergoing coronary angiography because of chest pain syndromes, believed to be indicative of obstructive atherosclerosis of the epicardial coronary arteries, are found to have normal angiograms. In the past two decades, a number of studies have reported that abnormalities in the function and structure of the coronary microcirculation may occur in patients without obstructive atherosclerosis, but with risk factors or with myocardial diseases as well as in patients with obstructive atherosclerosis; furthermore, coronary microvascular dysfunction (CMD) can be iatrogenic. In some instances, CMD represents an epiphenomenon, whereas in others it is an important marker of risk or may even contribute to the pathogenesis of cardiovascular and myocardial diseases, thus becoming a therapeutic target. This review article provides an update on the clinical relevance of CMD in different clinical settings and also the implications for therapy. PMID:24366916

  4. Erectile dysfunction.

    Science.gov (United States)

    Wylie, Kevan

    2008-01-01

    Erectile dysfunction is a common problem affecting sexual function in men. Approximately one in 10 men over the age of 40 is affected by this condition and the incidence is age related. Erectile dysfunction is a sentinel marker for several reversible conditions including peripheral and coronary vascular disease, hypertension and diabetes mellitus. Endothelial dysfunction is a common factor between the disease states. Concurrent conditions such as depression, late-onset hypogonadism, Peyronie's disease and lower urinary tract symptoms may significantly worsen erectile function, other sexual and relationship issues and penis dysmorphophobia. A focused physical examination and baseline laboratory investigations are mandatory. Management consists of initiating modifiable lifestyle changes, psychological and psychosexual/couples interventions and pharmacological and other interventions. In combination and with treatment of concurrent comorbid states, these interventions will often bring about successful resolution of symptoms and avoid the need for surgical interventions.

  5. Strapping for temporomandibular joint dysfunction

    Directory of Open Access Journals (Sweden)

    Babu Abraham

    2008-01-01

    Full Text Available Temporomandibular joint dysfunction (TMJD is a common problem seen in many of the dental clinics. Management of this depends on an accurate diagnosis of the cause for the TMJD. Physical therapy and rehabilitation play a vital role in the management of these dysfunctions. Physical therapy is useful in treating post-traumatic stiffness of the TMJ while strapping of the TMJ for a dysfunction along with conventional physical therapy is of benefit in terms of reduction in click, decrease in pain, and an improvement in function.

  6. Strapping for temporomandibular joint dysfunction.

    Science.gov (United States)

    Babu, Abraham Samuel; John, Sandhya Mary; Unni, Amith

    2008-01-01

    Temporomandibular joint dysfunction (TMJD) is a common problem seen in many of the dental clinics. Management of this depends on an accurate diagnosis of the cause for the TMJD. Physical therapy and rehabilitation play a vital role in the management of these dysfunctions. Physical therapy is useful in treating post-traumatic stiffness of the TMJ while strapping of the TMJ for a dysfunction along with conventional physical therapy is of benefit in terms of reduction in click, decrease in pain, and an improvement in function.

  7. Does the type and severity of brain injury predict hypothalamo-pituitary dysfunction? Does post-traumatic hypopituitarism predict worse outcome?

    DEFF Research Database (Denmark)

    Klose, M.; Feldt-Rasmussen, U.

    2008-01-01

    of reliable predictors is of utmost importance in order to secure a cost-effective screening strategy. It has not yet been possible to identify early hormone alterations as a useful tool for the prediction of long-term post-traumatic hypopituitarism, whereas indicators of increased trauma severity have been...... reported as predictive in an increasing number of studies. Outcome studies have moreover indicated that post-traumatic hypopituitarism is of clinical significance, which may justify introduction of neuroendocrine screening in TBI. Much larger cohorts are, however, still needed for further evaluation...

  8. Nobiletin attenuates adverse cardiac remodeling after acute myocardial infarction in rats via restoring autophagy flux.

    Science.gov (United States)

    Wu, Xiaoqian; Zheng, Dechong; Qin, Yuyan; Liu, Zumei; Zhang, Guiping; Zhu, Xiaoyan; Zeng, Lihuan; Liang, Zhenye

    2017-10-14

    Our previous study showed that autophagy flux was impaired with sustained heart ischemia, which exacerbated adverse cardiac remodeling after acute myocardial infarction (AMI). Here we investigated whether Nobiletin, a citrus polymethoxylated flavonoids, could restore the autophagy flux and improve cardiac prognosis after AMI. AMI was induced by ligating left anterior descending (LAD) coronary artery in rats. Nobiletin improved the post-infarct cardiac dysfunction significantly and attenuated adverse cardiac remodeling. Meanwhile, Nobiletin protected H9C2 cells against oxygen glucose deprivation (OGD) in vitro. The impaired autophagy flux due to ischemia was ameliorated after Nobiletin treatment by testing the autophagy substrate, LC3BⅡ and P62 protein level both in vivo and in vitro. GFP-mRFP-LC3 adenovirus transfection also supported that Nobiletin restored the impaired autophagy flux. Specifically, the autophagy flux inhibitor, chloroquine, but not 3 MA, alleviated Nobiletin-mediated protection against OGD. Notably, Nobiletin does not affect the activation of classical upstream autophagy signaling pathways. However, Nobiletin increased the lysosome acidation which also supported that Nobiletin accelerated autophagy flux. Taken together, our findings suggested that Nobiletin restored impaired autophagy flux and protected against acute myocardial infarction, suggesting a potential role of autophagy flux in Nobiletin-mediated myocardial protection. Copyright © 2017 Elsevier Inc. All rights reserved.

  9. Up-regulation of cardiac nitric oxide synthase 1-derived nitric oxide after myocardial infarction in senescent rats.

    Science.gov (United States)

    Damy, Thibaud; Ratajczak, Philippe; Robidel, Estelle; Bendall, Jennifer K; Oliviéro, Patricia; Boczkowski, Jorge; Ebrahimian, Talin; Marotte, Françoise; Samuel, Jane-Lise; Heymes, Christophe

    2003-10-01

    Nitric oxide (NO) has been implicated in the development of heart failure, although the source, significance, and functional role of the different NO synthase (NOS) isoforms in this pathology are controversial. The presence of a neuronal-type NOS isoform (NOS1) in the cardiac sarcoplasmic reticulum has been recently discovered, leading to the hypothesis that NOS1-derived NO may notably alter myocardial inotropy. However, the regulation and role(s) of NOS1 in cardiac diseases remain to be determined. Using an experimental model of myocardial infarction (MI) in senescent rats, we demonstrated a significant increase in cardiac NOS1 expression and activity in MI, coupled with the translocation of this enzyme to the sarcolemma through interactions with caveolin-3. The enhanced NOS1 activity counteracts the decrease in cardiac NOS3 expression and activity observed in heart failure. We demonstrated an increased interaction between NOS1 and its regulatory protein HSP90 in post-MI hearts, a potential mechanism for the higher NOS1 activity in this setting. Finally, preferential in vivo inhibition of NOS1 activity enhanced basal post-MI left ventricular dysfunction in senescent rats. These results provide the first evidence that increased NOS1-derived NO production may play a significant role in the autocrine regulation of myocardial contractility after MI in aging rats.

  10. Erectile dysfunction

    African Journals Online (AJOL)

    that increase blood flow to the penis. The blood ... The pressure of the blood in the chambers makes the ... What are the risk factors for erectile dysfunction? The most .... losing excessive weight and increasing physical activity, may improve the ...

  11. 血清尿酸与急性心肌梗死合并慢性肾功能不全患者预后的关系%Association between serum uric acid level and prognosis of patients with acute myocardial infarction andchronic renal dysfunction

    Institute of Scientific and Technical Information of China (English)

    赵宇飞; 程自平; 王麟

    2016-01-01

    Objective To determine the association between serum uric acid level and prognosis of patients withacute myocardial infarc-tion and chronic renal dysfunction.Methods Totally 512 acute myocardial infarction patients with chronic renal dysfunction were en-rolled in this study.These patients were assigned into two groups:high uric acid group(n =200)and low uric acid group(n =312). Basic clinical characters were analyzed and major adverse cardiovascular events(MACEs)were observed during 48-month follow-up. Results The results showed that during 48-month follow-up,death of any cause occurred in 1.0% patients(2 of 200)in low uric acid group,as compared with 5.3% in the high uric acid group (17 of 312)(hazard ratio,5.379;95% confidence interval,1.204 to 24.035;P =0.028).The incidences of stroke,heart failure and revascularization weresignificantly higher in high uric acidgroup.Con-clusions High serum uric acid level increases the incidences of death,revascularization,stroke and heart failure in acute myocardial infarction patients with chronic renal dysfunction.%目的:探讨血清尿酸水平对合并有慢性肾功能不全的急性心肌梗死患者远期预后的影响。方法选取512例合并有慢性肾功能不全的急性心肌梗死患者,按血清尿酸水平分为低尿酸组(n =200)和高尿酸组(n =312),分析各组病变血管、临床生化指标、合并症以及治疗情况,并对所有患者进行48个月随访,观察各组远期严重心血管不良事件。结果低尿酸组中共有2例患者死亡,高尿酸组中17例患者死亡(风险比:5.379;95%置信区间,1.204~24.035;P =0.028)。高尿酸组卒中、心衰和血运重建发生率均高于低尿酸组,且差异有统计学意义。结论合并有慢性肾功能不全的急性心肌梗死患者血清尿酸水平升高会导致患者远期死亡率、卒中发生率、心衰发生率和血运重建发生率增加。

  12. Association between the polymorphism of A9570G in angiotensin I converting enzyme 2 gene and cardiac dysfunction and ventricular remodeling after myocardial infarction%ACE2基因多态性与心肌梗死后心功能不全及心室重构的相关性研究

    Institute of Scientific and Technical Information of China (English)

    陈文忠; 周永健; 周劲东; 李志樑; 徐春生

    2010-01-01

    Objective To determine the effects of polymorphism of A9570G in angiotensin I converting enzyme 2 gene ( ACE2) gene on cardiac dysfunction and ventricular remodeling after myocardial infarction. Methods 252 patients with old myccardial infarction were included in this study. They were classified according to their polymorphisms of ACE 2 gene analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Echocardiograms were used to determine left ventricular end diastolic diameters (LVEDd) , Left ventricular mass index (LVMI) , mitral flow pattern early diastolic and late diastolic peak flow ratio (E/A) and left ventricular ejection fraction ( LVEF). Results In male, LVEDd, LVMI, and LVEF had significant difference among ACE2 genotypes ( t = 2. 609,3.527and 2.063, P =0.010,0.001 and 0.041), and no significant differences in E/A( t =0.689,P =0.492). In female,LVEDd, LVMI, E/A and LVEF had no significant difference among ACE2 genotypes( F =0. 848, 0.077,0. 985 and 1.611, P = 0. 432,0. 926,0. 377 and 0. 205 ). Conclusion The polymorphism of A9570G in ACE2 gene may be associated with cardiac dysfunction and ventricular remodeling after myocardial infarction in male. ACE 2 gene polymorphism may be a genetic factor on cardiac dysfunction and ventricular remodeling after myocardial infarction.%目的 研究血管紧张素转换酶2基因A9570G多态性与心肌梗死后心功能不全及心室重构的关系.方法 收集252例陈旧性心肌梗死患者,采取外周血2ml提取DNA,多聚酶链扩增反应及限制性内切酶法检测ACE2基因A9570G基因型,按基因型进行分组,采用超声心动图比较不同基因型间患者LVEF,E/A,LVEDd及LVMI的差异.结果 在男性,G基因型组LVEF、LVEDd、LVMI与A基因型组比较,差异有统计学意义(t=2.609、3.527、2.063,P0.05);在女性,3种基因型间患者LVEF、E/A、LVEDd及LVMI差异均无统计学意义(P>0.05).结论 ACE2基因A9570G多态性与男性心肌梗死后

  13. Implantable cardiac monitors in high-risk post-infarction patients with cardiac autonomic dysfunction and moderately reduced left ventricular ejection fraction: Design and rationale of the SMART-MI trial.

    Science.gov (United States)

    Hamm, Wolfgang; Rizas, Konstantinos D; Stülpnagel, Lukas von; Vdovin, Nikolay; Massberg, Steffen; Kääb, Stefan; Bauer, Axel

    2017-08-01

    Most deaths after myocardial infarction (MI) occur in patients with left ventricular ejection fraction (LVEF) >35%, for whom no specific prophylactic strategies exist. Deceleration capacity (DC) of heart rate and periodic repolarization dynamics (PRD) are noninvasive electrophysiological markers depending on the vagal and sympathetic tone. The combination of abnormal DC and/or PRD identifies a new high-risk group among postinfarction patients with LVEF 36%-50%. This new high-risk group has similar characteristics with respect to prognosis and patient numbers to those of the established high-risk group identified by LVEF ≤ 35%. The SMART-MI trial is an investigator-initiated randomized prospective multicenter trial that tests the efficacy of implantable cardiac monitors (ICM) in this new high-risk group. The study will enroll approximately 1,600 survivors of acute MI with sinus rhythm and an LVEF of 35%-50% in 17 centers in Germany who will be tested for presence of cardiac autonomic dysfunction. Four hundred patients with either abnormal DC (≤2.5 ms) and/or PRD (≥5.75deg(2)) will be randomized in a 1:1 fashion to intensive follow-up via telemonitoring using an ICM device (experimental arm) or conventional follow-up (control arm). For the ICM arm, specific treatment paths have been developed according to current guidelines. The primary end point is time to detection of predefined serious arrhythmic events during follow-up, including atrial fibrillation ≥6minutes, nonsustained ventricular tachycardia (cycle length≤320 ms; ≥40 beats), atrioventricular block ≥IIb, and sustained ventricular tachycardia/ventricular fibrillation. The median follow-up period is 18months with a minimum follow-up of 6months. The effect of remote monitoring on clinical outcomes will be tested as secondary outcome measure (ClinicalTrials.gov NCT02594488). Copyright © 2017 Elsevier Inc. All rights reserved.

  14. The observation about the effect of cognitive behavioral therapy in post stroke depression and nervous dysfunction%认知行为疗法对脑卒中后抑郁及神经功能康复的影响

    Institute of Scientific and Technical Information of China (English)

    梁翠萍; 孙素娟; 张卫红; 孙军雪; 刘夕霞

    2011-01-01

    Objective : To explore the effect of cognitive behavioral therapy on patients with post - stroke depression and nervous dysfunction. Methods : The 178 patients of post - stroke depression were randomly divided into treatment group and control group,89patients in each group. Treatment group accepted cognitive behavioral therapy on the hase of conventional therapy and control group accepted conventional therapy. The Self - Rating Depress Scale and Neurological Function Deficit Scale were used in the two groups before and after the treatment. Results : After 5 weeks. the scores of Self - Rating Depression and Neurological Function Deficit in the therapy group were lower than in the control group( P < 0. 01 ). Conclusion : Cognitive behavioral therapy can significantly improve the depression and promote nervous dysfunction in stroke.%目的:探讨认知行为疗法对脑卒中后抑郁及神经功能康复的临床疗效.方法:以178例脑卒中后抑郁患者为研究对象,依随机的形式分为治疗组和对照组,各89例,两组患者均采用常规治疗,治疗组则在此基础之上给予认知行为疗法.治疗前、后分别采用抑郁量表和神经功能缺损程度量表进行测评.结果:治疗组治疗5周后抑郁量表评分和神经功能缺损评分明显低于对照组,有显著性差异(P<0.01).结论:认知行为疗法对改善脑卒中后抑郁、促进神经功能康复效果显著.

  15. Combretastatin A4 disodium phosphate-induced myocardial injury

    Science.gov (United States)

    Tochinai, Ryota; Nagata, Yuriko; Ando, Minoru; Hata, Chie; Suzuki, Tomo; Asakawa, Naoyuki; Yoshizawa, Kazuhiko; Uchida, Kazumi; Kado, Shoichi; Kobayashi, Toshihide; Kaneko, Kimiyuki; Kuwahara, Masayoshi

    2016-01-01

    Histopathological and electrocardiographic features of myocardial lesions induced by combretastatin A4 disodium phosphate (CA4DP) were evaluated, and the relation between myocardial lesions and vascular changes and the direct toxic effect of CA4DP on cardiomyocytes were discussed. We induced myocardial lesions by administration of CA4DP to rats and evaluated myocardial damage by histopathologic examination and electrocardiography. We evaluated blood pressure (BP) of CA4DP-treated rats and effects of CA4DP on cellular impedance-based contractility of human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs). The results revealed multifocal myocardial necrosis with a predilection for the interventricular septum and subendocardial regions of the apex of the left ventricular wall, injury of capillaries, morphological change of the ST junction, and QT interval prolongation. The histopathological profile of myocardial lesions suggested that CA4DP induced a lack of myocardial blood flow. CA4DP increased the diastolic BP and showed direct effects on hiPS-CMs. These results suggest that CA4DP induces dysfunction of small arteries and capillaries and has direct toxicity in cardiomyocytes. Therefore, it is thought that CA4DP induced capillary and myocardial injury due to collapse of the microcirculation in the myocardium. Moreover, the direct toxic effect of CA4DP on cardiomyocytes induced myocardial lesions in a coordinated manner. PMID:27559241

  16. Classification of myocardial infarction

    DEFF Research Database (Denmark)

    Saaby, Lotte; Poulsen, Tina Svenstrup; Hosbond, Susanne Elisabeth

    2013-01-01

    The classification of myocardial infarction into 5 types was introduced in 2007 as an important component of the universal definition. In contrast to the plaque rupture-related type 1 myocardial infarction, type 2 myocardial infarction is considered to be caused by an imbalance between demand...... and supply of oxygen in the myocardium. However, no specific criteria for type 2 myocardial infarction have been established....

  17. Post-stroke hand dysfunction treated with acupuncture at Zhongzhu(TE 3) and Waiguan(TE 5)%针刺中渚、外关治疗脑卒中后手功能障碍

    Institute of Scientific and Technical Information of China (English)

    程先宽; 王征美; 孙岚; 李玉华

    2011-01-01

    目的:观察针刺中渚、外关改善脑卒中后手功能障碍的临床疗效.方法:将60例脑卒中后手功能障碍患者随机分为观察组和对照组,每组30例,两组均给予常规药物治疗及物理治疗、作业治疗等康复训练.观察组加针刺患手中渚、外关.两组治疗前后分别进行神经功能缺损评分、手功能、步行能力、日常生活活动能力(ADL)改良巴氏指数量表等评定.结果:两组患者治疗后,手功能、步行能力、ADL、NIHSS评分较治疗前均有明显改善(均P<0.01).观察组手功能、步行能力、ADL改善较对照组更为明显(均P<0.05).结论:脑卒中后手功能障碍患者常规药物治疗及康复训练配合针刺中渚、外关治疗,能明显改善脑卒中后手功能障碍,提高步行能力.提高日常生活活动能力,提高康复疗效.%Objective To observe the curative effects of post-stroke hand dysfunction treated with acupuncture at Zhongzhu(TE 3) and Waiguan(TE 5).Methods Sixty cases of post-stroke hand dysfunction were randomly divided into an observation group(30 cases) and a control group(30 cases).Routine medicine, physical therapy, occupational therapy and other rehabilitation trainings were applied in both groups; Zhongzhu(TE 3) and Waiguan(TE 5) were punctured in observation group.Scores of nervous functions deficit by the National Institutes of Health Stroke Scale (NIHSS), hand function, walking ability, activities of daily living (ADL) by Modified Barthel Index Scale were evaluated in both groups before and after treatment.Results After treatment, the scores of hand function, walking ability, ADL and NIHSS were improved in both groups(all P<0.01), and the hand function, walking ability and ADL in observation group were superior to those in control group (all P<0.05).Conclusion Routine medicine and rehabilitation trainings combined with acupuncture at Zhongzhu (TE 3) and Waiguan (TE 5) to treat post-stroke hand dysfunction can obviously

  18. Pulmonary arterial hypertension secondary to chronic left-sided cardiac dysfunction in dogs.

    Science.gov (United States)

    Stepien, Rebecca L

    2009-09-01

    Pulmonary arterial hypertension is a description of a physiological finding rather than a diagnosis. Pulmonary arterial pressure is the result of interactions among pulmonary blood flow (right ventricular cardiac output), pulmonary vascular impedance and post-capillary pressure (typically reflecting left atrial pressure). When elevations in pulmonary arterial pressure (systolic/diastolic pulmonary arterial pressure > approximately 30/19 mmHg at rest) are accompanied by increased left atrial pressure, pulmonary arterial hypertension may be considered secondary to left-heart failure. Introduction of Doppler methods to diagnose pulmonary arterial hypertension has increased the awareness of the prevalence and importance of pulmonary arterial hypertension dogs with left-heart failure. Increasing understanding of the mechanism of development of pulmonary venous hypertension and reactive pulmonary arterial hypertension in dogs with left-heart disease has led to the development of successful additive therapies for progressive clinical signs in the setting of chronic therapy for congestive heart failure due to left-sided valvular and myocardial dysfunction. Because effective therapies for pulmonary arterial hypertension secondary to chronic left-sided cardiac dysfunction are now available, screening for pulmonary arterial hypertension should be a regular part of the Doppler echocardiographic examination in a clinical setting of chronic therapy for left-sided congestive heart failure due to valvular or myocardial disease.

  19. Ketamine and midazolam differently impact post-intubation hemodynamic profile when used as induction agents during emergency airway management in hemodynamically stable patients with ST elevation myocardial infarction.

    Science.gov (United States)

    Zuin, Marco; Rigatelli, Gianluca; Dell'Avvocata, Fabio; Faggian, Giuseppe; Conte, Luca; Giatti, Sara; Michielan, Flavio; Roncon, Loris

    2017-09-09

    We investigated the incidence of post-intubation hypotension (PIH) in hemodynamically stable patients with STEMI requiring rapid sequences intubation (RSI) and medicated with ketamine or midazolam as induction agent. STEMI patients admitted between 1st January 2009 and 1st January 2017 who did not receive any type of inotropic support before the endotracheal intubation (ETI) was reviewed. PIH was defined as a reduction greater than 20% or a drop of systolic blood pressure (SBP) below 90 mmHg within 10 min from the administration of the induction agent [ketamine (1 mg/kg) or midazolam (0.3 mg/kg)]. Over the study period, 136 patients (66 male and 70 females, mean age 72.25 ± 7.33 years) met the inclusion criteria. Patients treated with midazolam and ketamine were 63 and 73, respectively. PIH was observed in 38 (27.9%) patients after 10 min from ETI. Midazolam patients had a significant lower SBP at both 5 and 10 min after induction (97.75 ± 8.06 vs 100.81 ± 8.08, p = 0.029 and 92.83 ± 7.53 vs 101.58 ± 7.29, p predictors of PIH in STEMI patients treated with midazolam, as induction agent, before ETI. Midazolam was more likely than ketamine to cause significant PIH when used as an induction agent for RSI in hemodynamically stable patients with STEMI.

  20. Post cardiac injury syndrome

    DEFF Research Database (Denmark)

    Nielsen, S L; Nielsen, F E

    1991-01-01

    The post-pericardiotomy syndrome is a symptom complex which is similar in many respects to the post-myocardial infarction syndrome and these are summarized under the diagnosis of the Post Cardiac Injury Syndrome (PCIS). This condition, which is observed most frequently after open heart surgery, i...... on the coronary vessels, with cardiac tamponade and chronic pericardial exudate. In the lighter cases, PCIS may be treated with NSAID and, in the more severe cases, with systemic glucocorticoid which has a prompt effect....

  1. Transient myocardial ischemia after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction...... the prevalence of ambulatory or transient myocardial ischemia is lower than in patients with chronic, stable coronary artery disease. A greater proportion of ischemic episodes, however, are silent than in other subgroups with ischemic heart disease. Early after the infarction, transient myocardial ischemia...... exhibits a circadian variation with a peak activity occurring in the late evening hours. Patients with non-Q wave infarction have more transient myocardial ischemia, whereas thrombolytic therapy seems to result in less residual ischemia. Exercise testing is more sensitive than ambulatory monitoring...

  2. Transient myocardial ischemia after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction...... the prevalence of ambulatory or transient myocardial ischemia is lower than in patients with chronic, stable coronary artery disease. A greater proportion of ischemic episodes, however, are silent than in other subgroups with ischemic heart disease. Early after the infarction, transient myocardial ischemia...... exhibits a circadian variation with a peak activity occurring in the late evening hours. Patients with non-Q wave infarction have more transient myocardial ischemia, whereas thrombolytic therapy seems to result in less residual ischemia. Exercise testing is more sensitive than ambulatory monitoring...

  3. Oral Dysfunction

    OpenAIRE

    鈴木, 規子; スズキ, ノリコ; Noriko, SUZUKI

    2004-01-01

    The major oral functions can be categorized as mastication, swallowing, speech and respiratory functions. Dysfunction of these results in dysphagia, speech disorders and abnormal respiration (such as Sleep Apnea). These functions relate to dentistry in the occurrence of : (1) oral preparatory and oral phases, (2) articulation disorders and velopharyngeal incompetence (VPI), and (3) mouth breathing, respiratory and blowing disorders. These disorders are related to oral and maxillofacial diseas...

  4. [Myocardial infarction caused by exertion].

    Science.gov (United States)

    Bernard, F; Weber, S

    1997-01-01

    Myocardial infarction is the main cause of sudden death during physical exercise, particularly in subjects over 40 and may even occur in high-performance young athletes. Sports and physical activity have a beneficial effect in preventing cardiovascular diseases, but certain rules of prudence must be followed to avoid the risk of a severe coronary event. Myocardial infarction always occurs in particularly susceptible subjects with several risk factors, predominantly smoking, hypercholesterolemia, family history of atherosclerosis. Dietary factors, either before, during or after the exercise, are always found. Distribution of coronary lesions differs with age. Before 40 years,