WorldWideScience

Sample records for acute reperfused myocardial

  1. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade

    NARCIS (Netherlands)

    Henriques, JPS; Zijlstra, F; van 't Hof, AWJ; de Boer, MJ; Gosselink, M; Hoorntje, JCA; Suryapranata, H; Dambrink, Jan Hendrik Everwijn

    2003-01-01

    Background-Angiographic successful reperfusion in acute myocardial infarction has been defined as TIMI 3 flow. However, TIMI 3 flow does not always result in effective myocardial reperfusion. Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We hypothesized that

  2. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade

    NARCIS (Netherlands)

    Henriques, Jose P. S.; Zijlstra, Felix; van 't Hof, Arnoud W. J.; de Boer, Menko-Jan; Dambrink, Jan-Henk E.; Gosselink, Marcel; Hoorntje, Jan C. A.; Suryapranata, Harry

    2003-01-01

    Angiographic successful reperfusion in acute myocardial infarction has been defined as TIMI 3 flow. However, TIMI 3 flow does not always result in effective myocardial reperfusion. Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We hypothesized that optimal

  3. Myocardium and microvessel endothelium apoptosis at day 7 following reperfused acute myocardial infarction.

    Science.gov (United States)

    Kang, Sheng; Yang, Yue-jin; Wu, Yi-ling; Chen, Yu-tong; Li, Li; Tian, Yi

    2010-01-01

    This study was to investigate the salvaged myocardial and microvascular endothelial cells apoptosis at the first week of reperfused acute myocardial infarction (AMI). Sixteen mini swines (20-30 kg) were randomly assigned to the sham-operated group and the AMI group. The acute myocardial infarction and reperfusion model was created, and pathologic myocardial tissue was collected at day 7 following left anterior descending coronary artery reperfusion, and detected by transmission electron microscope, in situ cell apoptosis detection (TUNEL method), Real-time Quantitative Polymerase Chain Reaction and Western blot. In the AMI group, the infarcted area showed the myolysis, fibroblast and injuried endothelial cells under transmission electron microscope. The infarcted area had higher apoptotic index of microvascular endothelial cells than the marginal area, the normal area, and the sham-operated area (all Pinfarcted area were higher than those in the marginal area, the normal area, and the sham-operated area (all Pinfarcted and marginal areas compared with the normal area and the sham-operated area. The overexpressions of Fas and Bax or the low expression of Bcl-2 in the infarcted and marginal heart tissue may play an important role in the acceleration of myocardial and endothelial apoptosis at 7th day following reperfused acute myocardial infarction. Copyright 2009 Elsevier Inc. All rights reserved.

  4. Effects of Chronic and Acute Zinc Supplementation on Myocardial Ischemia-Reperfusion Injury in Rats.

    Science.gov (United States)

    Ozyıldırım, Serhan; Baltaci, Abdulkerim Kasim; Sahna, Engin; Mogulkoc, Rasim

    2017-07-01

    The present study aims to explore the effects of chronic and acute zinc sulfate supplementation on myocardial ischemia-reperfusion injury in rats. The study registered 50 adult male rats which were divided into five groups in equal numbers as follows: group 1, normal control; group 2, sham; group 3, myocardial ischemia reperfusion (My/IR): the group which was fed on a normal diet and in which myocardial I/R was induced; group 4, myocardial ischemia reperfusion + chronic zinc: (5 mg/kg i.p. zinc sulfate for 15 days); and group 5, myocardial ischemia reperfusion + acute zinc: the group which was administered 15 mg/kg i.p. zinc sulfate an hour before the operation and in which myocardial I/R was induced. The collected blood and cardiac tissue samples were analyzed using spectrophotometric method to determine levels of MDA, as an indicator of tissue injury, and GSH, as an indicator of antioxidant activity. The highest plasma and heart tissue MDA levels were measured in group 3 (p zinc administration and markedly by chronic zinc supplementation.

  5. Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists

    Science.gov (United States)

    Neri, Margherita; Pascale, Natascha; Pomara, Cristoforo

    2017-01-01

    Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI. PMID:28286377

  6. Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice.

    Science.gov (United States)

    Muzumdar, Radhika H; Huffman, Derek M; Calvert, John W; Jha, Saurabh; Weinberg, Yoni; Cui, Lingguang; Nemkal, Anjana; Atzmon, Gil; Klein, Laura; Gundewar, Susheel; Ji, Sang Yong; Lavu, Madhav; Predmore, Benjamin L; Lefer, David J

    2010-10-01

    Humanin (HN), an endogenous antiapoptotic peptide, has previously been shown to protect against Alzheimer's disease and a variety of cellular insults. We evaluated the effects of a potent analog of HN (HNG) in an in vivo murine model of myocardial ischemia and reperfusion. Male C57BL6/J mice (8 to 10 week old) were subjected to 45 minutes of left coronary artery occlusion followed by a 24-hour reperfusion. HNG or vehicle was administered IP 1 hour prior or at the time of reperfusion. The extent of myocardial infarction per area-at-risk was evaluated at 24 hours using Evans Blue dye and 2-3-5-triphenyl tetrazolium chloride staining. Left ventricular function was evaluated at 1 week after ischemia using high-resolution, 2D echocardiography (VisualSonics Vevo 770). Myocardial cell signaling pathways and apoptotic markers were assessed at various time points (0 to 24 hours) following reperfusion. Cardiomyocyte survival and apoptosis in response to HNG were assessed in vitro. HNG reduced infarct size relative to the area-at-risk in a dose-dependent fashion, with a maximal reduction at the dose of 2 mg/kg. HNG therapy enhanced left ventricular ejection fraction and preserved postischemic left ventricular dimensions (end-diastolic and end-systolic), resulting in improved cardiac function. Treatment with HNG significantly increased phosphorylation of AMPK and phosphorylation of endothelial nitric oxide synthase in the heart and attenuated Bcl-2-associated X protein and B-cell lymphoma-2 levels following myocardial ischemia and reperfusion. HNG improved cardiomyocyte survival and decreased apoptosis in response to daunorubicin in vitro. These data show that HNG provides cardioprotection in a mouse model of myocardial ischemia and reperfusion potentially through activation of AMPK-endothelial nitric oxide synthase-mediated signaling and regulation of apoptotic factors. HNG may represent a novel agent for the treatment of acute myocardial infarction.

  7. Myocardial Hemorrhage After Acute Reperfused ST-Segment–Elevation Myocardial Infarction

    Science.gov (United States)

    Carrick, David; Haig, Caroline; Ahmed, Nadeem; McEntegart, Margaret; Petrie, Mark C.; Eteiba, Hany; Hood, Stuart; Watkins, Stuart; Lindsay, M. Mitchell; Davie, Andrew; Mahrous, Ahmed; Mordi, Ify; Rauhalammi, Samuli; Sattar, Naveed; Welsh, Paul; Radjenovic, Aleksandra; Ford, Ian; Oldroyd, Keith G.

    2016-01-01

    Background— The success of coronary reperfusion therapy in ST-segment–elevation myocardial infarction (MI) is commonly limited by failure to restore microvascular perfusion. Methods and Results— We performed a prospective cohort study in patients with reperfused ST-segment–elevation MI who underwent cardiac magnetic resonance 2 days (n=286) and 6 months (n=228) post MI. A serial imaging time-course study was also performed (n=30 participants; 4 cardiac magnetic resonance scans): 4 to 12 hours, 2 days, 10 days, and 7 months post reperfusion. Myocardial hemorrhage was taken to represent a hypointense infarct core with a T2* value of hemorrhage 2 days post MI was associated with clinical characteristics indicative of MI severity and inflammation. Myocardial hemorrhage was a multivariable associate of adverse remodeling (odds ratio [95% confidence interval]: 2.64 [1.07–6.49]; P=0.035). Ten (4%) patients had a cardiovascular cause of death or experienced a heart failure event post discharge, and myocardial hemorrhage, but not microvascular obstruction, was associated with this composite adverse outcome (hazard ratio, 5.89; 95% confidence interval, 1.25–27.74; P=0.025), including after adjustment for baseline left ventricular end-diastolic volume. In the serial imaging time-course study, myocardial hemorrhage occurred in 7 (23%), 13 (43%), 11 (33%), and 4 (13%) patients 4 to 12 hours, 2 days, 10 days, and 7 months post reperfusion. The amount of hemorrhage (median [interquartile range], 7.0 [4.9–7.5]; % left ventricular mass) peaked on day 2 (Phemorrhage and microvascular obstruction follow distinct time courses post ST-segment–elevation MI. Myocardial hemorrhage was more closely associated with adverse outcomes than microvascular obstruction. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT02072850. PMID:26763281

  8. Dexrazoxane Shows No Protective Effect in the Acute Phase of Reperfusion during Myocardial Infarction in Pigs.

    Science.gov (United States)

    Kamat, Pranitha; Vandenberghe, Stijn; Christen, Stephan; Bongoni, Anjan K; Meier, Bernhard; Rieben, Robert; Khattab, Ahmed A

    2016-01-01

    Calcium and iron overload participate in the mechanisms of ischemia/reperfusion (I/R) injury during myocardial infarction (MI). Calcium overload induces cardiomyocyte death by hypercontraction, while iron catalyses generation of reactive oxygen species (ROS). We therefore hypothesized that dexrazoxane, an intracellular metal chelator, would attenuate I/R injury. MI was induced in pigs by occlusion of the left anterior descending artery for 1 hour followed by 2 hours reperfusion. Thirty minutes before reperfusion either 5 mg/ml dexrazoxane (n = 5) or saline (n = 5) was infused intravenously. Myocardial necrosis as percentage of the area at ischemic risk was found to be similar in both groups (77.2 ± 18% for dexrazoxane and 76.4 ± 14% for saline group) as determined by triphenyl tetrazolium chloride staining of the ischemic myocardium. Also, serum levels of troponin-I were similar in both groups. A conductance catheter was used to measure left ventricular pressure and volume at all times. Markers for tissue damage due to ROS (HNE), endothelial cell activation (CD31) and inflammation (IgG, C3b/c, C5b9, MCP-1) were assessed on tissue and/or in serum. No significant differences were observed between the groups for the parameters analyzed. To conclude, in this clinically relevant model of early reperfusion after acute myocardial ischemia, dexrazoxane lacked attenuating effects on I/R injury as shown by the measured parameters.

  9. Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia Reperfusion in Rats

    Energy Technology Data Exchange (ETDEWEB)

    Takhtfooladi, Hamed Ashrafzadeh; Asl, Adel Haghighi Khiabanian [Department of Pathobiology, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Shahzamani, Mehran [Department of Cardiovascular Surgery, Isfahan University of Medical Sciences, Tehran (Iran, Islamic Republic of); Takhtfooladi, Mohammad Ashrafzadeh, E-mail: dr-ashrafzadeh@yahoo.com [Young Researchers and Elites Club, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Allahverdi, Amin [Department of Surgery, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Khansari, Mohammadreza [Department of Physiology, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of)

    2015-08-15

    Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries. This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. Thirty healthy mature male Wistar rats were allocated randomly into three groups: Group I (sham), Group II (IR), and Group III (IR + tramadol). Ischemia was induced in anesthetized rats by left femoral artery clamping for 3 h, followed by 3 h of reperfusion. Tramadol (20 mg/kg, intravenous) was administered immediately prior to reperfusion. At the end of the reperfusion, animals were euthanized, and hearts were harvested for histological and biochemical examination. The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were higher in Groups I and III than those in Group II (p < 0.05). In comparison with other groups, tissue malondialdehyde (MDA) levels in Group II were significantly increased (p < 0.05), and this increase was prevented by tramadol. Histopathological changes, including microscopic bleeding, edema, neutrophil infiltration, and necrosis, were scored. The total injuryscore in Group III was significantly decreased (p < 0.05) compared with Group II. From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model.

  10. B-type natriuretic peptide as a predictor of ischemia/reperfusion injury immediately after myocardial reperfusion in patients with ST-segment elevation acute myocardial infarction.

    Science.gov (United States)

    Arakawa, Kentaro; Himeno, Hideo; Kirigaya, Jin; Otomo, Fumie; Matsushita, Kensuke; Nakahashi, Hidefumi; Shimizu, Satoru; Nitta, Manabu; Takamizawa, Tetsu; Yano, Hideto; Endo, Mitsuaki; Kanna, Masahiko; Kimura, Kazuo; Umemura, Satoshi

    2016-02-01

    In animal models of acute myocardial infarction (AMI), B-type natriuretic peptide (BNP) administered before and during coronary occlusion limits infarct size. However, the relation between plasma BNP levels and ischemia/reperfusion injury remains unclear. 302 patients with ST-segment elevation AMI (STEMI) received emergency percutaneous coronary intervention within six hours from the onset. The patients were divided into two groups according to the plasma BNP level before angiography: group L (n=151), BNP ≤ 32.2 pg/ml; group H (n=151), BNP >32.2 pg/ml. The Selvester QRS-scoring system was used to estimate infarct size. The rate of ischemia/reperfusion injury immediately after reperfusion, defined as reperfusion ventricular arrhythmias (26% vs. 11%, p=0.001) and ST-segment re-elevation (44% vs. 22%, p=0.008), was higher in group L than in group H. Group L had a greater increase in the QRS score during percutaneous coronary intervention (3.55 ± 0.17 vs. 2.09 ± 0.17, preperfusion injury (odds ratio, 2.620; preperfusion injury according to decreasing quartiles of BNP level, as compared with the highest quartile, were 1.536, 3.692 and 4.964, respectively (p trend=0.002). Plasma BNP level before percutaneous coronary intervention may be a predictor of ischemia/reperfusion injury and the resultant extent of myocardial damage. Our findings suggest that high plasma BNP levels might have a clinically important protective effect on ischemic myocardium in patients with STEMI who receive percutaneous coronary intervention. © The European Society of Cardiology 2015.

  11. Nitric oxide treatments as adjuncts to reperfusion in acute myocardial infarction: a systematic review of experimental and clinical studies.

    Science.gov (United States)

    Bice, Justin S; Jones, Bethan R; Chamberlain, Georgia R; Baxter, Gary F

    2016-03-01

    Unmodified reperfusion therapy for acute myocardial infarction (AMI) is associated with irreversible myocardial injury beyond that sustained during ischemia. Studies in experimental models of ischemia/reperfusion and in humans undergoing reperfusion therapy for AMI have examined potential beneficial effects of nitric oxide (NO) supplemented at the time of reperfusion. Using a rigorous systematic search approach, we have identified and critically evaluated all the relevant experimental and clinical literature to assess whether exogenous NO given at reperfusion can limit infarct size. An inclusive search strategy was undertaken to identify all in vivo experimental animal and clinical human studies published in the period 1990-2014 where NO gas, nitrite, nitrate or NO donors were given to ameliorate reperfusion injury. Articles were screened at title and subsequently at abstract level, followed by objective full text analysis using a critical appraisal tool. In twenty-one animal studies, all NO treatments except nitroglycerin afforded protection against measures of reperfusion injury, including infarct size, creatinine kinase release, neutrophil accumulation and cardiac dysfunction. In three human AMI RCT's, there was no consistent evidence of infarct limitation associated with NO treatment as an adjunct to reperfusion. Despite experimental evidence that most NO treatments can reduce infarct size when given as adjuncts to reperfusion, the value of these interventions in clinical AMI is unproven. Our study raises issues for the design of further clinical studies and emphasises the need for improved design of animal studies to reflect more accurately the comorbidities and other confounding factors seen in clinical AMI.

  12. Technetium-99m pyrophosphate/thallium-201 dual-isotope SPECT imaging predicts reperfusion injury in patients with acute myocardial infarction after reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Akutsu, Yasushi; Kaneko, Kyouichi; Kodama, Yusuke; Li, Hui-Ling; Nishimura, Hideki; Hamazaki, Yuji; Kobayashi, Youichi [Showa University School of Medicine, Division of Cardiology, Department of Medicine, Tokyo (Japan); Suyama, Jumpei; Shinozuka, Akira; Gokan, Takehiko [Showa University School of Medicine, Department of Radiology, Tokyo (Japan)

    2009-02-15

    Microcirculatory failure after reperfusion is clinically indicated to cause reperfusion injury whereas excessive intracellular calcium ion overload is experimentally proved as a key mechanism of reperfusion injury. We hypothesized that technetium-99m ({sup 99m}Tc) pyrophosphate (Tc-PYP) uptake in injured but viable infarct-related myocardium with preserved myocardial perfusion after reperfusion estimated by thallium-201 ({sup 201}Tl) uptake would be associated with final functional recovery. Dual-isotope Tc-PYP/{sup 201}Tl single-photon emission computed tomography (SPECT) was performed 2 days after successful reperfusion therapy in patients with first acute myocardial infarction, and 50 patients (63 {+-} 13 years old, female 22%) with preserved {sup 201}Tl uptakes of {>=}50% in reperfused myocardium was followed for 1 month. Tc-PYP uptake was assessed as the heart-to-sternum (H/S) ratio. Two-dimensional echocardiography was also performed 2 days and 1 month after reperfusion to evaluate functional recovery. High Tc-PYP uptake, defined as the H/S ratio {>=}0.81, was predictive of chronic phase no functional recovery (73.7% in 14 of 19 patients with high uptake vs 16.1% in five of 31 patients without those, p < 0.0001). After adjustment for potential confounding variables, including electrocardiographic persistent ST segment elevation at 1 h after reperfusion, high Tc-PYP uptake remained independently predictive of no functional recovery with odds ratio of 8.7 (95% confidential interval = 2 to 38.7; p = 0.005). High Tc-PYP uptake in reperfused but viable infarct-related myocardium was a powerful predictor of no functional recovery, which may reflect excessive intracellular calcium ion overload caused by reperfusion injury. Tc-PYP/{sup 201}Tl dual-isotope SPECT imaging can provide prognostic information after reperfusion. (orig.)

  13. Ultrasonic tissue characterization with integrated backscatter. Acute myocardial ischemia, reperfusion, and stunned myocardium in patients

    Energy Technology Data Exchange (ETDEWEB)

    Milunski, M.R.; Mohr, G.A.; Perez, J.E.; Vered, Z.; Wear, K.A.; Gessler, C.J.; Sobel, B.E.; Miller, J.G.; Wickline, S.A. (Washington Univ., St. Louis, MO (USA))

    1989-09-01

    We have previously shown in studies of experimental animals that myocardium exhibits a cardiac cycle-dependent variation of integrated backscatter that reflects regional myocardial contractile performance and that is blunted promptly after arterial occlusion and recovers after reperfusion. To define the clinical utility of ultrasonic tissue characterization with integrated backscatter for detection of acute myocardial infarction and reperfusion, 21 patients (14 men and seven women) were studied in the cardiac care unit within the first 24 hours (mean time, 11.3 hours; range, 3.5-23.8 hours) after the onset of symptoms indicative of acute myocardial infarction with conventional two-dimensional and M-mode echocardiography and with analysis of integrated backscatter. The magnitude of cyclic variation of integrated backscatter was measured from several sites within acute infarct regions and normal regions remote from the infarct zone for each patient. The average magnitude of cyclic variation among all patients (n = 21) was 4.8 +/- 0.5 dB in normal regions compared with 0.8 +/- 0.3 dB in infarct regions (p less than 0.05) within the first 24 hours after the onset of symptoms. Among the patients who had two studies, 15 (mean, 7.1 days; range, 2-31 days for second study) underwent coronary arteriography to define vessel patency. In patients with vessels with documented patency (n = 10), the magnitude of cyclic variation in infarct regions increased over time from 1.3 +/- 0.6 to 2.5 +/- 0.5 dB from the initial to final study (p less than 0.05). Patients with occluded infarct-related arteries (n = 5) exhibited no significant recovery of cyclic variation (0.3 +/- 0.3-0.6 +/- 0.3 dB). A blinded analysis of standard two-dimensional echocardiographic images revealed no significant recovery of wall thickening in either group over the same time intervals.

  14. Reperfusion therapy for ST elevation acute myocardial infarction 2010/2011

    DEFF Research Database (Denmark)

    Kristensen, Steen D; Laut, Kristina G; Fajadet, Jean

    2014-01-01

    AIMS: Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion therapy in ST-elevation myocardial infarction (STEMI). We conducted this study to evaluate the contemporary status on the use and type of reperfusion therapy in patients admitted with STEMI in the European Society...

  15. Relation of elevated levels of plasma myeloperoxidase to impaired myocardial microcirculation after reperfusion in patients with acute myocardial infarction

    NARCIS (Netherlands)

    Yunoki, Kei; Naruko, Takahiko; Komatsu, Ryushi; Shirai, Nobuyuki; Nakagawa, Masashi; Sugioka, Kenichi; Ikura, Yoshihiro; Kusano, Kengo Fukushima; Itoh, Akira; Haze, Kazuo; Yoshiyama, Minoru; Becker, Anton E.; Ueda, Makiko

    2010-01-01

    Previous studies have shown that oxidative stress and endothelial dysfunction are related to impaired myocardial microcirculation after reperfusion. Moreover, elevated myeloperoxidase (MPO) levels are associated with endothelial dysfunction. Plasma MPO levels were measured in patients with

  16. Evaluating coronary reperfusion during acute myocardial infarction in a canine model by gadolinium-DTPA-enhanced magnetic resonance imaging

    Energy Technology Data Exchange (ETDEWEB)

    Tanabe, Kazuaki; Ishibashi, Yutaka; Shimada, Toshio (Shimane Medical Univ., Izumo (Japan)) (and others)

    1993-05-01

    In previous studies, magnetic resonance imaging (MRI) using contrast agents was found to be useful in distinguishing reperfused infarcts from nonreperfused infarcts. However, there have been only a few detailed studies using consecutive MR images for the assessment of myocardial reperfusion during an acute infarction and also no studies have been performed using a percutaneous transluminal coronary occlusion model (closed chest model). We induced acute myocardial infarction in dogs by occluding and then reperfusing the coronary artery with a balloon catheter. ECG-gated MR images were taken using the spin-echo technique before and after Gd-DTPA injection during both coronary artery occlusion and after reperfusion. We defined the intensity ratio (IR) as the signal intensity at the ischemic area divided by that at the nonischemic area on MR images and compared each image by the IR. Without Gd-DTPA, there was no difference between infarcted and normally perfused myocardium. Infarcted myocardium had a low signal intensity (IR=0.68[+-]0.14) soon after Gd-DTPA injection. This difference diminished with time. After reperfusion the infarcted myocardium had a high signal intensity (IR: 1.76[+-]0.34). We conclude that Gd-DTPA-enhanced MRI can distinguish reperfused from nonreperfused infarcts soon after Gd-DTPA administration. (author).

  17. Natriuretic peptide infusion reduces myocardial injury during acute ischemia/reperfusion

    DEFF Research Database (Denmark)

    Kousholt, Birgitte S.; Larsen, Jens Kjærgaard Rolighed; Bisgaard, Line Stattau

    2012-01-01

    in the ischemic left ventricular region (Pinjury in acute ischemia–reperfusion, possibly through indirect mechanisms (e.g. increased diuresis and vasodilation). The results suggest a role for natriuretic peptide therapy......Aim: The aim of this study was to determine whether a natriuretic peptide infusion during reperfusion can reduce cardiomyocyte ischemia–reperfusion damage. Materials and methods: The effect of B-type natriuretic peptide (BNP) activity was assessed in vitro and in vivo: the cellular effect...... was determined by assessment of intracellular caspase activity and troponin T release from cultured HL-1 cells subjected to short-term hypoxia–reperfusion. Cardiac effects were further examined in pigs (n=25) that had been subjected to 1 h of regional cardiac ischemia, followed by 3 h of reperfusion. Results: HL...

  18. 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.

  19. Down-regulation of lncRNA KCNQ1OT1 protects against myocardial ischemia/reperfusion injury following acute myocardial infarction.

    Science.gov (United States)

    Li, Xin; Dai, Yingnan; Yan, Shujun; Shi, Yanli; Han, Baihe; Li, Jingxiu; Cha, Li; Mu, Jianjun

    2017-09-30

    This study aimed to investigate the protective effects of long non-coding RNA KCNQ1OT1 against myocardial ischemia/reperfusion (I/R) injury following acute myocardial infarction, as well as its regulatory mechanism. We used the cardiac muscle H9c2 cells under condition of oxygen glucose deprivation followed by reperfusion (OGD/R) to induce myocardial I/R injury. Then H9C2 cells were transfected with si-NC, si-KCNQ1OT1, pc-NC, pc-KCNQ1OT1, si-AdipoR1 and si-AdipoR2, respectively. The myocardial cell viability and apoptosis were respectively detected. In addition, the expression levels of inflammatory factors, apoptosis-related proteins and p38 MAPK/NF-κB pathway-related proteins were detected. Besides, an inhibitor of p38 MAPK/NF-κB pathway SB203580 was used to treat cells to verify the relationship between KCNQ1OT1 and p38 MAPK/NF-κB pathway. The expression of KCNQ1OT1 was significantly up-regulated in OGD/R-induced myocardial H9C2 cells. The OGD/R-induced decreased cell viability and AdipoR1 expression could be reversed after suppression of KCNQ1OT1. In addition, suppression of KCNQ1OT1 reduced OGD/R-induced increased expressions of TNF-α, IL-6 and IL-1β and OGD/R-induced increased cell apoptosis, which were reversed after knockdown of AdipoR1. Besides, suppression of KCNQ1OT1 significantly down-regulated the OGD/R-induced increased expression of p-p38 and p-NF-κB, which were also reversed after knockdown of AdipoR1. Moreover, SB203580, an inhibitor of p38 MAPK/NF-κB signal pathway, could further enhance the inhibitory effects of KCNQ1OT1 suppression on the expression of p-p38, TNF-α, IL-6, IL-1β and p-NF-κB in OGD/R-induced myocardial H9C2 cells. Suppression of KCNQ1OT1 may prevent myocardial I/R injury following acute myocardial infarction via regulating AdipoR1 and involving in p38 MAPK/NF-κB signal pathway. Copyright © 2017 Elsevier Inc. All rights reserved.

  20. Transplantation of Allogeneic Pericytes Improves Myocardial Vascularization and Reduces Interstitial Fibrosis in a Swine Model of Reperfused Acute Myocardial Infarction.

    Science.gov (United States)

    Alvino, Valeria Vincenza; Fernández-Jiménez, Rodrigo; Rodriguez-Arabaolaza, Iker; Slater, Sadie; Mangialardi, Giuseppe; Avolio, Elisa; Spencer, Helen; Culliford, Lucy; Hassan, Sakinah; Sueiro Ballesteros, Lorena; Herman, Andrew; Ayaon-Albarrán, Ali; Galán-Arriola, Carlos; Sánchez-González, Javier; Hennessey, Helena; Delmege, Catherine; Ascione, Raimondo; Emanueli, Costanza; Angelini, Gianni Davide; Ibanez, Borja; Madeddu, Paolo

    2018-01-22

    Transplantation of adventitial pericytes (APCs) promotes cardiac repair in murine models of myocardial infarction. The aim of present study was to confirm the benefit of APC therapy in a large animal model. We performed a blind, randomized, placebo-controlled APC therapy trial in a swine model of reperfused myocardial infarction. A first study used human APCs (hAPCs) from patients undergoing coronary artery bypass graft surgery. A second study used allogeneic swine APCs (sAPCs). Primary end points were (1) ejection fraction as assessed by cardiac magnetic resonance imaging and (2) myocardial vascularization and fibrosis as determined by immunohistochemistry. Transplantation of hAPCs reduced fibrosis but failed to improve the other efficacy end points. Incompatibility of the xenogeneic model was suggested by the occurrence of a cytotoxic response following in vitro challenge of hAPCs with swine spleen lymphocytes and the failure to retrieve hAPCs in transplanted hearts. We next considered sAPCs as an alternative. Flow cytometry, immunocytochemistry, and functional/cytotoxic assays indicate that sAPCs are a surrogate of hAPCs. Transplantation of allogeneic sAPCs benefited capillary density and fibrosis but did not improve cardiac magnetic resonance imaging indices of contractility. Transplanted cells were detected in the border zone. Immunologic barriers limit the applicability of a xenogeneic swine model to assess hAPC efficacy. On the other hand, we newly show that transplantation of allogeneic sAPCs is feasible, safe, and immunologically acceptable. The approach induces proangiogenic and antifibrotic benefits, though these effects were not enough to result in functional improvements. © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

  1. DELAYED REPERFUSION FOR SAVING VITAL MYOCARDIUM IN THE ACUTE PERIOD OF MYOCARDIAL INFARCTION WITH ELEVATION OF ST SEGMENT.

    Science.gov (United States)

    Gazarvan, G G

    Reperfusion therupy in case of acule inl , voc'ardial infiction is especialli desirble within 12 hr cfierfirs/ clinical manifestalions as show in stidies with the use of thrombolytic therapy (TLT). Its efficiency for saving ischemic myocardum decreqses as the time from the onset of pain syndrome increasrs. Nevertheless, patients admitted to the clinic in the period deemed infavourable for TLT still preserve large part of vital myocardium even if in the risk zone. Delayed saving myocardum impossible by TLT can be ensured by transdermal coronary interventions. The depence of myocardial necrois on the duration of occlution of coronary artery is as well recognized as the necessity of early interventions. Transdermal coronary interventions can be perforned within days 2 or 3 after onset of acute myocarial infraction if it was impracticable in an earlier period.

  2. Early detection of the no-reflow phenomenon in reperfused acute myocardial infarction using technetium-99m tetrofosmin imaging

    Energy Technology Data Exchange (ETDEWEB)

    Hamada, Shinichi; Nakamura, Seishi; Murakami, Takashi; Fujimoto, Toshinori; Watanabe, Junko; Baden, Masato [Division of Cardiology, Takarazuka Hospital, Hyogo (Japan); Sugiura, Tetsuro; Hatada, Kengo; Iwasaka, Toshiji [Cardiovascular Center, Kansai Medical University, Osaka (Japan)

    1999-03-01

    Evaluation of myocardial perfusion in the early stage of acute myocardial infarction (MI) is clinically important for adjunctive therapies to minimize infarct size. To determine the role of early scintigraphic detection of impaired myocardial reperfusion after primary coronary angioplasty (PTCA) in patients with acute MI, semiquantitative technetium-99m tetrofosmin single-photon emission tomographic (SPET) imaging was performed before primary PTCA (before; area at risk), 60 min after PTCA (after) and at 1 month (1 M; final infarct) in 35 patients with acute MI. The left ventricle was divided into 13 segments and the defect score was calculated as the sum of the perfusion defect of each segment, from 3 (complete defect) to 0 (normal perfusion). A significant myocardial perfusion change after PTCA was defined as a change in the defect score (before minus after PTCA) of {>=}4. The echocardiographic asynergic score was defined as the number of asynergic (severe hypokinetic or akinetic) segments corresponding to the analogous segments on SPET images, and recovery of wall motion was calculated as absolute change in the asynergic score (before PTCA minus 1 M). Among the 35 patients, 15 (43%) had a change in the defect score of <4 (no reflow: group 1) while 20 had a change in the defect score of {>=}4 (reflow: group 2). There were no significant differences between the two groups with respect to the time between admission to PTCA, revascularization time, collateral grade or Thrombolysis in Myocardial Infarction (TIMI) flow grade before PTCA. Despite the lack of a difference in area at risk between the two groups (group 1 = 12.8{+-}4.3 and group 2 = 15.1{+-}4.7), final infarct size in group 1 was significantly larger compared with that in group 2 (8.1{+-}4.3 vs 4.9{+-}3.0, P<0.001). Recovery of wall motion was significantly smaller in group 1 than in group 2 (4.3{+-}1.7 to 3.5{+-}1.5 vs 4.1{+-}2.1 to 1.6{+-}1.6, P<0.001). In conclusion, a small change (<4) in defect score

  3. Intracoronary and systemic melatonin to patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Løvland Halladin, Natalie; Busch, Sarah Ekeløf; Jensen, Svend Eggert

    2014-01-01

    Ischaemia-reperfusion injury following acute myocardial infarctions (AMI) is an unavoidable consequence of the primary percutaneous coronary intervention (pPCI) procedure. A pivotal mechanism in ischaemia-reperfusion injury is the production of reactive oxygen species following reperfusion...

  4. Temporal change of enhancement after gadolinium injection on contrast-enhanced CMR in reperfused acute myocardial infarction.

    Science.gov (United States)

    Matsumoto, Hidenari; Matsuda, Tetsuya; Miyamoto, Kenichi; Shimada, Toshihiko; Ushimaru, Shunpei; Mikuri, Mikiko; Yamazaki, Taketoshi

    2015-01-01

    A recent report demonstrated that early enhancement on contrast-enhanced cardiac magnetic resonance (CE-CMR) correlated with myocardial edema detected by T2-weighted CMR in reperfused acute myocardial infarction (AMI). However, the time at which the enhancement in salvaged myocardium disappears is yet to be determined. We aimed to examine the time course of the enhancement with the use of different quantification techniques and to compare the extent of enhancement with the myocardial edema. CE-CMR was performed at 2-20 min after gadolinium administration in 32 AMI patients. The extent of enhancement (% myocardium) was quantified by manual delineation and the threshold methods of 2-5 SDs above remote myocardium. In subendocardial infarct, the enhancement was greatest at 2 min regardless of the quantification techniques and decreased with time, particularly in the first 6 min. In transmural infarct, the change in the size of enhancement was modest although the time course of enhancement varied according to the quantification techniques. The sizes of enhancement were not significantly different between 15 and 20 min regardless of the techniques and infarct transmurality. The best agreement with myocardial edema was found at 2 min with average differences of 0.5% and -1.2% and limits of agreement of ±20.2% and ±21.2% for the manual and 2-SD techniques, respectively. The optimal timing for delineation of salvaged myocardium on CE-CMR is at 2min when the manual or 2-SD technique was employed. Imaging needs to be completed in a short time (ideally within a minute) because of rapid reduction of enhancement in salvaged myocardium. Copyright © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

  5. SDF-1/CXCR4 mediates acute protection of cardiac function through myocardial STAT3 signaling following global ischemia/reperfusion injury

    Science.gov (United States)

    Huang, Chunyan; Gu, Hongmei; Zhang, Wenjun; Manukyan, Mariuxi C.; Shou, Weinian

    2011-01-01

    Stromal cell-derived factor-1α (SDF-1) has been reported to mediate cardioprotection through the mobilization of stem cells into injured tissue and an increase in local angiogenesis after myocardial infarction. However, little is known regarding whether SDF-1 induces acute protection following global myocardial ischemia/reperfusion (I/R) injury and if so, by what molecular mechanism. SDF-1 binding to its cognate receptor CXCR4 has been shown to activate STAT3 in a variety of cells. STAT3 is a cardioprotective factor and may mediate SDF-1/CXCR4-induced acute protection. We hypothesized that SDF-1 would improve myocardial function through CXCR4-increased STAT3 activation following acute I/R. Isolated mouse hearts were subjected to 25-min global ischemia/40-min reperfusion and divided into groups of 1) vehicle; 2) SDF-1; 3) AMD3100, a CXCR4 inhibitor; 4) SDF-1 + AMD3100; 5) Stattic, a STAT3 inhibitor; 6) SDF-1 + Stattic; 7) cardiomyocyte-restricted ablation of STAT3 (STAT3KO); 8) STAT3KO + SDF-1; 9) Ly294002, an inhibitor of the Akt pathway; and 10) SDF-1 + Ly294002. Reagents were infused into hearts within 5 min before ischemia. SDF-1 administration significantly improved postischemic myocardial functional recovery in a dose-dependent manner. Additionally, pretreatment with SDF-1 reduced cardiac apoptotic signaling and increased myocardial STAT3 activation following acute I/R. Inhibition of the SDF-1 receptor CXCR4 neutralized these protective effects by SDF-1 in hearts subjected to I/R. Notably, inhibition of the STAT3 pathway or use of STAT3KO hearts abolished SDF-1-induced acute protection following myocardial I/R. Our results represent the first evidence that the SDF-1/CXCR4 axis upregualtes myocardial STAT3 activation and, thereby, mediates acute cardioprotection in response to global I/R. PMID:21821779

  6. Effects of single-dose atorvastatin on interleukin-6, interferon gamma, and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Zhao, X.J. [Affiliated Hospital of Binzhou Medical University, Department of Cardiology, Binzhou, China, Department of Cardiology, Affiliated Hospital of Binzhou Medical University, Binzhou (China); Liu, X.L. [Qilu Hospital, Shandong University, Department of Cardiology, Jinan, China, Department of Cardiology, Qilu Hospital, Shandong University, Jinan (China); He, G.X. [Third Military Medical University, Southwest Hospital, Department of Cardiology, Chongqing, China, Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing (China); Xu, H.P. [Affiliated Hospital of Binzhou Medical University, Department of Cardiology, Binzhou, China, Department of Cardiology, Affiliated Hospital of Binzhou Medical University, Binzhou (China)

    2014-03-03

    The mechanisms of statins relieving the no-reflow phenomenon and the effects of single-dose statins on it are not well known. This study sought to investigate the effects of inflammation on the no-reflow phenomenon in a rabbit model of acute myocardial infarction and reperfusion (AMI/R) and to evaluate the effects of single-dose atorvastatin on inflammation and myocardial no-reflow. Twenty-four New Zealand white male rabbits (5-6 months old) were randomized to three groups of eight: a sham-operated group, an AMI/R group, and an atorvastatin-treated group (10 mg/kg). Animals in the latter two groups were subjected to 4 h of coronary occlusion followed by 2 h of reperfusion. Serum levels of interleukin (IL)-6 were measured by enzyme-linked immunosorbent assay. The expression of interferon gamma (IFN-γ) in normal and infarcted (reflow and no-reflow) myocardial tissue was determined by immunohistochemical methods. The area of no-reflow and necrosis was evaluated pathologically. Levels of serum IL-6 were significantly lower in the atorvastatin group than in the AMI/R group (P<0.01). Expression of IFN-γ in infarcted reflow and no-reflow myocardial tissue was also significantly lower in the atorvastatin group than in the AMI/R group. The mean area of no-reflow [47.01% of ligation area (LA)] was significantly smaller in the atorvastatin group than in the AMI/R group (85.67% of LA; P<0.01). The necrosis area was also significantly smaller in the atorvastatin group (85.94% of LA) than in the AMI/R group (96.56% of LA; P<0.01). In a secondary analysis, rabbits in the atorvastatin and AMI/R groups were divided into two groups based on necrosis area (90% of LA): a small group (<90% of LA) and a large group (>90% of LA). There was no significant difference in the area of no-reflow between the small (61.40% of LA) and large groups (69.87% of LA; P>0.05). Single-dose atorvastatin protected against inflammation and myocardial no-reflow and reduced infarct size during AMI/R in

  7. An Observational study of prehospital and hospital delay in reperfusion for acute myocardial infarction at a University Hospital in India

    Directory of Open Access Journals (Sweden)

    Rahul Choudhary

    2016-01-01

    Full Text Available Objective: Cardiovascular disease is the leading cause of death among Indian adults, and approximately 50% of deaths usually occur during the 1st hour after symptom onset before arriving at the hospital. A study was planned to evaluate the prehospital and hospital delay in patients with acute myocardial infarction (AMI. Methods: This was a prospective observational study of 390 patients with AMI admitted to the Department of Cardiology between March 2014 and August 2015. Detailed patient demographics, socioeconomic status, and prehospital and hospital delay were reviewed. Results: The mean age of presentation for male and female was 57 ± 12.91 and 61.5 ± 12.83 years, respectively. The mean prehospital delay, time to act after chest pain, and travel time were 9.08 ± 6.3, 7.16 ± 6.1, and 1.84 ± 0.8 h, respectively, and only three (9.7% patients reached the hospital within 2 h after symptom onset. Out of 300 patients who received reperfusion therapy, thrombolysis was done in 276 (92% patients while primary percutaneous coronary intervention was performed in only 24 (8% patients. Mean door-to-needle (D-N time and door-to-device time for those who received reperfusion therapy were 27.8 ± 4.3 and 78.95 ± 9.5 min, respectively. A multivariate logistic regression analysis revealed that the prehospital delay was significantly associated with older age, female sex, rural background, diabetes, having atypical pain, and lack of knowledge regarding the seriousness of chest pain. Conclusion: Approximately 79% of total prehospital delay was due to patient-related factors; old age, female sex, rural background, diabetes, atypical angina, and lack of knowledge being the significant attributes. D-N time and door-to-device time were within the limits of those recommended by current guidelines.

  8. The relation between hypointense core, microvascular obstruction and intramyocardial haemorrhage in acute reperfused myocardial infarction assessed by cardiac magnetic resonance imaging

    Energy Technology Data Exchange (ETDEWEB)

    Kandler, Diana; Luecke, Christian; Grothoff, Matthias; Andres, Claudia; Lehmkuhl, Lukas; Nitzsche, Stefan; Riese, Franziska; Gutberlet, Matthias [University Leipzig - Heart Centre, Department of Diagnostic and Interventional Radiology, Leipzig (Germany); Mende, Meinhard [University Leipzig, Coordination Centre for Clinical Trials, Leipzig (Germany); Waha, Suzanne de; Desch, Steffen; Lurz, Philipp; Eitel, Ingo [University Leipzig - Heart Centre, Department of Internal Medicine/ Cardiology, Leipzig (Germany)

    2014-12-15

    Intramyocardial haemorrhage (IMH) and microvascular obstruction (MVO) represent reperfusion injury after reperfused ST-elevation myocardial infarction (STEMI) with prognostic impact and ''hypointense core'' (HIC) appearance in T{sub 2}-weighted images. We aimed to distinguish between IMH and MVO by using T{sub 2}{sup *}-weighted cardiovascular magnetic resonance imaging (CMR) and analysed influencing factors for IMH development. A total of 151 patients with acute STEMI underwent CMR after primary angioplasty. T{sub 2}-STIR sequences were used to identify HIC, late gadolinium enhancement to visualise MVO and T{sub 2}{sup *}-weighted sequences to detect IMH. IMH{sup +}/IMH{sup -} patients were compared considering infarct size, myocardial salvage, thrombolysis in myocardial infarction (TIMI) flow, reperfusion time, ventricular volumes, function and pre-interventional medication. Seventy-six patients (50 %) were IMH{sup +}, 82 (54 %) demonstrated HIC and 100 (66 %) MVO. IMH was detectable without HIC in 16 %, without MVO in 5 % and HIC without MVO in 6 %. Multivariable analyses revealed that IMH was associated with significant lower left ventricular ejection fraction and myocardial salvage index, larger left ventricular volume and infarct size. Patients with TIMI flow grade ≤1 before angioplasty demonstrated IMH significantly more often. IMH is associated with impaired left ventricular function and higher infarct size. T{sub 2} and HIC imaging showed moderate agreement for IMH detection. T{sub 2}{sup *} imaging might be the preferred CMR imaging method for comprehensive IMH assessment. (orig.)

  9. Comparison between visual grading and planimetric quantification of microvascular obstruction extent assessment in reperfused acute myocardial infarction.

    Science.gov (United States)

    Sirol, Marc; Gzara, Heger; Gayat, Etienne; Dautry, Raphael; Gellen, Barnabas; Logeart, Damien; Soyer, Philippe; Vicaut, Eric; Mercadier, Jean-Jacques

    2016-07-01

    Current methods for infarct size and microvascular obstruction (MVO) quantification by cardiac magnetic resonance (CMR) imaging rely on planimetry. This method is time-consuming. We sought to evaluate a direct assessment of MVO severity based on visual evaluation and to compare it to a reference method. CMR was performed in 112 consecutive patients after reperfused myocardial infarction. MVO was estimated by direct visual assessment based on a three-grade severity scale (MVO 1, mild; MVO 2, moderate; MVO 3, severe) on late gadolinium-enhancement (LGE). MVO was present in 69 patients (61.6 %). Quantitative MVO extent significantly increased accordingly to visual MVO grading (p < 0.01). Correlation between visual grading and quantitative assessment was excellent (r = 0.92, IQR 0.88-0.95, p < 0.001). CMR inter- and intraobserver variability for visual MVO evaluation was low (κ = 0.93 and κ = 0.96, respectively), whereas quantitative MVO assessment suffered from moderate agreement (interobserver, bias = -0.81 ± 1.8 g LV; intraobserver, -0.83 ± 2.1 g LV). Visual evaluation was significantly faster than reference method (0.65 ± 0.37 vs. 10.2 ± 2.9 min, p < 0.0001). MVO severity based on direct visual assessment on LGE images is feasible, rapid, reproducible and agrees very well with quantitative methods, with a very low inter- and intraobserver variability. Our approach could be used for routine evaluation in patients undergoing CMR after acute myocardial infarction. • Microvascular obstruction direct visual evaluation is feasible, rapid and highly reproducible. • Microvascular obstruction direct visual evaluation correlates well with quantification by planimetry. • Microvascular obstruction or no-reflow phenomenon is determined on late gadolinium-enhanced images. • Cardiac MRI is useful for myocardial damage assessment after myocardial infarction.

  10. Predictive values of early rest/24 hour delay Tl-201 perfusion SPECT for wall motion improvement in patients with acute myocardial infarction after reperfusion

    International Nuclear Information System (INIS)

    Hyun, In Young; Kwan, June

    1998-01-01

    We studied early rest/24 hour delay Tl-201 perfusion SPECT for prediction of wall motion improvement after reperfusion in patients with acute myocardial infarction. Among 17 patients (male/female=11/6, age: 59±13) with acute myocardial infarction, 15 patients were treated with percutaneous transcoronary angioplasty (direct:2, delay:11) and intravenous urokinase (2). Spontaneous resolution occurred in infarct related arteries of 2 patients. We confirmed TIMI 3 flow of infarct-related artery after reperfusion in all patients with coronary angiography. We performed rest Tl-201 perfusion SPECT less then 6 hours after reperfusion and delay Tl-201 perfusion SPECT next day. Tl-201 uptake was visually graded as 4 point score from normal (0) to severe defect (3). Rest Tl-201 uptake ≤2 or combination of rest Tl-201 uptake ≤2 or late reversibility were considered to be viable. Myocardial wall motion was graded as 5 point score from normal (1) to dyskinesia (5). Myocardial wall motion was considered to be improved when a segment showed an improvement ≥1 grade in follow up echo compared with the baseline values. Among 98 segments with wall motion abnormality, the severity of myocardial wall motion decrease was as follow: mild hypokinesia: 18/98 (18%), severe hypokinesia: 28/98 (29%), akinesia: 51/98 (52%), dyskinesia: 1/98 (1%). The wall motion improved in 85%. Redistribution (13%), and reverse redistribution (4%) were observed in 24 hour delay SPECT. Positive predictive value (PPV) and negative predictive value (NPV) of combination of late reversibility and rest Tl-201uptake were 99%, and 54%.PPV and NPV of rest Tl-201 uptake were 100% and 52% respectively. Predictive values of comibination of rest Tl-201 uptake and late reversibility were not significantly different compared with predictive values of rest Tl-201 uptake only. We conclude that early Tl-201 perfusion SPECT predict myocardial wall motion improvement with excellent positive but relatively low negative

  11. Natriuretic peptide infusion reduces myocardial injury during acute ischemia/reperfusion

    DEFF Research Database (Denmark)

    Kousholt, Birgitte S.; Larsen, Jens Kjærgaard Rolighed; Bisgaard, Line Stattau

    2012-01-01

    Aim: The aim of this study was to determine whether a natriuretic peptide infusion during reperfusion can reduce cardiomyocyte ischemia–reperfusion damage. Materials and methods: The effect of B-type natriuretic peptide (BNP) activity was assessed in vitro and in vivo: the cellular effect...... in apoptotic changes in the BNP-stimulated cells. Pigs tolerated the BNP and CD-NP (a CNP analogue) infusion well, with a decrease in systemic blood pressure (~15 mmHg) and increased diuresis compared with the controls. Left ventricular pressure decreased in the pigs that received BNP infusion compared...... with controls (P=0.02). A similar trend was observed in the pigs that received CD-NP infusion, although this was not significant (P=0.3). BNP and CD-NP infusion in pigs reduced total cardiac troponin T release by 46 and 40%, respectively (P=0.0015 and 0.0019), and were associated with improved RNA integrity...

  12. Natriuretic peptide infusion reduces myocardial injury during acute ischemia/reperfusion

    DEFF Research Database (Denmark)

    Kousholt, Birgitte S.; Larsen, Jens Kjærgaard Rolighed; Bisgaard, Line Stattau

    2012-01-01

    Aim: The aim of this study was to determine whether a natriuretic peptide infusion during reperfusion can reduce cardiomyocyte ischemia–reperfusion damage. Materials and methods: The effect of B-type natriuretic peptide (BNP) activity was assessed in vitro and in vivo: the cellular effect...... in apoptotic changes in the BNP-stimulated cells. Pigs tolerated the BNP and CD-NP (a CNP analogue) infusion well, with a decrease in systemic blood pressure (∼15 mmHg) and increased diuresis compared with the controls. Left ventricular pressure decreased in the pigs that received BNP infusion compared...... with controls (P=0.02). A similar trend was observed in the pigs that received CD-NP infusion, although this was not significant (P=0.3). BNP and CD-NP infusion in pigs reduced total cardiac troponin T release by 46 and 40%, respectively (P=0.0015 and 0.0019), and were associated with improved RNA integrity...

  13. Treatment of reperfusion injury with recombinant ADAMTS13 in a porcine model of acute myocardial infarction

    NARCIS (Netherlands)

    Eerenberg, E.S.; Teunissen, P.F.A.; Van Den Born, B.J.; Meijers, J.C.; Hollander, M.; Aly, M.; Niessen, H.W.M.; Kamphuisen, P.W.; Levi, M.; Van Royen, N.

    Background: No reflow and decreased microvascular perfusion after percutaneous coronary intervention increase morbidity and mortality in ST-elevation myocardial infarction (STEMI) patients. No reflow may be mediated by platelet vessel wall interaction that is governed by von Willebrand factor.

  14. Acute reperfusion without recanalization

    DEFF Research Database (Denmark)

    Makris, Nikolaos; Chamard, Leila; Mikkelsen, Irene K

    2017-01-01

    Acute reperfusion despite persistent arterial occlusion may occur in up to 30% of ischemic stroke patients. Recruitment of leptomeningeal collaterals may explain this phenomenon. Using dynamic susceptibility-contrast perfusion imaging (DSC-PI), we assessed acute changes in collateral flow among...... patients without recanalization. From a multicenter prospective database (I-KNOW), 46 patients with magnetic resonance angiography visible occlusion in whom both reperfusion and recanalization were assessed within 6 h of onset were identified. Maps of collateral flow at arterial, capillary and late venous...... phases were generated from DSC-PI through inter-frame registration, baseline signal subtraction and temporal summation, and graded blind to all other relevant clinical and radiological data using the Higashida scale. Flow direction and the acute evolution of collaterals were evaluated against...

  15. A Translational Study of a New Therapeutic Approach for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin into Reperfused Myocardium Reduces Ischemia-Reperfusion Injury in a Preclinical Porcine Model.

    Science.gov (United States)

    Ichimura, Kenzo; Matoba, Tetsuya; Nakano, Kaku; Tokutome, Masaki; Honda, Katsuya; Koga, Jun-Ichiro; Egashira, Kensuke

    2016-01-01

    There is an unmet need to develop an innovative cardioprotective modality for acute myocardial infarction, for which interventional reperfusion therapy is hampered by ischemia-reperfusion (IR) injury. We recently reported that bioabsorbable poly(lactic acid/glycolic acid) (PLGA) nanoparticle-mediated treatment with pitavastatin (pitavastatin-NP) exerts a cardioprotective effect in a rat IR injury model by activating the PI3K-Akt pathway and inhibiting inflammation. To obtain preclinical proof-of-concept evidence, in this study, we examined the effect of pitavastatin-NP on myocardial IR injury in conscious and anesthetized pig models. Eighty-four Bama mini-pigs were surgically implanted with a pneumatic cuff occluder at the left circumflex coronary artery (LCx) and telemetry transmitters to continuously monitor electrocardiogram as well as to monitor arterial blood pressure and heart rate. The LCx was occluded for 60 minutes, followed by 24 hours of reperfusion under conscious conditions. Intravenous administration of pitavastatin-NP containing ≥ 8 mg/body of pitavastatin 5 minutes before reperfusion significantly reduced infarct size; by contrast, pitavastatin alone (8 mg/body) showed no therapeutic effects. Pitavastatin-NP produced anti-apoptotic effects on cultured cardiomyocytes in vitro. Cardiac magnetic resonance imaging performed 4 weeks after IR injury revealed that pitavastatin-NP reduced the extent of left ventricle remodeling. Importantly, pitavastatin-NP exerted no significant effects on blood pressure, heart rate, or serum biochemistry. Exploratory examinations in anesthetized pigs showed pharmacokinetic analysis and the effects of pitavastatin-NP on no-reflow phenomenon. NP-mediated delivery of pitavastatin to IR-injured myocardium exerts cardioprotective effects on IR injury without apparent adverse side effects in a preclinical conscious pig model. Thus, pitavastatin-NP represents a novel therapeutic modality for IR injury in acute myocardial

  16. Acute myocardial infarction: serial cardiac MR imaging shows a decrease in delayed enhancement of the myocardium during the 1st week after reperfusion.

    Science.gov (United States)

    Ibrahim, Tareq; Hackl, Thomas; Nekolla, Stephan G; Breuer, Martin; Feldmair, Michael; Schömig, Albert; Schwaiger, Markus

    2010-01-01

    To evaluate the time course of delayed gadolinium enhancement of infarcted myocardium by using serial contrast agent-enhanced (CE) cardiac magnetic resonance (MR) images obtained during the acute, subacute, and chronic stages of infarction. The study protocol was reviewed and approved by the local ethics committee, and written informed consent was obtained. Seventeen patients with reperfused acute myocardial infarction (AMI) underwent cine and CE cardiac MR a median of 1, 7, 35, and 180 days after reperfusion. Infarct size determined on the basis of delayed enhancement MR imaging at different times was compared by using nonparametric tests and Bland-Altman analysis. Extent of myocardial enhancement was compared with single photon emission computed tomographic (SPECT) measures of infarct size with Spearman correlation. Regional myocardial enhancement extent and contractility were analyzed with nonparametric tests. Infarct size was 18.3% of total myocardial LV volume on day 1 after AMI and decreased to 12.9% on day 7, 11.3% on day 35, and 11.6% on day 180 (all P infarct size on day 7, as compared with day 1 enhancement size, declined by 57.1% within the epicardium and by 6.3% within the endocardium (both P Infarct size on day 7 showed only minor changes at subsequent imaging and yielded a high correlation with SPECT measurements of infarct size (r = 0.84). Infarct size on day 7 inversely correlated with long-term wall thickening (P infarction. Thus, timing of CE cardiac MR imaging is crucial for accurate measurement of myocardial infarct size early after AMI.

  17. MR imaging distinction between occlusive and reperfused myocardial infarctions with a myocardial persistent contrast medium

    International Nuclear Information System (INIS)

    Saeed, M.; Wagner, S.; Wendland, M.; Derugin, N.; Pomeroy, O.; Higgins, C.B.

    1988-01-01

    Paramagnetic contrast agents have limitations for myocardial enhancement of the area at risk after acute occlusion and for differentiating occlusive and reperfused infarctions. A new contrast medium was used in an attempt to discriminate occlusive and reperfused infarctions. The pattern of enhancement was compared in occlusive (6-hour occlusion, 13 rats) and reperfused (2-hour occlusion and 4-hour reperfusion, ten rats) infarctions with electrocardiogram-gated MR imaging. MR imaging of infarcted areas was histologically and histochemically documented. Rats received 100-mM Mn-DPDP. The reperfused infarct showed transmural enhancement early after Mn-DPDP administration. However, occlusive infarcts showed no early enhancement. The difference in the pattern was significant. Mn-DPDP has the potential to distinguish between the occlusive and reperfused infarctions

  18. Comparison of infarct size changes with delayed contrast-enhanced magnetic resonance imaging and electrocardiogram QRS scoring during the 6 months after acutely reperfused myocardial infarction

    DEFF Research Database (Denmark)

    Bang, L.E.; Ripa, R.S.; Grande, P.

    2008-01-01

    that has infarcted. There are no comparison of serial changes on ECG and DE-MRI measuring infarct size. AIM: The general aim of this study was to describe the acute, healing, and chronic phases of the changes in infarct size estimated by the ECG and DE-MRI. The specific aim was to compare estimates......INTRODUCTION: Magnetic resonance imaging using the delayed contrast-enhanced (DE-MRI) method can be used for characterizing and quantifying myocardial infarction (MI). Electrocardiogram (ECG) score after the acute phase of MI can be used to estimate the portion of left ventricular myocardium...... of the Selvester QRS scoring system and DE-MRI to identify the difference between the extent of left ventricle occupied by infarction in the acute and chronic phases. METHODS: In 31 patients (26 men, age 56 +/- 9) with reperfused ST-elevation MI (11 anterior, 20 inferior), standard 12-lead ECG and DE-MRI were...

  19. Coronary artery calcification score is an independent predictor of the no-reflow phenomenon after reperfusion therapy in acute myocardial infarction.

    Science.gov (United States)

    Modolo, Rodrigo; Figueiredo, Valeria N; Moura, Filipe A; Almeida, Breno; Quinaglia e Silva, José C; Nadruz, Wilson; Lemos, Pedro A; Coelho, Otavio R; Blaha, Michael J; Sposito, Andrei C

    2015-11-01

    Abundant evidence shows that coronary artery calcification (CAC) is a strong marker of structural and functional changes within the artery wall. Thus far, the implications of CAC in patients with acute coronary syndromes remain unclear. We aimed to investigate whether the CAC score is associated with impaired reperfusion during the acute phase of ST-elevation myocardial infarction (STEMI). We enrolled 60 consecutive STEMI patients to undergo cardiac computed tomography for assessment of the CAC score within 1 week after STEMI. Coronary thrombus burden, coronary blood flow (TIMI flow), and myocardial blush grade (MBG) were evaluated systematically. Patients with maximal TIMI flow and MBG were grouped as optimal reperfusion (n=27) and their counterparts as no-reflow (NR, n=33). There were no differences in the clinical characteristics between groups. Patients in the NR group had higher heart rate, coronary angiographic severity, and CAC score. CAC score greater than 100 was associated independently with the presence of NR (odds ratio 4.4, 95% confidence interval 1.17-16.3). The CAC score of nonculprit coronary arteries was higher in NR individuals than in their counterparts (P=0.04). In addition, the CAC score of the isnfarct-related artery correlated negatively with the TIMI-flow rate (r=-0.54, P<0.001) and with the MBG (r=-0.32, P=0.04). The CAC score is associated with the presence of the NR phenomenon in STEMI patients.

  20. CURRENT REPERFUSION THERAPY POSSIBILITIES IN MYOCARDIAL INFARCTION AND ISCHEMIC STROKE

    Directory of Open Access Journals (Sweden)

    E. V. Konstantinova

    2015-01-01

    Full Text Available Myocardial infarction and ischemic stroke remain to be of the greatest medical and social importance because of their high prevalence, disability, and mortality rates. Intractable thrombotic occlusion of the respective artery leads to the formation of an ischemic lesion focus in the tissue of the heart or brain. Emergency reperfusion serves to decrease a necrotic focus, makes its formation reversible, and reduces patient death rates. The paper considers main reperfusion therapy lines: medical (with thrombolytic drugs and mechanical (with primary interventions one and their combination in treating patients with acute myocardial and cerebral ischemia. Each reperfusion procedure is discussed in view of its advantages, disadvantages, available guidelines, and possibilities of real clinical practice. Tenecteplase is assessed in terms of its efficacy, safety, and capacities for bolus administration, which allows its use at any hospital and at the pre-hospital stage. Prehospital thrombolysis permits reperfusion therapy to bring much closer to the patient and therefore aids in reducing time to reperfusion and in salvaging as much the myocardial volume as possible. The rapidest recovery of myocardial and cerebral perfusion results in a decreased necrotic area and both improved immediate and late prognosis. The results of randomized clinical trials studying the possibilities of the medical and mechanical methods to restore blood flow are analyzed in the context of evidence-based medicine. The reason why despite the available contraindications, limited efficiency, and the risk of hemorrhagic complications, thrombolytic therapy remains the method of choice for prehospital reperfusion, an alternative to primary percutaneous coronary intervention (PCI if it cannot be carried out in patients with myocardial infarction at the stated time, and the only treatment ischemic stroke treatment that has proven its efficiency and safety in clinical trials is under

  1. Evolving therapies for myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Ibáñez, Borja; Heusch, Gerd; Ovize, Michel; Van de Werf, Frans

    2015-04-14

    The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion injury). During the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have been widely incorporated into clinical practice. The remarkable reduction in death rates achieved with these therapies has resulted in a shift in emphasis from efforts to reduce mortality to a focus on tackling the downstream consequence of survival: post-infarction heart failure. Infarct size is the main determinant of long-term mortality and chronic heart failure, and thus, the possibility of limiting the extent of necrosis during an ST-segment elevation myocardial infarction is of great individual and socioeconomic value. After the great success of therapies to reduce ischemic injury, the time has come to focus efforts on therapies to reduce reperfusion injury, but in the recent few years, few interventions have successfully passed the proof-of-concept stage. In this review, we examine the past, present, and future therapies to reduce ischemia/reperfusion injury. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

  2. 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.)

  3. Major prognostic impact of persistent microvascular obstruction as assessed by contrast-enhanced cardiac magnetic resonance in reperfused acute myocardial infarction

    International Nuclear Information System (INIS)

    Cochet, Alexandre A.; Lalande, Alain; Walker, Paul M.; Touzery, Claude; Brunotte, Francois; Lorgis, Luc; Beer, Jean-Claude; Cottin, Yves; Zeller, Marianne; Wolf, Jean-Eric

    2009-01-01

    The aim of this study was to compare the prognostic significance of microvascular obstruction (MO) and persistent microvascular obstruction (PMO) as assessed by cardiac magnetic resonance (CMR) in patients with acute myocardial infarction (AMI). CMR was performed in 184 patients within the week following successfully reperfused first AMI. First-pass images were performed to evaluate extent of MO and late gadolinium-enhanced images to assess PMO and infarct size (IS). Major adverse cardiac events (MACE) were collected at 1-year follow-up. MO and PMO were found in 127 (69%) and 87 (47%) patients, respectively. By using univariate logistic regression analysis, high Global Registry of Acute Coronary Events (GRACE) risk score (odds ratio [OR] 95% confidence interval [CI]: 3.6 [1.8-7.4], p < 0.001), IS greater than 10% (OR [95% CI]: 2.7 [1.1-6.9], p = 0.036), left ventricular ejection fraction less than 40% (OR [95% CI]: 2.4 [1.1-5.2], p = 0.027), presence of MO (OR [95% CI]: 3.1 [1.3-7.3], p = 0.004) and presence of PMO (OR [95% CI]:10 [4.1-23.9], p < 0.001) were shown to be significantly associated with the outcome. By using multivariate analysis, presence of MO (OR [95% CI]: 2.5 [1.0-6.2], p = 0.045) or of PMO (OR [95% CI]: 8.7 [3.6-21.1], p < 0.001), associated with GRACE score, were predictors of MACE. Presence of microvascular obstruction and persistent microvascular obstruction is very common in AMI patients even after successful reperfusion and is associated with a dramatically higher risk of subsequent cardiovascular events, beyond established prognostic markers. Moreover, our data suggest that the prognostic impact of PMO might be superior to MO. (orig.)

  4. Lebetin 2, a Snake Venom-Derived Natriuretic Peptide, Attenuates Acute Myocardial Ischemic Injury through the Modulation of Mitochondrial Permeability Transition Pore at the Time of Reperfusion.

    Directory of Open Access Journals (Sweden)

    Bochra Tourki

    Full Text Available Cardiac ischemia is one of the leading causes of death worldwide. It is now well established that natriuretic peptides can attenuate the development of irreversible ischemic injury during myocardial infarction. Lebetin 2 (L2 is a new discovered peptide isolated from Macrovipera lebetina venom with structural similarity to B-type natriuretic peptide (BNP. Our objectives were to define the acute cardioprotective actions of L2 in isolated Langendorff-perfused rat hearts after regional or global ischemia-reperfusion (IR. We studied infarct size, left ventricular contractile recovery, survival protein kinases and mitochondrial permeability transition pore (mPTP opening in injured myocardium. L2 dosage was determined by preliminary experiments at its ability to induce cyclic guanosine monophosphate (cGMP release without changing hemodynamic effects in normoxic hearts. L2 was found to be as effective as BNP in reducing infarct size after the induction of either regional or global IR. Both peptides equally improved contractile recovery after regional IR, but only L2 increased coronary flow and reduced severe contractile dysfunction after global ischemia. Cardioprotection afforded by L2 was abolished after isatin or 5-hydroxydecanote pretreatment suggesting the involvement of natriuretic peptide receptors and mitochondrial KATP (mitoKATP channels in the L2-induced effects. L2 also increased survival protein expression in the reperfused myocardium as evidenced by phosphorylation of signaling pathways PKCε/ERK/GSK3β and PI3K/Akt/eNOS. IR induced mitochondrial pore opening, but this effect was markedly prevented by L2 treatment. These data show that L2 has strong cardioprotective effect in acute ischemia through stimulation of natriuretic peptide receptors. These beneficial effects are mediated, at least in part, by mitoKATP channel opening and downstream activated survival kinases, thus delaying mPTP opening and improving IR-induced mitochondrial

  5. Determinants of myocardial hemorrhage after coronary reperfusion in the anesthetized dog

    International Nuclear Information System (INIS)

    Higginson, L.A.J.; White, F.; Heggtveit, H.A.; Sanders, T.M.; Bloor, C.M.; Covell, J.W.

    1982-01-01

    Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 10 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitate reflow. Complete flow data were available in eight reperfused and 10 analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium. Pathologic examination indicatd that hemorrhage did not occur into otherwise microscopically normal myocardium. These studies indicate that hemorrhage or reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and this occurs only into myocardium already markedly compromised at the time of reperfusion

  6. Myocardial protection from ischemia-reperfusion injury post coronary revascularization.

    Science.gov (United States)

    Binder, Andrew; Ali, Asghar; Chawla, Raveen; Aziz, Hammad A; Abbate, Antonio; Jovin, Ion S

    2015-01-01

    Effective primary and secondary prevention and advances in cardiac surgery have significantly improved the care and outcomes of patients with myocardial ischemia. While timely reperfusion has proved to be an invaluable tool, ischemia-reperfusion injury represents a mechanism that may limit its effectiveness. Numerous experimental studies have shown effective protection from ischemia-reperfusion injury in animal models, but translation into clinical practice has been less successful. This article summarizes the role of ischemia-reperfusion injury in the pathophysiology of ischemic heart disease and gives an overview of the various modalities that have been developed in order to provide myocardial protection from reperfusion injury in clinical practice.

  7. Liraglutide-induced reduction of myocardial ischemia- reperfusion ...

    African Journals Online (AJOL)

    ischemia/reperfusion injury. Jci Insight 2016; 1(19): e90931. 16. Wang Y, Zhang H, Chai F, Liu X, Berk M. The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression. BMC Psychiatry 2014; 14(1): 349. 17. Liu Z, Chen JM, ...

  8. Effects of nicorandil on cardiac sympathetic nerve activity after reperfusion therapy in patients with first anterior acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kasama, Shu; Toyama, Takuji; Suzuki, Tadashi; Kurabayashi, Masahiko [Gunma University School of Medicine, Department of Cardiovascular Medicine, Maebashi (Japan); Kumakura, Hisao; Takayama, Yoshiaki; Ichikawa, Shuichi [Cardiovascular Hospital of Central Japan, Gunma (Japan)

    2005-03-01

    Ischaemic preconditioning (PC) is a cardioprotective phenomenon in which short periods of myocardial ischaemia result in resistance to decreased contractile dysfunction during a subsequent period of sustained ischaemia. Nicorandil, an ATP-sensitive potassium channel opener, can induce PC effects on sympathetic nerves during myocardial ischaemia. However, its effects on cardiac sympathetic nerve activity (CSNA) and left ventricular remodelling have not been determined. In this study, we sought to determine whether nicorandil administration improves CSNA in patients with acute myocardial infarction (AMI). We studied 58 patients with first anterior AMI, who were randomly assigned to receive nicorandil (group A) or isosorbide dinitrate (group B) after primary coronary angioplasty. The nicorandil or isosorbide dinitrate was continuously infused for >48 h. The extent score (ES) was determined from {sup 99m}Tc-pyrophosphate scintigraphy, and the total defect score (TDS) was determined from {sup 201}Tl scintigraphy 3-5 days after primary angioplasty. The left ventricular end-diastolic volume (LVEDV) and left ventricular ejection fraction (LVEF) were determined by left ventriculography 2 weeks later. The delayed heart/mediastinum count (H/M) ratio, delayed TDS and washout rate (WR) were determined from {sup 123}I-meta-iodobenzylguanidine (MIBG) images 3 weeks later. The left ventriculography results were re-examined 6 months after treatment. Fifty patients originally enrolled in the trial completed the entire protocol. After treatment, no significant differences were observed in ES or left ventricular parameters between the two groups. However, in group A (n=25), the TDSs determined from {sup 201}Tl and {sup 123}I-MIBG were significantly lower (26{+-}6 vs 30{+-}5, P<0.01, and 32{+-}8 vs 40{+-}6, P<0.0001, respectively), the H/M ratio significantly higher (1.99{+-}0.16 vs 1.77{+-}0.30, P<0.005) and the WR significantly lower (36%{+-}8% vs 44%{+-}12%, P<0.005) than in group B

  9. Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction.

    Science.gov (United States)

    Christia, Panagiota; Bujak, Marcin; Gonzalez-Quesada, Carlos; Chen, Wei; Dobaczewski, Marcin; Reddy, Anilkumar; Frangogiannis, Nikolaos G

    2013-08-01

    Mouse models of myocardial infarction are essential tools for the study of cardiac injury, repair, and remodeling. Our current investigation establishes a systematic approach for quantitative evaluation of the inflammatory and reparative response, cardiac function, and geometry in a mouse model of reperfused myocardial infarction. Reperfused mouse infarcts exhibited marked induction of inflammatory cytokines that peaked after 6 hr of reperfusion. In the infarcted heart, scar contraction and chamber dilation continued for at least 28 days after reperfusion; infarct maturation was associated with marked thinning of the scar, accompanied by volume loss and rapid clearance of cellular elements. Echocardiographic measurements of end-diastolic dimensions correlated well with morphometric assessment of dilative remodeling in perfusion-fixed hearts. Hemodynamic monitoring was used to quantitatively assess systolic and diastolic function; the severity of diastolic dysfunction following myocardial infarction correlated with cardiomyocyte hypertrophy and infarct collagen content. Expression of molecular mediators of inflammation and cellular infiltration needs to be investigated during the first 72 hr, whereas assessment of dilative remodeling requires measurement of geometric parameters for at least four weeks after the acute event. Rapid initiation and resolution of the inflammatory response, accelerated scar maturation, and extensive infarct volume loss are important characteristics of infarct healing in mice.

  10. Estimated gain in life expectancy : A simple tool to select optimal reperfusion treatment in individual patients with evolving myocardial infarction

    NARCIS (Netherlands)

    M.J. van der Vlugt (Maureen); A.E.R. Arnold (Alfred); J.W. Deckers (Jaap); M.L. Simoons (Maarten); H. Boersma (Eric)

    1996-01-01

    textabstractCurrently several modes of reperfusion therapy for acute myocardial infarction are available. Streptokinase, accelerated alteplase and direct angioplasty are the most frequently used. These options are increasingly effective, but are also increasingly complex and costly. Since,

  11. Renal insufficiency was correlated with 2-year mortality for rural female patients with ST-segment elevation acute myocardial infarction after reperfusion therapy: a multicenter, prospective study.

    Science.gov (United States)

    Gao, Yuan; Jiang, Daming; Zhang, Bo; Sun, Yujiao; Ren, Lina; Fan, Dandan; Qi, Guoxian

    2015-12-24

    Renal insufficiency (RI) following ST-segment elevation acute myocardial infarction (STEMI) is associated with a worse clinical prognosis. We investigated the impact of RI on long-term mortality in rural female patients with STEMI and evaluated prognostic factors. A prospective cohort study of 436 consecutive rural female patients who were successfully treated with reperfusion therapy for STEMI between May 2009 and August 2011 in secondary care hospitals in Liaoning province northeastern China and followed up for 2 years. Patients were divided into three groups by estimated glomerular filtration rate (eGFR): Normal group, eGFR ≥90 mL/min/1.73 m(2) (n = 233). Moderate group, eGFR 60-90 mL/min/1.73 m(2) (n = 108). RI group, eGFR <60 mL/min/1.73 m(2) (n = 95). The primary outcome was 2-year mortality. During follow-up (mean 741 ± 118 days), the RI group had a significantly higher mortality than the other groups (24.21 % vs. 6.87 % and 10.19 %, p < 0.001). The RI group had significantly higher hospital mortality (7.37 % p = 0.045 vs. Normal group). RI increased the risk of hospital mortality (hazard ratio (HR) 1.832, 95 % CI 1.017-3.091, p = 0.033), and increased the risk of 2-year mortality (HR 3.872, 95 % CI 2.004-6.131, p < 0.001). Multivariate analysis showed eGFR <90 ml/min/1.73 m(2) and age ≥75 years as independent predictors of mortality at 2 years. In detail these were eGFR 60-90 ml/min/1.73 m(2) with HR 2.081, 95%CI 1.250-2.842, p < 0.001; eGFR <60 ml/min/1.73 m(2) with HR 3.872, 95%CI 2.004-6.131, p < 0.001; age ≥75 with HR 1.461, 95%CI 1.011-1.952, p = 0.024. RI had a powerful correlation with long-term mortality for rural female patients with STEMI after reperfusion therapy.

  12. Timing of ischemic onset estimated from the electrocardiogram is better than historical timing for predicting outcome after reperfusion therapy for acute anterior myocardial infarction: a DANish trial in Acute Myocardial Infarction 2 (DANAMI-2) substudy

    DEFF Research Database (Denmark)

    Sejersten, Maria; Ripa, Rasmus S; Grande, Peer

    2007-01-01

    BACKGROUND: Acute treatment strategy and subsequently prognosis are influenced by the duration of ischemia in patients with ST-elevation acute myocardial infarction (AMI). However, timing of ischemia may be difficult to access by patient history (historical timing) alone. We hypothesized that an ...

  13. Predictors of 30-Day Mortality in the Era of Reperfusion for Acute Myocardial Infarction : Results From an International Trial of 41021 Patients

    NARCIS (Netherlands)

    K.L. Lee (Kerry); L.H. Woodlief (Lynn); E.J. Topol (Eric); W.G. Weaver; A. Betriu; J.J. Col (Jacques); M.L. Simoons (Maarten); P.E. Aylward (Philip Edmund); R.M. Califf (Robert); F.J.J. van de Werf (Frans)

    1995-01-01

    textabstractBACKGROUND: Despite remarkable advances in the treatment of acute myocardial infarction, substantial early patient mortality remains. Appropriate choices among alternative therapies and the use of clinical resources depend on an estimate of the patient's risk. Individual patients reflect

  14. Myocardial kinetics of (201)Thallium, (99m)Tc-tetrofosmin, and (99m)Tc-sestamibi in an acute ischemia-reperfusion model using isolated rat heart.

    Science.gov (United States)

    Fukushima, Kenji; Momose, Mitsuru; Kondo, Chisato; Kusakabe, Kiyoko; Kasanuki, Hiroshi

    2007-07-01

    (201)Thallium (TL), (99m)Tc-tetrofosmin (TF), and (99m)Tc-sestamibi (MIBI) are extensively used as myocardial perfusion agents. The objective of the present study was to evaluate their kinetics under acute ischemia-reperfusion. Isolated rat hearts, perfused by the Langendorff method at a constant flow rate of 10 ml/min, were allotted to normal control, mild ischemia, and severe ischemia groups, in which 20-min tracer wash-in was conducted followed by a 25-min tracer washout. No-flow ischemia (15 min for mild ischemia groups; 30 min for severe ischemia groups) was induced before conducting wash-in and washout in the ischemia groups. Whole-heart radioactivity was determined with an external gamma detector. Myocardial flow rate (K (1), ml/min) and clearance rate (k (2), min(-1)) were calculated. K (1TL), K (1TF), and K (1MIBI) decreased according to the severity of ischemia (K (1TL) 5.32 +/- 0.53, 4.76 +/- 0.70, and 1.44 +/- 0.59; K (1TF) 3.80 +/- 0.70, 2.73 +/- 0.99, and 1.09 +/- 0.45; and K (1MIBI) 3.45 +/- 1.10, 2.15 +/- 0.82, and 1.05 +/- 0.13, in the normal control, mild, and severe ischemia groups, respectively). K (1) was significantly higher for TL than for the (99m)Tc tracers (P < 0.05), but the (99m)Tc tracers had equivalent K (1) values. k (2TL) increased significantly (P < 0.05) in the ischemia groups (k (2TL) 0.062 +/- 0.013, 0.11 +/- 0.045, and 0.12 +/- 0.035), but showed no significant difference between the ischemia groups. k (2MIBI) and k (2TF) were significantly (P < 0.05) lower than k (2TL) and increased significantly (P < 0.05) in the severe ischemia group (k (2TF) 0.0056 +/- 0.0022, 0.0037 +/- 0.0015, and 0.024 +/- 0.015; and k (2MIBI) 0.00072 +/- 0.0011, 0.00038 +/- 0.00076, and 0.042 +/- 0.034). k (2MIBI) was significantly (P < 0.05) lower than k (2TF) in the normal control and mild ischemia groups. Tracer extraction was higher for TL than for the (99m)Tc tracers and all tracers decreased according to the severity of ischemia-reperfusion in the

  15. Cardiovascular magnetic resonance of the myocardium at risk in acute reperfused myocardial infarction: comparison of T2-weighted imaging versus the circumferential endocardial extent of late gadolinium enhancement with transmural projection.

    Science.gov (United States)

    Ubachs, Joey F A; Engblom, Henrik; Erlinge, David; Jovinge, Stefan; Hedström, Erik; Carlsson, Marcus; Arheden, Håkan

    2010-03-29

    In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. Recently, T2-weighted cardiovascular magnetic resonance (CMR) has been introduced as a new method for assessing MaR several days after the acute event. Furthermore, it has been suggested that the endocardial extent of infarction as assessed by late gadolinium enhanced (LGE) CMR can also be used to quantify the MaR. Hence, we sought to assess the ability of endocardial extent of infarction by LGE CMR to predict MaR as compared to T2-weighted imaging. Thirty-seven patients with early reperfused first-time ST-segment elevation myocardial infarction underwent CMR imaging within the first week after percutaneous coronary intervention. The ability of endocardial extent of infarction by LGE CMR to assess MaR was evaluated using T2-weighted imaging as the reference method. MaR determined with T2-weighted imaging (34 +/- 10%) was significantly higher (p infarction (23 +/- 12%). There was a weak correlation between the two methods (r2 = 0.17, p = 0.002) with a bias of -11 +/- 12%. Myocardial salvage determined with T2-weighted imaging (58 +/- 22%) was significantly higher (p myocardial salvage determined with endocardial extent of infarction (45 +/- 23%). No MaR could be determined by endocardial extent of infarction in two patients with aborted myocardial infarction. This study demonstrated that the endocardial extent of infarction as assessed by LGE CMR underestimates MaR in comparison to T2-weighted imaging, especially in patients with early reperfusion and aborted myocardial infarction.

  16. Effects of intracoronary melatonin on ischemia-reperfusion injury in ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Ekeløf, Sarah V; Halladin, Natalie L; Jensen, Svend E

    2016-01-01

    Acute coronary occlusion is effectively treated by primary percutaneous coronary intervention. However, myocardial ischemia-reperfusion injury is at the moment an unavoidable consequence of the procedure. Oxidative stress is central in the development of ischemia-reperfusion injury. Melatonin......, an endogenous hormone, acts through antioxidant mechanisms and could potentially minimize the myocardial injury. The aim of the experimental study was to examine the cardioprotective effects of melatonin in a porcine closed-chest reperfused infarction model. A total of 20 landrace pigs were randomized...... to a dosage of 200 mg (0.4 mg/mL) melatonin or placebo (saline). The intervention was administered intracoronary and intravenous. Infarct size, area at risk and microvascular obstruction were determined ex vivo by cardiovascular magnetic resonance imaging. Myocardial salvage index was calculated. The plasma...

  17. Remote Ischemic Perconditioning to Reduce Reperfusion Injury During Acute ST-Segment-Elevation Myocardial Infarction: A Systematic Review and Meta-Analysis.

    Science.gov (United States)

    McLeod, Shelley L; Iansavichene, Alla; Cheskes, Sheldon

    2017-05-17

    Remote ischemic conditioning (RIC) is a noninvasive therapeutic strategy that uses brief cycles of blood pressure cuff inflation and deflation to protect the myocardium against ischemia-reperfusion injury. The objective of this systematic review was to determine the impact of RIC on myocardial salvage index, infarct size, and major adverse cardiovascular events when initiated before catheterization. Electronic searches of Medline, Embase, and Cochrane Central Register of Controlled Trials were conducted and reference lists were hand searched. Randomized controlled trials comparing percutaneous coronary intervention (PCI) with and without RIC for patients with ST-segment-elevation myocardial infarction were included. Two reviewers independently screened abstracts, assessed quality of the studies, and extracted data. Data were pooled using random-effects models and reported as mean differences and relative risk with 95% confidence intervals. Eleven articles (9 randomized controlled trials) were included with a total of 1220 patients (RIC+PCI=643, PCI=577). Studies with no events were excluded from meta-analysis. The myocardial salvage index was higher in the RIC+PCI group compared with the PCI group (mean difference: 0.08; 95% confidence interval, 0.02-0.14). Infarct size was reduced in the RIC+PCI group compared with the PCI group (mean difference: -2.46; 95% confidence interval, -4.66 to -0.26). Major adverse cardiovascular events were lower in the RIC+PCI group (9.5%) compared with the PCI group (17.0%; relative risk: 0.57; 95% confidence interval, 0.40-0.82). RIC appears to be a promising adjunctive treatment to PCI for the prevention of reperfusion injury in patients with ST-segment-elevation myocardial infarction; however, additional high-quality research is required before a change in practice can be considered. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

  18. Myocardial scintigraphy in acute myocardial infarction

    International Nuclear Information System (INIS)

    Faerestrand, S.

    1984-01-01

    The sensitivity and specificity of 99m Tc-PYP myocardial scintigraphy for detecting an acute myocardial infarction were studied in 39 patients hospitalized because of central chest pain. One myocardial scintigraphic examination was done in each patient between the first and sixth day after the chest pain had started. Twenty-two patients had a myocardial infarction based on history, ECG and enzym values and myocardial scintigraphy was positive in twenty of these. Three patients with left bundle branch block and myocardial infarction all had a positive myocardial scintigram and the one patient with negative ECG and myocardial infarction also had a positive myocardial scintigram. The sensitivity is 91% and the specificity is 91.7% for 99m Tc-PYP myocardial scintigraphy in the detection of acute myocardial infarction. No complications were seen. (Auth.)

  19. Comparison of infarct size changes with delayed contrast-enhanced magnetic resonance imaging and electrocardiogram QRS scoring during the 6 months after acutely reperfused myocardial infarction

    DEFF Research Database (Denmark)

    Bang, L.E.; Ripa, R.S.; Grande, P.

    2008-01-01

    INTRODUCTION: Magnetic resonance imaging using the delayed contrast-enhanced (DE-MRI) method can be used for characterizing and quantifying myocardial infarction (MI). Electrocardiogram (ECG) score after the acute phase of MI can be used to estimate the portion of left ventricular myocardium...

  20. Quantitative T2 mapping after reperfusion therapy in patients with acute myocardial infarction: A comparison with late gadolinium enhancement and cine MR imaging.

    Science.gov (United States)

    Park, Chul Hwan; Choi, Eui-Young; Yoon, Young Won; Kwon, Hyuck Moon; Hong, Bum Kee; Lee, Byoung Kwon; Min, Pil-Ki; Greiser, Andreas; Paek, Mun Young; Hwang, Sung Ho; Kim, Tae Hoon

    2015-12-01

    This study evaluates myocardial edema by quantitative T2 mapping in patients with acute myocardial infarction (AMI) and compares the lateral extent of myocardial edema with those of infarcted and dysfunctional myocardium. Cardiac magnetic resonance images (MRIs) of 31 patients (M:F=29:2, mean age: 52.5±10.8years) with AMI were reviewed. On cine-MRI, all short axis images of the left ventricle (LV) were divided into 60 sectors. The regional wall motion of each sector was calculated as follows: systolic wall thickening (SWT, %)=[(LV wall thicknessES-LV wall thicknessED)/LV wall thicknessED]*100. Dysfunctional myocardium was defined as sectors with decreased SWT lower than 40%. On LGE-images, myocardial infarction was defined as an area of hyper-enhancement more than 5 SDs from the remote myocardium. On T2 map, myocardial edema was defined as an area in which T2 values were at least 2 SDs higher than those from remote myocardium. The lateral extents of infarcted myocardium, myocardial edema, and dysfunctional myocardium were calculated as the percentage of central angles ((central angle of the involved myocardium/360)*100 (%)) and then compared. The lateral extent of myocardial edema was slightly larger than that of infarcted myocardium (37.4±13.3% vs. 35±12.9%, pinfarcted myocardium or myocardial edema (pmyocardial edema beyond the infarcted myocardium might be narrow, but the dysfunctional myocardium could be significantly larger than myocardial edema, suggesting stunned myocardium without edema. Copyright © 2015 Elsevier Inc. All rights reserved.

  1. 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

  2. ECG and enzymatic indicators of therapeutic success after intravenous streptokinase for acute myocardial infarction

    DEFF Research Database (Denmark)

    Clemmensen, P; Grande, P; Pedersen, F

    1990-01-01

    Thrombolytic therapy has been documented to result in reperfusion of jeopardized myocardium and reduction in the size of the acute myocardial infarction (AMI). The effect of intravenous streptokinase on a creatine kinase-MB (CK-MB) reperfusion index and an ECG estimate of myocardial salvage was t...

  3. The role of secretory phospholipases as therapeutic targets for the treatment of myocardial ischemia reperfusion injury.

    Science.gov (United States)

    Ravindran, Sriram; Kurian, Gino A

    2017-08-01

    Myocardial reperfusion injury is a consequence of restoration of blood flow post ischemia. It is a complex process involving an acute inflammatory response activated by cytokines, chemokines, growth factors, and mediated by free radicals, calcium overload leading to mitochondrial dysfunction. Secretory phospholipases (sPLA2) are a group of pro-inflammatory molecules associated with diseases such as atherosclerosis, which increase the risk of reperfusion injury. This acute response leads to breakdown of phospholipids such as cardiolipin, found in the mitochondrial inner membrane, leading to disruption of energy producing enzymes of the electron transport chain. Thus the activation of secretory phospholipases has a direct link to the vascular occlusion and arrhythmia observed in myocardial reperfusion injury. Therapeutic agents targeting sPLA2 are under human trials and many are in the preclinical phase. This article reviews the pathological effects of various groups of secretory phospholipases (I, II, V and X) implicated in myocardial ischemia reperfusion injury and the phospholipase inhibitors under development. Considering the fact that human trials in this class of drugs is limited, sPLA2 as a potential target for drug development is emphasized. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  4. Low dose prospective ECG-gated delayed enhanced dual-source computed tomography in reperfused acute myocardial infarction comparison with cardiac magnetic resonance

    Energy Technology Data Exchange (ETDEWEB)

    Wang Rui, E-mail: rui_wang1979@yahoo.cn [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Zhang Zhaoqi, E-mail: zhaoqi5000@vip.sohu.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Xu Lei, E-mail: leixu2001@hotmail.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Ma Qin, E-mail: tel1367@gmail.com [Department of Emergency, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); He Yi, E-mail: heyi139@sina.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Lu Dongxu, E-mail: larry.hi@163.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Yu Wei, E-mail: yuwei02@gmail.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China); Fan Zhanming, E-mail: fanzm120@tom.com [Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, 100029 Beijing (China)

    2011-11-15

    Purpose: To determine whether prospective electrocardiogram (ECG)-gated delayed contrast-enhanced dual-source computed tomography (DCE-DSCT) can accurately delineate the extension of myocardial infarction (MI) compared with delayed enhanced cardiac MR (DE-MR). Material and methods: Eleven patients were examined using dual-source CT and cardiac MR in 2 weeks after a first reperfused MI. DCE-DSCT scan protocol was performed with prospective ECG-gating sequential scan model 7 min after contrast administration. In a 17-model, infarcted myocardium detected by DE-MR was categorized as transmural and subendocardial extension. Segment of infarcted location and graded transmurality were compared between DCE-MDCT and DE-MR. Results: In all eleven patients, diagnostic quality was obtained for depicting delayed enhanced myocardium. Agreement between DCE-DSCT and MR was good on myocardial segment based comparison (kappa = 0.85, p < 0.001), and on transmural and subendocardial infarction type comparison (kappa = 0.82, p < 0.001, kappa = 0.52, p < 0.001, respectively). CT value was higher on infarcted region than that of normal region (100.02 {+-} 9.57 HU vs. 72.63 {+-} 7.32 HU, p < 0.001). Radiation dose of prospectively ECG-gating protocol were 0.99 {+-} 0.08 mSv (0.82-1.19 mSv). Conclusions: Prospective ECG-gated DCE-DSCT can accurately assess the extension and the patterns of myocardial infarction with low radiation dose.

  5. Cell therapy in reperfused acute myocardial infarction does not improve the recovery of perfusion in the infarcted myocardium: a cardiac MR imaging study.

    Science.gov (United States)

    Robbers, Lourens F H J; Nijveldt, Robin; Beek, Aernout M; Hirsch, Alexander; van der Laan, Anja M; Delewi, Ronak; van der Vleuten, Pieter A; Tio, René A; Tijssen, Jan G P; Hofman, Mark B M; Piek, Jan J; Zijlstra, Felix; van Rossum, Albert C

    2014-07-01

    To investigate the effects of cell therapy on myocardial perfusion recovery after treatment of acute myocardial infarction (MI) with primary percutaneous coronary intervention (PCI). In this HEBE trial substudy, which was approved by the institutional review board (trial registry number ISRCTN95796863), the authors assessed the effects of intracoronary infusion with bone marrow-derived mononuclear cells (BMMCs) or peripheral blood-derived mononuclear cells (PBMCs) on myocardial perfusion recovery by using cardiac magnetic resonance (MR) imaging after revascularization. In 152 patients with acute MI treated with PCI, cardiac MR imaging was performed after obtaining informed consent-before randomization to BMMC, PBMC, or standard therapy (control group)-and repeated at 4-month follow-up. Cardiac MR imaging consisted of cine, rest first-pass perfusion, and late gadolinium enhancement imaging. Perfusion was evaluated semiquantitatively with signal intensity-time curves by calculating the relative upslope (percentage signal intensity change). The relative upslope was calculated for the MI core, adjacent border zone, and remote myocardium. Perfusion differences among treatment groups or between baseline and follow-up were assessed with the Wilcoxon signed rank or Mann-Whitney U test. At baseline, myocardial perfusion differed between the MI core (median, 6.0%; interquartile range [IQR], 4.1%-8.0%), border zone (median, 8.4%; IQR, 6.4%-10.2%), and remote myocardium (median, 12.2%; IQR, 10.5%-15.9%) (P < .001 for all), with equal distribution among treatment groups. These interregional differences persisted at follow-up (P < .001 for all). No difference in perfusion recovery was found between the three treatment groups for any region. After revascularization of ST-elevation MI, cell therapy does not augment the recovery of resting perfusion in either the MI core or border zone. © RSNA, 2014.

  6. August rats are more resistant to arrhythmogenic effect of myocardial ischemia and reperfusion than Wistar rats.

    Science.gov (United States)

    Belkina, L M; Kirillina, T N; Pshennikova, M G; Arkhipenko, Yu V

    2002-06-01

    As differentiated from Wistar rats, myocardial ischemia and reperfusion produce no ventricular fibrillation in August rats. Pretreatment with nitric oxide synthase inhibitor Nw-nitro-L-arginine increased mortality rate in August rats with acute myocardial infarction from 20 to 40%. Under these conditions mortality rate in Wistar rats increased from 50 to 71%. Interstrain differences in the resistance of these animals to the arrhythmogenic effect of ischemia are probably associated with higher activity of the nitric oxide system in August rats compared to Wistar rats.

  7. Predicting ischemic mitral regurgitation in patients with acute ST-elevation myocardial infarction: Does time to reperfusion really matter and what is the role of collateral circulation?

    Science.gov (United States)

    Valuckiene, Zivile; Budrys, Povilas; Jurkevicius, Renaldas

    2016-01-15

    Ischemic mitral regurgitation (MR) is an adverse prognostic factor. We aimed to assess the role of time delay from symptom onset to reperfusion, and the impact of collateral circulation to incidence of MR in relation to established echocardiographic and clinical risk factors. Patients with STEMI presenting within 12 h from symptom onset and treated with primary percutaneous coronary intervention (PPCI) at Hospital of Lithuanian University of Health Sciences were enrolled. Echocardiography was performed after PPCI. Based on MR grade, patients were divided into no significant MR (NMR, grade 0-I MR, N = 102) and ischemic MR (IMR, grade ≥ 2 MR, N = 71) groups. Well-developed collaterals were defined as grade ≥ 2 by Rentrop classification. Continuous variables were compared by independent samples Student's T-test. Multivariate logistic regression analysis was used to identify independent predictors of ischemic MR. Time to reperfusion, MI localization, TIMI flow before/after PCI was similar between the groups. IMR group patients were elder, more often females and non-smokers, had lower body mass index, higher prevalence of multi-vessel coronary artery disease (CAD), better-developed collateral supply, greater left ventricular end-diastolic diameter index, left atrial index, pulmonary artery systolic pressure and lower ejection fraction. Multivariate logistic regression analysis revealed that ischemic MR is predicted by female gender, well-developed collateral supply, presence of multi-vessel CAD, and lower EF. In acute STEMI significant MR is unrelated to ischemic time and is predicted by female gender, lower EF, multi-vessel CAD and well-developed collateral supply to the infarct region.

  8. Exenatide reduces reperfusion injury in patients with ST-segment elevation myocardial infarction

    DEFF Research Database (Denmark)

    Lønborg, Jacob; Vejlstrup, Niels; Kelbæk, Henning

    2011-01-01

    Aims Exenatide, a glucagon-like-peptide-1 analogue, increases myocardial salvage in experimental settings with coronary occlusion and subsequent reperfusion. We evaluated the cardioprotective effect of exenatide at the time of reperfusion in patients with ST-segment elevation myocardial infarction.......11). No difference was observed in left ventricular function or 30-day clinical events. No adverse effects of exenatide were observed. Conclusion In patients with STEMI undergoing pPCI, administration of exenatide at the time of reperfusion increases myocardial salvage....

  9. The Formin, DIAPH1, is a Key Modulator of Myocardial Ischemia/Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Karen M. O'Shea

    2017-12-01

    Full Text Available The biochemical, ionic, and signaling changes that occur within cardiomyocytes subjected to ischemia are exacerbated by reperfusion; however, the precise mechanisms mediating myocardial ischemia/reperfusion (I/R injury have not been fully elucidated. The receptor for advanced glycation end-products (RAGE regulates the cellular response to cardiac tissue damage in I/R, an effect potentially mediated by the binding of the RAGE cytoplasmic domain to the diaphanous-related formin, DIAPH1. The aim of this study was to investigate the role of DIAPH1 in the physiological response to experimental myocardial I/R in mice. After subjecting wild-type mice to experimental I/R, myocardial DIAPH1 expression was increased, an effect that was echoed following hypoxia/reoxygenation (H/R in H9C2 and AC16 cells. Further, compared to wild-type mice, genetic deletion of Diaph1 reduced infarct size and improved contractile function after I/R. Silencing Diaph1 in H9C2 cells subjected to H/R downregulated actin polymerization and serum response factor-regulated gene expression. Importantly, these changes led to increased expression of sarcoplasmic reticulum Ca2+ ATPase and reduced expression of the sodium calcium exchanger. This work demonstrates that DIAPH1 is required for the myocardial response to I/R, and that targeting DIAPH1 may represent an adjunctive approach for myocardial salvage after acute infarction.

  10. Gadolinium-enhanced magnetic resonance imaging in acute myocardial infarction

    International Nuclear Information System (INIS)

    Dijkman, P.R.M. van; Wall, E.E. van der; Roos, A. de; Doornbos, J.; Laarse, A. van der; Voorthuisen, A.E. van; Bruschke, A.V.G.; Rossum, A.C. van

    1990-01-01

    To evaluate he usefulness of the paramagnetic contrast agent Gadolinium-DTPA (diethylenetriaminepentaacetic acid) in Magnetic Resonance. Imaging of acute myocardial infarction, we studied a total of 45 patients with a first acute myocardial infarction by ECG-gated magnetic resonance imaging before and after intravenous administration of 0.1 mmol/kg Gadolinium-DTPA. All patients received thrombolytic treatment by intravenous streptokinase. The magnetic resonance imaging studies were preformed after a meam of 88 h (range 15-241) after the acute onset of acute myocardial infarction. Five patients without evidence of cardiac disease served as controls. Spin-echo measurements (TE 30 ms) were made using a Philips Gyroscan (0.5 Tesla) or a Teslacon II (0.6 Tesla). The 45 patients were divided into four groups of patients. In Group I( patients) Gadolinium-DTPA improved the detection of myocardial infarction by Gadolinium-DTPA. In Group II (20 patients) the magnetic resonance imaging procedure was repeated every 10 min for up to 40 min following administration of Gadolinium-DTPA. Optimal contrast enhancement was obtained 20-25 min after Gadolinium-DTPA. In Group III (27 patients) signal intensities were significantly higher in the patients who underwent the magnetic resonance imaging study more than 72 h (mean 120) after the acute event, suggesting increased acculumation of Gadolinium-DTPA in a more advanced stage of the infarction process. In Group IV (45 patients) Gadolinium-DTPA was administered in an attempt to distinguish between reperfused and nonreperfused myocardial areas after thrombolytic treatment for acute myocardial infarction. The signal intensities did not differ, but reperfused areas showed a more homogeneous aspect whereas nonreperfused areas were visualized as a more heterogeneous contrast enhancement. It is concluded that magnetic resonance imaging using the contrast agent Gadolinium-DTPA significantly improves the detection of infarcted myocardial areas

  11. Cardiac-Specific SOCS3 Deletion Prevents In Vivo Myocardial Ischemia Reperfusion Injury through Sustained Activation of Cardioprotective Signaling Molecules.

    Directory of Open Access Journals (Sweden)

    Takanobu Nagata

    Full Text Available Myocardial ischemia reperfusion injury (IRI adversely affects cardiac performance and the prognosis of patients with acute myocardial infarction. Although myocardial signal transducer and activator of transcription (STAT 3 is potently cardioprotective during IRI, the inhibitory mechanism responsible for its activation is largely unknown. The present study aimed to investigate the role of the myocardial suppressor of cytokine signaling (SOCS-3, an intrinsic negative feedback regulator of the Janus kinase (JAK-STAT signaling pathway, in the development of myocardial IRI. Myocardial IRI was induced in mice by ligating the left anterior descending coronary artery for 1 h, followed by different reperfusion times. One hour after reperfusion, the rapid expression of JAK-STAT-activating cytokines was observed. We precisely evaluated the phosphorylation of cardioprotective signaling molecules and the expression of SOCS3 during IRI and then induced myocardial IRI in wild-type and cardiac-specific SOCS3 knockout mice (SOCS3-CKO. The activation of STAT3, AKT, and ERK1/2 rapidly peaked and promptly decreased during IRI. This decrease correlated with the induction of SOCS3 expression up to 24 h after IRI in wild-type mice. The infarct size 24 h after reperfusion was significantly reduced in SOCS3-CKO compared with wild-type mice. In SOCS3-CKO mice, STAT3, AKT, and ERK1/2 phosphorylation was sustained, myocardial apoptosis was prevented, and the expression of anti-apoptotic Bcl-2 family member myeloid cell leukemia-1 (Mcl-1 was augmented. Cardiac-specific SOCS3 deletion led to the sustained activation of cardioprotective signaling molecules including and prevented myocardial apoptosis and injury during IRI. Our findings suggest that SOCS3 may represent a key factor that exacerbates the development of myocardial IRI.

  12. Effect of 5-aminosalicylic acid on myocardial capillary permeability following ischaemia and reperfusion

    DEFF Research Database (Denmark)

    Hansen, P R; Svendsen, Jesper Hastrup; Høst, N B

    1992-01-01

    The aim was to evaluate the effect of 5-aminosalicylic acid on myocardial capillary permeability for small hydrophilic molecules after ischaemia and reperfusion.......The aim was to evaluate the effect of 5-aminosalicylic acid on myocardial capillary permeability for small hydrophilic molecules after ischaemia and reperfusion....

  13. Association of time to reperfusion with left ventricular function and heart failure in patients with acute myocardial infarction treated with primary percutaneous coronary intervention: a systematic review.

    Science.gov (United States)

    Goel, Kashish; Pinto, Duane S; Gibson, C Michael

    2013-04-01

    Shorter time to reperfusion is associated with a significant reduction in mortality; however, its association with heart failure (HF) is not clearly documented. We conducted a systematic review to examine the association between time to reperfusion and incident HF and/or left ventricular dysfunction. MEDLINE/OVID, EMBASE, Cochrane Library, and Web of Science databases were searched from January 1974 to May 2012 for studies that reported the association between time to reperfusion and incident HF or left ventricular ejection fraction (LVEF) in patients undergoing primary percutaneous coronary intervention. Of 362 nonduplicate abstracts, 71 studies were selected for full-text review. Thirty-three studies were included in the final review, of which 16 were single-center studies, 7 were population-based studies, 7 were subanalyses from randomized controlled trials, and 3 were based on national samples. The pooled data demonstrate that every 1-hour delay in time to reperfusion is associated with a 4% to 12% increased risk of new-onset HF and a 4% relative increase in the risk of incident HF during follow-up. Early reperfusion was associated with a 2% to 8% greater LVEF before discharge and a 3% to 12% larger improvement in absolute LVEF at follow-up compared with the index admission. This systematic review presents evidence that longer time to reperfusion is not only associated with worsened left ventricular systolic function and new-onset HF at the time of index admission, but also with increased risk of HF and reduced improvement in left ventricular systolic function during follow-up. Copyright © 2013 Mosby, Inc. All rights reserved.

  14. Myocardial ischemia-reperfusion injury, antioxidant enzyme systems, and selenium: a review.

    Science.gov (United States)

    Venardos, Kylie M; Perkins, Anthony; Headrick, John; Kaye, David M

    2007-01-01

    Coronary heart disease (CHD) remains the greatest killer in the Western world, and although the death rate from CHD has been falling, the current increased prevalence of major risk factors including obesity and diabetes, suggests it is likely that CHD incidence will increase over the next 20 years. In conjunction with preventive strategies, major advances in the treatment of acute coronary syndromes and myocardial infarction have occurred over the past 20 years. In particular the ability to rapidly restore blood flow to the myocardium during heart attack, using interventional cardiologic or thrombolytic approaches has been a major step forward. Nevertheless, while 'reperfusion' is a major therapeutic aim, the process of ischemia followed by reperfusion is often followed by the activation of an injurious cascade. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial cause of the injury. ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function. ROS have been shown to be generated following routine clinical procedures such as coronary bypass surgery and thrombolysis, due to the unavoidable episode of ischemia-reperfusion. Furthermore, they have been associated with poor cardiac recovery post-ischemia, with recent studies supporting a role for them in infarction, necrosis, apoptosis, arrhythmogenesis and endothelial dysfunction following ischemia-reperfusion. In normal physiological condition, ROS production is usually homeostatically controlled by endogenous free radical scavengers such as superoxide dismutase, catalase, and the glutathione peroxidase and thioredoxin reductase systems. Accordingly, targeting the generation of ROS with various antioxidants has been shown to reduce injury following oxidative stress, and improve

  15. The effects of the fibrin-derived peptide Bβ15-42 in acute and chronic rodent models of myocardial ischemia-reperfusion

    NARCIS (Netherlands)

    Zacharowski, K.; Zacharowski, P.A.; Friedl, P.; Mastan, P.; Koch, A.; Boehm, O.; Rother, R.P.; Reingruber, S.; Henning, R.; Emeis, J.J.; Petzelbauer, P.

    2007-01-01

    Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. Therefore, the National Heart, Lung, and Blood Institute convened a working group to discuss reasons for such failure. As a result, the

  16. [Bonsai induced acute myocardial infarction].

    Science.gov (United States)

    Ayhan, Hüseyin; Aslan, Abdullah Nabi; Süygün, Hakan; Durmaz, Tahir

    2014-09-01

    Incidences of drug abuse and cannabis have increased in young adults, recently. Cannabis induced myocardial infarction has rarely been reported in these people. There is no any literature about a synthetic cannabinoid, being recently most popular Bonsai, to cause myocardial infarction. In this case report we presented a 33-year-old male patient who developed acute myocardial infarction after taking high doses of Bonsai.

  17. Review Paper: Myocardial Rupture After Acute Myocardial Infarction ...

    African Journals Online (AJOL)

    Myocardial rupture complications after acute myocardial infarction are infrequent but lethal. They mainly involve rupture of the ventricular free wall, ventricular septum, papillary muscle, or combined. We compare features of different kinds of myocardial ruptures after acute myocardial infarction by reviewing the clinical ...

  18. REPERFUSION THERAPY IN ACUTE CORONARY SYNDROME WITH ST SEGMENT ELEVATION

    Directory of Open Access Journals (Sweden)

    A. L. Alyavi

    2016-01-01

    Full Text Available Aim. To compare effect of percutaneous balloon angioplasty (PCA and a systemic thrombolysis (STL on the central and intracardiac hemodynamics in patients with acute coronary syndrome (ACS with ST segment elevation.Material and methods. 80 patients with ACS with ST segment elevation were included in the study. Patients were split into 2 groups depending on reperfusion strategy. PCA was performed in 55 patients (first group. 25 patients of the second group had STL with Streptokinase, i/v, 1 500 000 units per hour. Echocardiography was performed in all patients at admission and after 3 and 7 days of treatment to evaluate intracardiac hemodynamics.Results. Both reperfusion methods significantly increase of ejection fraction (EF and maximal output speed of left ventricle (LV. Increase of LV EF in patients after PCA was higher than this in patients after STL. PCA improved LV diastolic function; STL did not change this characteristic. After PCA working diagnosis of ACS was transformed to the following final diagnosis: acute myocardial infarction (AMI with Q, AMI without Q and unstable angina in 37,5, 30,4 and 32,1% of patients, respectively. After STL diagnosis of AMI with Q was defined in all patients.Conclusion. PCA in patients with ACS with ST segment elevation results in fast improvement of global systolic and diastolic LV function. Besides, PCA prevents AMI with Q in a half of these patients.

  19. The effect of Euryale ferox (Makhana), an herb of aquatic origin, on myocardial ischemic reperfusion injury.

    Science.gov (United States)

    Das, Samarjit; Der, Peter; Raychaudhuri, Utpal; Maulik, Nilanjana; Das, Dipak K

    2006-09-01

    Fox nut or gorgon nut (Euryale ferox--Family Nymphaeaceae), popularly known as Makhana, has been widely used in traditional oriental medicine to cure a variety of diseases including kidney problems, chronic diarrhea, excessive leucorrhea and hypofunction of the spleen. Based on the recent studies revealing antioxidant activities of Euryale ferox and its glucosides composition, we sought to determine if Euryale ferox seeds (Makhana) could reduce myocardial ischemic reperfusion injury. Two different models were used: acute model, where isolated rat hearts were preperfused for 15 min with Krebs Henseleit bicarbonate (KHB) buffer containing three different doses of makhana (25, 125 or 250 microg/ml) followed by 30 min of ischemia and 2 h of reperfusion; and chronic model, where rats were given two different doses of makhana (250 and 500 mg/kg/day) for 21 days, after which isolated hearts were subjected to 30 min of ischemia followed by 2 h of reperfusion. In both cases, the hearts of the Makhana treated rats were resistant to ischemic reperfusion injury as evidenced by their improved post-ischemic ventricular function and reduced myocardial infarct size. Antibody array technique was used to identify the cardioprotective proteins. The Makhana-treated hearts had increased amounts of thioredoxin-1 (Trx-1) and thioredoxin-related protein-32 (TRP32) compared to the control hearts. Western blot analysis confirmed increased expression of TRP32 and thioredoxin proteins. In vitro studies revealed that Makhana extracts had potent reactive oxygen species scavenging activities. Taken together, the results of this study demonstrate cardioprotective properties of Makhana and suggest that such cardioprotective properties may be linked with the ability of makhana to induce TRP32 and Trx-1 proteins and to scavenge ROS.

  20. A mismatch index based on the difference between measured left ventricular ejection fraction and that estimated by infarct size at three months following reperfused acute myocardial infarction

    DEFF Research Database (Denmark)

    Carlsen, Esben A; Bang, Lia E; Lønborg, Jacob

    2014-01-01

    BACKGROUND AND AIM: The reduction of left ventricular ejection fraction (LVEF) following ST-segment elevation myocardial infarction (STEMI) is a result of infarcted myocardium and may involve dysfunctional but viable myocardium. An index that may quantitatively determine whether LVEF is reduced b...

  1. Increased inflammatory response and neovascularization in reperfused vs. nonreperfused murine myocardial infarction

    NARCIS (Netherlands)

    Vandervelde, S; van Amerongen, MJ; Tio, RA; Petersen, AH; van Luyn, MJA; Harmsen, MC

    2006-01-01

    Introduction: Fundamental knowledge of the inflammatory response after myocardial infarction (MI) is indispensable for intervention toward cardiac regeneration. Although reperfusion is preferred as clinical therapy, for basic research, also permanent ligation MI models are widely used. Methods: In

  2. Large myocardial infarction with myocardium calcium deposits associated with reperfusion injury.

    Science.gov (United States)

    Rios, Elisabete; Mancio, Jennifer; Rodrigues-Pereira, Pedro; Magalhães, Domingos; Bartosch, Carla

    2014-01-01

    The clinical and autopsy findings of a 66-year-old man with myocardial infarction complicated by reperfusion injury are described, highlighting the presence of large myocardium calcium deposits. Copyright © 2014 Elsevier Inc. All rights reserved.

  3. Implication of Tc-99m tetrofosmin myocardial scintigraphy in patients with acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kajiya, Teishi; Yasaka, Yoshinori; Kurogane, Hiroyuki; Hayashi, Takatoshi; Takarada, Akira; Yoshida, Akihiro; Mori, Masuki; Itagaki, Tuyoshi; Yoshida, Yutaka [Himeji Cardiovascular Center, Hyogo (Japan)

    1997-02-01

    Usefulness of the 99mTc-tetrofosmin (TF) scintigraphy was evaluated for acute coronary events. Subjects were 182 patients with pectoralgia, who involved 110 cases with myocardial infarction (MI) and 72 cases with unstable angina. Following echocardiography for evaluation of wall move, they were subjected to imaging with gamma camera or with SPECT after intravenous administration of 99mTc-TF (222 MBq) before treatment for re-perfusion. The area at risk for evaluation was a sum of defect scores graded from 0 (normal) to 3 (defect) on images. Low local perfusion was seen in 101 cases of 102 acute MI and lowered blood flow, in 48 patients with unstable angina. FT scintigraphy was useful in the following points; diagnosis by exclusion was possible for acute ischemic heart disease, myocardial salvage after the treatment could be quantified, blood flow in ischemic region before the treatment was indicative of myocardial viability at that region. (K.H.)

  4. MR imaging of acute myocardial infarction

    International Nuclear Information System (INIS)

    Revel, D.; Dandis, G.; Pichard, J.B.; Ovize, M.; DeLorgeril, M.; Amiel, M.

    1990-01-01

    This paper reports on superparamagnetic iron oxide particles (AMI-25) evaluated in comparison with paramagnetic Gd-DOTA for the MR evaluation of acute myocardial infarct size. Twelve openchest dogs underwent 2 hours of LAD occlusion followed by 6 hours of reperfusion. AMI-25 and Gd-DOTA were intravenously injected 1 hour and 10 minutes before euthanasia, respectively, in two groups of six dogs. Gradient-echo and T1- and T2-weighted spin-echo images were obtained in six AMI-25-injected excised hearts, and T1- and T2-weighted images in six Gd-DOTA injected excised hearts. Infarct size was evaluated by planimetry of each 8-mm-thick transverse slice after ex vivo double staining and correlated with the planimetry of each 8-mm-thick transverse MR section

  5. Approaches to Improving Cardiac Structure and Function During and After an Acute Myocardial Infarction: Acute and Chronic Phases.

    Science.gov (United States)

    Kloner, Robert A; Dai, Wangde; Hale, Sharon L; Shi, Jianru

    2016-07-01

    While progress has been made in improving survival following myocardial infarction, this injury remains a major source of mortality and morbidity despite modern reperfusion therapy. While one approach has been to develop therapies to reduce lethal myocardial cell reperfusion injury, this concept has not translated to the clinics, and several recent negative clinical trials raise the question of whether reperfusion injury is important in humans undergoing reperfusion for acute ST segment elevation myocardial infarction. Therapy aimed at reducing myocardial cell death while the myocytes are still ischemic is more likely to further reduce myocardial infarct size. Developing new therapies to further reduce left ventricular remodeling after the acute event is another approach to preserving structure and function of the heart after infarction. Such therapy may include chronic administration of pharmacologic agents and/or therapies developed from the field of regenerative cardiology, including cellular or non-cellular materials such as extracellular matrix. The optimal therapy will be to administer agents that both reduce myocardial infarct size in the acute phase of infarction as well as reduce adverse left ventricular remodeling during the chronic or healing phase of myocardial infarction. Such a dual approach will help optimize the preservation of both cardiac structure and function. © The Author(s) 2015.

  6. Effects of enflurane, isoflurane, sevoflurane and desflurane on reperfusion injury after regional myocardial ischaemia in the rabbit heart in vivo

    NARCIS (Netherlands)

    Preckel, B.; Schlack, W.; Comfère, T.; Obal, D.; Barthel, H.; Thämer, V.

    1998-01-01

    It is known that volatile anaesthetics protect myocardial tissue against ischaemic and reperfusion injury in vitro. In this investigation, we have determined the effects of the inhalation anaesthetics, enflurane, isoflurane, sevoflurane and desflurane, administered only during early reperfusion, on

  7. Pharmaco-mechanic antithrombotic strategies to reperfusion of the infarct-related artery in patients with ST-elevation acute myocardial infarctions.

    Science.gov (United States)

    Kala, Petr; Miklik, Roman

    2013-06-01

    Primary percutaneous coronary intervention is the best treatment of patients with ST elevation myocardial infarction (STEMI). When managing a STEMI patient, our approach must be rapid and aggresive in order to interrupt the pathological process of thrombus formation and stabilization. The therapy must be initiated prior to angiography (pretreatment), continued during the procedure (periprocedural), recovery phase (in-hospital), and follow-up. The treatment strategies resulting in thrombus dissolution/extraction have focused on optimization of both pharmacological and interventional therapies. At present, there is no optimal evidence-based approach to all patients with STEMI, and the treatment of these patients needs to be modified with respect to the risk profile, availability of medical resources, and our experience. In this review, we summarize current pharmacological and interventional strategies used in the setting of STEMI and discuss potential benefits of novel dosing regimens and combinations of drugs and techniques.

  8. Comparative analysis of intramyocardial autotransplantation of postnatal stem cells from peripheral blood and adipose tissue in patients with acute phase of myocardial infarction, ST segment elevation, after effective thrombolytic reperfusion and coronary artery stenting

    NARCIS (Netherlands)

    Kharlamov, A. N.; Smolenskaya, O. G.; Gabinsky, Ya. L.; Bos, E. K.

    2007-01-01

    Aim. To compare various techniques of peripheral blood and adipose tissue stem cell (SC) transplantation and identify its optimal method for acute phase of myocardial infarction (MI). Material and methods. The study included 90 patients with acute MI. The participants were randomized into three

  9. Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis.

    Science.gov (United States)

    Tao, Lichan; Bei, Yihua; Lin, Shenghui; Zhang, Haifeng; Zhou, Yanli; Jiang, Jingfa; Chen, Ping; Shen, Shutong; Xiao, Junjie; Li, Xinli

    2015-01-01

    Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis. © 2015 S. Karger AG, Basel.

  10. Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

    Directory of Open Access Journals (Sweden)

    Lichan Tao

    2015-08-01

    Full Text Available Background/Aims: Acute myocardial infarction (AMI represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R injury However it remains unclear whether, and (if so how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

  11. Featured Article: Pharmacological postconditioning with delta opioid attenuates myocardial reperfusion injury in isolated porcine hearts.

    Science.gov (United States)

    Seewald, Maria; Coles, James A; Sigg, Daniel C; Iaizzo, Paul A

    2017-05-01

    Ischemic preconditioning has been utilized to protect the heart from ischemia prior to ischemia onset, whereas postconditioning is employed to minimize the consequences of ischemia at the onset of reperfusion. The underlying mechanisms and pathways of ischemic pre- and postconditioning continue to be investigated as therapeutic targets. We evaluated the administration of a delta opioid agonist or cariporide on various parameters associated with myocardial reperfusion injury upon reperfusion of isolated porcine hearts. The hearts were reperfused in vitro with a Krebs buffer containing either: (1) 1 µM Deltorphin D (delta opioid specific agonist, n = 6); (2) 3 µM cariporide (sodium-hydrogen exchange inhibitor, n = 4); or (3) no treatment (control, n = 6). Subsequently, postischemic hemodynamic performance, arrhythmia burden, relative tissue perfusion, and development of necrosis were assessed over a 2 h reperfusion period. Postconditioning with Deltorphin D significantly improved diastolic relaxation (Tau, P reperfusion. Additionally, these treated hearts demonstrated increased tissue perfusion after 2 h ( P reperfusion injury, suggesting a postconditioning effect of these agents. We hypothesize that the induced benefits of delta opioids, in part, are associated with decreased calcium influx on reperfusion, independent of sodium-hydrogen exchange inhibition. Such agents may have a potential role in minimizing reperfusion injury associated with coronary stenting, bypass surgery, myocardial infarction, cardiac transplantation, or with the utilization of heart preservation systems. Impact statement In this study, we found that postconditioning with Deltorphin D significantly improved diastolic relaxation and decreased the incidence of ventricular arrhythmias during early reperfusion. Furthermore, these treated hearts demonstrated increased tissue perfusion after 2 h, suggesting improved microvascular function. Delta opioid agonists

  12. MerTK Cleavage on Resident Cardiac Macrophages Compromises Repair After Myocardial Ischemia Reperfusion Injury.

    Science.gov (United States)

    DeBerge, Matthew; Yeap, Xin Yi; Dehn, Shirley; Zhang, Shuang; Grigoryeva, Lubov; Misener, Sol; Procissi, Daniel; Zhou, Xin; Lee, Daniel C; Muller, William A; Luo, Xunrong; Rothlin, Carla; Tabas, Ira; Thorp, Edward B

    2017-09-29

    Clinical benefits of reperfusion after myocardial infarction are offset by maladaptive innate immune cell function, and therapeutic interventions are lacking. We sought to test the significance of phagocytic clearance by resident and recruited phagocytes after myocardial ischemia reperfusion. In humans, we discovered that clinical reperfusion after myocardial infarction led to significant elevation of the soluble form of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, soluble MER), a critical biomarker of compromised phagocytosis by innate macrophages. In reperfused mice, macrophage Mertk deficiency led to decreased cardiac wound debridement, increased infarct size, and depressed cardiac function, newly implicating MerTK in cardiac repair after myocardial ischemia reperfusion. More notably, Mertk(CR ) mice, which are resistant to cleavage, showed significantly reduced infarct sizes and improved systolic function. In contrast to other cardiac phagocyte subsets, resident cardiac MHCII LO CCR2 - (major histocompatibility complex II/C-C motif chemokine receptor type 2) macrophages expressed higher levels of MerTK and, when exposed to apoptotic cells, secreted proreparative cytokines, including transforming growth factor-β. Mertk deficiency compromised the accumulation of MHCII LO phagocytes, and this was rescued in Mertk(CR ) mice. Interestingly, blockade of CCR2-dependent monocyte infiltration into the heart reduced soluble MER levels post-ischemia reperfusion. Our data implicate monocyte-induced MerTK cleavage on proreparative MHCII LO cardiac macrophages as a novel contributor and therapeutic target of reperfusion injury. © 2017 American Heart Association, Inc.

  13. Glaucocalyxin A Ameliorates Myocardial Ischemia-Reperfusion Injury in Mice by Suppression of Microvascular Thrombosis

    Science.gov (United States)

    Liu, Xiaohui; Xu, Dongzhou; Wang, Yuxin; Chen, Ting; Wang, Qi; Zhang, Jian; You, Tao; Zhu, Li

    2016-01-01

    Background The aim of this study was to evaluate the cardio-protective roles of glaucocalyxin A (GLA) in myocardial ischemia-reperfusion injury and to explore the underlying mechanism. Material/Methods Myocardial ischemia-reperfusion in wild-type C57BL/6J mice was induced by transient ligation of the left anterior descending artery. GLA or vehicle (solvent) was administrated intraperitoneally to the mice before reperfusion started. After 24 h of myocardial reperfusion, ischemic size was revealed by Evans blue/TTC staining. Cardiac function was evaluated by echocardiography and microvascular thrombosis was assessed by immunofluorescence staining of affected heart tissue. We also measured the phosphorylation of AKT, ERK, P-GSK-3β, and cleaved caspase 3 in the myocardium. Results Compared to the solvent-treated control group, GLA administration significantly reduced infarct size (GLA 13.85±2.08% vs. Control 18.95±0.97%, pthrombosis (Pthrombosis. PMID:27716735

  14. Thrombolysis in acute myocardial infarction

    NARCIS (Netherlands)

    F. Vermeer (Frank)

    1987-01-01

    textabstractThe purpose of this study was to analyse the effects of thrombolytic therapy with intracoronary streptokinase in patients with acute myocardial infarction. Five centres participated in the study, the Thorax center in Rotterdam (237 patients), the Academic Hospital of the Free

  15. Effects of Liraglutide on Reperfusion Injury in Patients With ST-Segment-Elevation Myocardial Infarction.

    Science.gov (United States)

    Chen, Wei Ren; Chen, Yun Dai; Tian, Feng; Yang, Na; Cheng, Liu Quan; Hu, Shun Ying; Wang, Jing; Yang, Jun Jie; Wang, Shi Feng; Gu, Xiao Fang

    2016-12-01

    Liraglutide, a glucagon-like peptide-1 analog, was reported to reduce reperfusion injury in mice. We planned to evaluate the effects of liraglutide on reperfusion injury in patients with acute ST-segment-elevation myocardial infarction treated with primary percutaneous coronary intervention. A total of 96 patients with ST-segment-elevation myocardial infarction undergoing emergency primary percutaneous coronary intervention were randomized to receive either subcutaneous liraglutide or placebo. Study treatment was commenced 30 minutes before intervention (1.8 mg) and maintained for 7 days after the procedure (0.6 mg for 2 days, 1.2 mg for 2 days, followed by 1.8 mg for 3 days). The salvage index was calculated from myocardial area at risk, measured during the index admission (35±12 hours), and final infarct size measured at 91±5 days after primary percutaneous coronary intervention by cardiac magnetic resonance. At 3 months, the primary end point, a higher salvage index was found in the liraglutide group than in the placebo group in 77 patients evaluated with cardiac magnetic resonance (0.66±0.14 versus 0.55±0.15; P=0.001). The final infarct size was lower in the liraglutide group than that in the placebo group (15±12 versus 21±15 g; P=0.05). Serum high-sensitivity C-reactive protein level was lower in the liraglutide group (Preperfusion injury, making it a promising treatment for evaluation in larger trials. URL: https://www.clinicaltrials.gov. Unique identifier: NCT02001363. © 2016 American Heart Association, Inc.

  16. Hemorrhagic myocardial infarction after reperfusion detected by X-ray CT

    International Nuclear Information System (INIS)

    Tamura, Tsutomu; Toyoki, Takaaki; Ishikawa, Tomoko

    1992-01-01

    The purpose of this study was to determine whether computed tomography (CT) can detect hemorrhagic infarction occurring after intracoronary thrombolytic therapy (ICT) for acute myocardial infarction (AMI). In an experimental study, 12 dogs underwent 2-4 h of left anterior descending artery (LAD) occlusion, followed by reperfusion, and infusion of contrast material into the LAD. After CT examination, the heart was cut into transverse sections. A good correlation was obtained between the CT-enhanced area and the hemorrhagic area in the sliced heart section (r=0.895, p 0.1). The SPECT defect areas were consistently smaller than the CT enhancement areas. These results indicate that CT can detect hemorrhage into the myocardium after ICT, and that after ICT half the AMI patients showed hemorrhagic infarction. However, hemorrhage did not cause complete deterioration of the myocardium. (author)

  17. Acute oxygen-ozone administration to rats protects the heart from ischemia reperfusion infarct.

    Science.gov (United States)

    Di Filippo, C; Marfella, R; Capodanno, P; Ferraraccio, F; Coppola, L; Luongo, M; Mascolo, L; Luongo, C; Capuano, A; Rossi, F; D'Amico, M

    2008-10-01

    We tested here the effects of acute administration of an oxygen/ozone (O3) mixture on the myocardial tissue damage following an ischemic event. The study was done in Sprague-Dawley rats subjected to acute myocardial ischemia/reperfusion (I/R). 100; 150; and 300 microg/kg oxygen/O3 mixture were insufflated intraperitoneally 1 h prior to I/R. Myocardial infarct size measurement and immunhistochemistry or ELISA for nitrotyrosine, CD68, CD8,CD4 and caspase-3 were done. I/R produced a marked damage in the rat left ventricle with an infarct size as percentage of the area at risk (IS/ AR) of approximately 45 +/- 4% . Rats insufflated with a oxygen/O3 mixture showed a significant 2-h cardio-protection (e. g. infarct size over area at risk for the dose of 300 microg/kg was approximately 30 +/- 3%,) as compared with control rats (P <0.01). This effect was paralleled by a decrease in tissue levels of immunostaining for biomarkers of nitrosative stress (nitrotyrosine), inflammation (CD68) and immunity response (CD8 and CD4) between heart tissues from infarcted rats and infarcted O3 treated rats. These data indicate that the tissue and biochemical damages associated with myocardial ischemia/reperfusion can be counteracted by an acute O3 pretreatment.

  18. Amelioration of myocardial ischemic reperfusion injury with Calendula officinalis.

    Science.gov (United States)

    Ray, Diptarka; Mukherjee, Subhendu; Falchi, Mario; Bertelli, Aldo; Das, Dipak K

    2010-12-01

    Calendula officinalis of family Asteraceae, also known as marigold, has been widely used from time immemorial in Indian and Arabic cultures as an anti-inflammatory agent to treat minor skin wound and infections, burns, bee stings, sunburn and cancer. At a relatively high dose, calendula can lower blood pressure and cholesterol. Since inflammatory responses are behind many cardiac diseases, we sought to evaluate if calendula could be cardioprotective against ischemic heart disease Two groups of hearts were used: the treated rat hearts were perfused with calendula solution at 50 mM in KHB buffer (in mM: sodium chloride 118, potassium chloride 4.7, calcium chloride 1.7, sodium bicarbonate 25, potassium biphosphate 0.36, magnesium sulfate 1.2, and glucose 10) for 15 min prior to subjecting the heart to ischemia, while the control group was perfused with the buffer only. Calendula achieved cardioprotection by stimulating left ventricular developed pressure and aortic flow as well as by reducing myocardial infarct size and cardiomyocyte apoptosis. Cardioprotection appears to be achieved by changing ischemia reperfusion-mediated death signal into a survival signal by modulating antioxidant and anti-inflammatory pathways as evidenced by the activation of Akt and Bcl2 and depression of TNFα. The results further strengthen the concept of using natural products in degeneration diseases like ischemic heart disease.

  19. Imaging myocardial ischemia and reperfusion injury via Cy5.5 Annexin V

    Energy Technology Data Exchange (ETDEWEB)

    Tian, Rong [Sichuan Univ., Chengdu (China); Pan, Dong Feng [Univ. of Virginia, VA (United States)

    2012-09-15

    The aim of this article is to present the results of an imaging study of myocardial apoptosis induced by ischemia/reperfusion injury. Twenty nude mice were randomly divided into an experimental group, myocardial apoptosis was induced by ligation of the left anterior descending coronary artery (LAD)for 30 min. This was followed by reperfusion for 90 min. In the control group, the heart was exposed for the same length of time as in the experimental group. Cy5.5 annexin V (25{mu}g)was injected into both sets of mice after the onset of reperfusion. At 90 min post injection, the mice were imaged. The region of interest (ROI)was obtained, and the fluorescence intensity of the ROI was quantified. The animals were sacrificed, and myocardial apoptosis was assayed by TUNEL assay. Fluorescence intensity in the ischemia/reperfusion hearts was significantly higher than that in the control group (P<0.05). In the TUNEL assay, more apoptotic cells were observed in the experimental group than in the control group, correlating with imaging results. Fluorescence imaging of Cy5.5 annexin V in a mouse model of myocardial ischemia/reperfusion can be used in vivo as a noninvasive means of detecting ischemia/reperfusion induced apoptotic cells in the heart.

  20. Electrocardiography as a Tool for Validating Myocardial Ischemia–Reperfusion Procedures in Mice

    Science.gov (United States)

    Preda, Mihai B; Burlacu, Alexandrina

    2010-01-01

    This paper evaluates the modifications induced by ischemia and ischemia–reperfusion in mice after permanent or transient, respectively, ligation of the left coronary artery and establishes a correlation among the extent of ischemia, electrocardiograph features, and infarct size. The left coronary artery was ligated 1 mm distal from the tip of the left auricle. Histologic analysis revealed that 30-min ischemia (n = 9) led to infarction involving 9.7% ± 0.5% of the left ventricle, whereas 1-h ischemia (n = 9) resulted in transmural infarction of 16.1% ± 4.6% of the left ventricle. In contrast, 24-h ischemia (n = 8) and permanent ischemia (n = 8) induced similarly sized infarcts (33% ± 2% and 31.8% ± 0.7%, respectively), suggesting ineffective reperfusion after 24-h ischemia. Electrocardiography revealed that ligation of the left coronary artery led to ST height elevation (204 compared with 14 μV) and QTc prolongation (136 compared with 76 ms). Both parameters rapidly normalized on reperfusion, demonstrating that electrocardiography was important for validating correct ligation and reperfusion. In addition, electrocardiography predicted the severity of the myocardial damage induced by ischemia. Our results show that electrocardiographic changes present after 30-min ischemia were reversed on reperfusion; however, prolonged ischemia induced pathologic electrocardiographic patterns that remained even after reperfusion. The mouse model of myocardial ischemia–reperfusion can be improved by using electrocardiography to validate ligation and reperfusion during surgery and to predict the severity of infarction. PMID:21262130

  1. Electrocardiography as a tool for validating myocardial ischemia-reperfusion procedures in mice.

    Science.gov (United States)

    Preda, Mihai B; Burlacu, Alexandrina

    2010-12-01

    This paper evaluates the modifications induced by ischemia and ischemia-reperfusion in mice after permanent or transient, respectively, ligation of the left coronary artery and establishes a correlation among the extent of ischemia, electrocardiograph features, and infarct size. The left coronary artery was ligated 1 mm distal from the tip of the left auricle. Histologic analysis revealed that 30-min ischemia (n = 9) led to infarction involving 9.7% ± 0.5% of the left ventricle, whereas 1-h ischemia (n = 9) resulted in transmural infarction of 16.1% ± 4.6% of the left ventricle. In contrast, 24-h ischemia (n = 8) and permanent ischemia (n = 8) induced similarly sized infarcts (33% ± 2% and 31.8% ± 0.7%, respectively), suggesting ineffective reperfusion after 24-h ischemia. Electrocardiography revealed that ligation of the left coronary artery led to ST height elevation (204 compared with 14 μV) and QTc prolongation (136 compared with 76 ms). Both parameters rapidly normalized on reperfusion, demonstrating that electrocardiography was important for validating correct ligation and reperfusion. In addition, electrocardiography predicted the severity of the myocardial damage induced by ischemia. Our results show that electrocardiographic changes present after 30-min ischemia were reversed on reperfusion; however, prolonged ischemia induced pathologic electrocardiographic patterns that remained even after reperfusion. The mouse model of myocardial ischemia-reperfusion can be improved by using electrocardiography to validate ligation and reperfusion during surgery and to predict the severity of infarction.

  2. Glucose oxidation positively regulates glucose uptake and improves cardiac function recovery after myocardial reperfusion.

    Science.gov (United States)

    Li, Tingting; Xu, Jie; Qin, Xinghua; Hou, Zuoxu; Guo, Yongzheng; Liu, Zhenhua; Wu, Jianjiang; Zheng, Hong; Zhang, Xing; Gao, Feng

    2017-11-01

    Myocardial reperfusion decreases glucose oxidation and uncouples glucose oxidation from glycolysis. Therapies that increase glucose oxidation lessen myocardial ischemia-reperfusion (I/R) injury. However, the regulation of glucose uptake during reperfusion remains poorly understood. We found that glucose uptake was remarkably diminished in the myocardium following reperfusion in Sprague-Dawley rats as detected by 18 F-labeled and fluorescent-labeled glucose analogs, even though GLUT1 was upregulated by threefold and GLUT4 translocation remained unchanged compared with those of sham-treated rats. The decreased glucose uptake was accompanied by suppressed glucose oxidation. Interestingly, stimulating glucose oxidation by inhibition of pyruvate dehydrogenase kinase 4 (PDK4), a rate-limiting enzyme for glucose oxidation, increased glucose uptake and alleviated I/R injury. In vitro data in neonatal myocytes showed that PDK4 overexpression decreased glucose uptake, whereas its knockdown increased glucose uptake, suggesting that PDK4 has a role in regulating glucose uptake. Moreover, inhibition of PDK4 increased myocardial glucose uptake with concomitant enhancement of cardiac insulin sensitivity following myocardial I/R. These results showed that the suppressed glucose oxidation mediated by PDK4 contributes to the reduced glucose uptake in the myocardium following reperfusion, and enhancement of glucose uptake exerts cardioprotection. The findings suggest that stimulating glucose oxidation via PDK4 could be an efficient approach to improve recovery from myocardial I/R injury. Copyright © 2017 the American Physiological Society.

  3. Differences in Thallium-201 uptake in reperfused and nonreperfused myocardial infarction

    International Nuclear Information System (INIS)

    Melin, J.A.; Becker, L.C.; Bulkley, B.H.

    1983-01-01

    The respective importance of flow and cellular viability in determining initial myocardial thallium uptake was studied in reperfused and nonreperfused experimental myocardial infarction. Open-chest dogs were subjected to permanent coronary artery occlusion of 70-minute (n . 3) or 5-hour duration (n . 5), or to a 3-hour temporary occlusion followed by reflow (n . 14). Thallium uptake 10 minutes after intravenous injection was compared directly with radioactive microspheres in myocardial samples from excised hearts. Triphenyl tetrazolium chloride staining was used to differentiate necrotic and viable samples with confirmation by electron microscopy. In nonreperfused infarcts, thallium uptake occurred despite necrosis, and a close correlation was found between thallium uptake and regional myocardial blood flow. In reperfused infarcts, thallium uptake again occurred, but was reduced relative to flow in necrotic myocardium and, to a lesser extent, in reperfused viable areas. However, because of the high levels of reflow, actual thallium uptake was often more than 50% of normal in reperfused necrotic regions. This study demonstrates that the presence of thallium uptake is an unreliable indicator of myocardial injury and that reperfused necrotic tissue may have remarkably high levels of thallium uptake

  4. Nanoparticle-Mediated Delivery of Mitochondrial Division Inhibitor 1 to the Myocardium Protects the Heart From Ischemia-Reperfusion Injury Through Inhibition of Mitochondria Outer Membrane Permeabilization: A New Therapeutic Modality for Acute Myocardial Infarction.

    Science.gov (United States)

    Ishikita, Ayako; Matoba, Tetsuya; Ikeda, Gentaro; Koga, Jun-Ichiro; Mao, Yajing; Nakano, Kaku; Takeuchi, Osamu; Sadoshima, Junichi; Egashira, Kensuke

    2016-07-22

    Mitochondria-mediated cell death plays a critical role in myocardial ischemia-reperfusion (IR) injury. We hypothesized that nanoparticle-mediated drug delivery of mitochondrial division inhibitor 1 (Mdivi1) protects hearts from IR injury through inhibition of mitochondria outer membrane permeabilization (MOMP), which causes mitochondrial-mediated cell death. We formulated poly (lactic-co-glycolic acid) nanoparticles containing Mdivi1 (Mdivi1-NP). We recently demonstrated that these nanoparticles could be successfully delivered to the cytosol and mitochondria of cardiomyocytes under H2O2-induced oxidative stress that mimicked IR injury. Pretreatment with Mdivi1-NP ameliorated H2O2-induced cell death in rat neonatal cardiomyocytes more potently than Mdivi1 alone, as indicated by a lower estimated half-maximal effective concentration and greater maximal effect on cell survival. Mdivi1-NP treatment of Langendorff-perfused mouse hearts through the coronary arteries at the time of reperfusion reduced infarct size after IR injury more effectively than Mdivi1 alone. Mdivi1-NP treatment also inhibited Drp1-mediated Bax translocation to the mitochondria and subsequent cytochrome c leakage into the cytosol, namely, MOMP, in mouse IR hearts. MOMP inhibition was also observed in cyclophilin D knockout (CypD-KO) mice, which lack the mitochondrial permeability transition pore (MPTP) opening. Intravenous Mdivi1-NP treatment in vivo at the time of reperfusion reduced IR injury in wild-type and CypD-KO mice, but not Bax-KO mice. Mdivi1-NP treatment reduced IR injury through inhibition of MOMP, even in the absence of a CypD/MPTP opening. Thus, nanoparticle-mediated drug delivery of Mdivi1 may be a novel treatment strategy for IR injury. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  5. Reperfusion therapy of myocardial infarction in Mexico: A challenge for modern cardiology.

    Science.gov (United States)

    Martínez-Sánchez, Carlos; Arias-Mendoza, Alexandra; González-Pacheco, Héctor; Araiza-Garaygordobil, Diego; Marroquín-Donday, Luis Alfonso; Padilla-Ibarra, Jorge; Sierra-Fernández, Carlos; Altamirano-Castillo, Alfredo; Álvarez-Sangabriel, Amada; Azar-Manzur, Francisco Javier; Briseño-de la Cruz, José Luis; Mendoza-García, Salvador; Piña-Reyna, Yigal; Martínez-Ríos, Marco Antonio

    Mexico has been positioned as the country with the highest mortality attributed to myocardial infarction among the members of the Organization for Economic Cooperation and Development. This rate responds to multiple factors, including a low rate of reperfusion therapy and the absence of a coordinated system of care. Primary angioplasty is the reperfusion method recommended by the guidelines, but requires multiple conditions that are not reached at all times. Early pharmacological reperfusion of the culprit coronary artery and early coronary angiography (pharmacoinvasive strategy) can be the solution to the logistical problem that primary angioplasty rises. Several studies have demonstrated pharmacoinvasive strategy as effective and safe as primary angioplasty ST-elevation myocardial infarction, which is postulated as the choice to follow in communities where access to PPCI is limited. The Mexico City Government together with the National Institute of Cardiology have developed a pharmaco-invasive reperfusion treatment program to ensure effective and timely reperfusion in STEMI. The model comprises a network of care at all three levels of health, including a system for early pharmacological reperfusion in primary care centers, a digital telemedicine system, an inter-hospital transport network to ensure primary angioplasty or early percutaneous coronary intervention after fibrinolysis and a training program with certification of the health care personal. This program intends to reduce morbidity and mortality associated with myocardial infarction. Copyright © 2016 Instituto Nacional de Cardiología Ignacio Chávez. Publicado por Masson Doyma México S.A. All rights reserved.

  6. PREVENTION OF COMPLICATIONS CAUSED BY MYOCARDIAL ISCHEMIA-REPERFUSION IN NONCARDIAC SURGICAL PROCEDURES

    Directory of Open Access Journals (Sweden)

    I. A. Kozlov

    2016-01-01

    Full Text Available In the next 20 years, the aging population will be a major factor affecting the characteristics of perioperative anesthesia tactics. Domestic researchers have reported that the incidence of cardiac complications after general surgical procedures in patients with middle and old age is 9.1%, and mortality in these complications reached 45.5%. Analyzed current data on myocardial ischemia-reperfusion, the etiopathogenesis of perioperative cardiac complications, recurrence of their development and the possible consequences. It is concluded that prevention and timely treatment of complications resulting from ischemia-reperfusion of the myocardium, with noncardiac surgical interventions is an important tactical (prevention of perioperative myocardial infarction, arrhythmias, cardiac death and policy (prevention of cardiac remodeling and post-hospital disability of patients anaesthesiological tasks. Research carried out in the Nrgovsky Research Institute of General Reanimatology showed that in the real practice Detsky index, Lee index and echocardiographic left ventricular ejection fraction did not provide high accuracy prediction of cardiac events. More informative proved preoperative determination of blood N-terminal part of the pro-brain natriuretic peptide (NT-proBNP. In assessing the predictive ability of NT-proBNP area under the ROC-curve achieved 0.86. NT-proBNP value 358 pg/ml and above provided 77% sensitivity and 85% specificity. The comparative assessment and recommendations on the use to reduce the risk of cardiac complications of β-blockers, statins, calcium channel blockers, nitrates, clonidine, dexmedetomidine, levosimendan and phosphocreatine. Phosphocreatine, introduced in practice domestic cardiac surgery and transplantology more than 20 years ago, continues to be studied and used at the moment. Recently demonstrated that perioperative phosphocreatine usage appointment in older oncological patients with a high risk of cardiac

  7. Relation between reperfusion and hemorrhagic transformation in acute ischemic stroke

    International Nuclear Information System (INIS)

    Horsch, Alexander D.; Dankbaar, Jan Willem; Niesten, Joris M.; Seeters, Tom van; Schaaf, Irene C. van der; Velthuis, Birgitta K.; Graaf, Yolanda van der; Kappelle, L.J.

    2015-01-01

    Intravenous recombinant tissue plasminogen activator (IV-rtPA) is given in acute ischemic stroke patients to achieve reperfusion. Hemorrhagic transformation (HT) is a serious complication of IV-rtPA treatment and related to blood-brain barrier (BBB) injury. It is unclear whether HT occurs secondary to reperfusion in combination with ischemic BBB injury or is caused by the negative effect of IV-rtPA on BBB integrity. The aim of this study was to establish the association between reperfusion and the occurrence of HT. From the DUST study, patients were selected with admission and follow-up non-contrast CT (NCCT) and CT perfusion (CTP) imaging, and a perfusion deficit in the middle cerebral artery territory on admission. Reperfusion was categorized qualitatively as reperfusion or no-reperfusion by visual comparison of admission and follow-up CTP. Occurrence of HT was assessed on follow-up NCCT. The association between reperfusion and occurrence of HT on follow-up was estimated by calculating odds ratios (ORs) and 95 % confidence intervals (CIs) with additional stratification for IV-rtPA treatment. Inclusion criteria were met in 299 patients. There was no significant association between reperfusion and HT (OR 1.2 95%CI 0.5-3.1). In patients treated with IV-rtPA (n = 203), the OR was 1.3 (95%CI 0.4-4.0), and in patients not treated with IV-rtPA (n = 96), the OR was 0.8 (95%CI 0.1-4.5). HT occurred in 14 % of the IV-rtPA patients and in 7 % of patients without IV-rtPA (95%CI of difference -1 to 14 %). Our results suggest that the increased risk of HT after acute ischemic stroke treatment is not dependent on the reperfusion status. (orig.)

  8. Relation between reperfusion and hemorrhagic transformation in acute ischemic stroke

    Energy Technology Data Exchange (ETDEWEB)

    Horsch, Alexander D. [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Rijnstate Hospital, Department of Radiology, Arnhem (Netherlands); Dankbaar, Jan Willem; Niesten, Joris M.; Seeters, Tom van; Schaaf, Irene C. van der; Velthuis, Birgitta K. [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Graaf, Yolanda van der [Julius Center for Health Sciences and Primary Care, Utrecht (Netherlands); Kappelle, L.J. [University Medical Center, Department of Neurology, Utrecht Stroke Center, Utrecht (Netherlands); Collaboration: DUST investigators

    2015-12-15

    Intravenous recombinant tissue plasminogen activator (IV-rtPA) is given in acute ischemic stroke patients to achieve reperfusion. Hemorrhagic transformation (HT) is a serious complication of IV-rtPA treatment and related to blood-brain barrier (BBB) injury. It is unclear whether HT occurs secondary to reperfusion in combination with ischemic BBB injury or is caused by the negative effect of IV-rtPA on BBB integrity. The aim of this study was to establish the association between reperfusion and the occurrence of HT. From the DUST study, patients were selected with admission and follow-up non-contrast CT (NCCT) and CT perfusion (CTP) imaging, and a perfusion deficit in the middle cerebral artery territory on admission. Reperfusion was categorized qualitatively as reperfusion or no-reperfusion by visual comparison of admission and follow-up CTP. Occurrence of HT was assessed on follow-up NCCT. The association between reperfusion and occurrence of HT on follow-up was estimated by calculating odds ratios (ORs) and 95 % confidence intervals (CIs) with additional stratification for IV-rtPA treatment. Inclusion criteria were met in 299 patients. There was no significant association between reperfusion and HT (OR 1.2 95%CI 0.5-3.1). In patients treated with IV-rtPA (n = 203), the OR was 1.3 (95%CI 0.4-4.0), and in patients not treated with IV-rtPA (n = 96), the OR was 0.8 (95%CI 0.1-4.5). HT occurred in 14 % of the IV-rtPA patients and in 7 % of patients without IV-rtPA (95%CI of difference -1 to 14 %). Our results suggest that the increased risk of HT after acute ischemic stroke treatment is not dependent on the reperfusion status. (orig.)

  9. Reperfusion Therapy in ST-segment Elevation Myocardial Infarction – Data from a Pilot Registry of Myocardial Infarction

    Czech Academy of Sciences Publication Activity Database

    Monhart, Z.; Faltus, Václav; Grünfeldová, H.; Kadlečková, A.; Ryšavá, D.; Velimský, T.; Ballek, J.; Hubač, J.; Janský, P.; Zvárová, Jana

    Roc. 50, c. 2 (2008), s. 55-59 ISSN 0010-8650 R&D Projects: GA MŠk(CZ) 1M06014 Institutional research plan: CEZ:AV0Z10300504 Keywords : myocardial infarction * reperfusion therapy * mortality Subject RIV: BB - Applied Statistics, Operational Research

  10. Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias

    DEFF Research Database (Denmark)

    Collis, C S; Rice-Evans, C; Davies, Michael Jonathan

    1996-01-01

    the first 5 min of reperfusion were quantified. Drugs (all at 150 microM) were introduced during the last 2 min of ischaemia and remained throughout reperfusion. Although the monohydroxamate- and desferrioxamine-treated hearts showed a reduction in the incidence of ventricular tachycardia and fibrillation...

  11. The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression.

    Science.gov (United States)

    Wang, Yiming; Zhang, Hongming; Chai, Fangxian; Liu, Xingde; Berk, Michael

    2014-12-04

    Major depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R). Rats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat's left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl-2 and Bax. Compared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P escitalopram + DI/R group was significantly decreased (P escitalopram + DI/R groups (P escitalopram + DI/R group were significantly decreased (P escitalopram + DI/R group (P escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction.

  12. ECG and enzymatic indicators of therapeutic success after intravenous streptokinase for acute myocardial infarction

    DEFF Research Database (Denmark)

    Clemmensen, P; Grande, P; Pedersen, F

    1990-01-01

    Thrombolytic therapy has been documented to result in reperfusion of jeopardized myocardium and reduction in the size of the acute myocardial infarction (AMI). The effect of intravenous streptokinase on a creatine kinase-MB (CK-MB) reperfusion index and an ECG estimate of myocardial salvage...... was therefore studied in 65 patients with a first AMI, randomized to treatment with streptokinase (n = 33) or placebo (control group, n = 32). Reperfusion was defined as a CK-MB appearance rate constant (k1) greater than 0.185. The final AMI size was first predicted from the admission standard ECG by previously...... developed formulas based on ST segment elevation. The final AMI size was estimated from the QRS score on the predischarge ECG. Myocardial salvage was defined as a greater than or equal to 20% decrease from predicted to final AMI size. The k1 value in the control group was significantly lower than...

  13. Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents

    OpenAIRE

    Eisenmann, Eric D.; Rorabaugh, Boyd R.; Zoladz, Phillip R.

    2016-01-01

    Cardiovascular disease is the largest cause of mortality worldwide, and stress is a significant contributor to the development of cardiovascular disease. The relationship between acute and chronic stress and cardiovascular disease is well-evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia-reperfusion injury. Conversely, chronic stress is arrythmogenic and incr...

  14. Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

    Directory of Open Access Journals (Sweden)

    Liliang Shu

    2017-12-01

    Full Text Available Background/Aims: Troxerutin, also known as vitamin P4, has been commonly used in the treatment of chronic venous insufficiency (CVI disease. However, its effect on in vivo myocardial ischemia/reperfusion (I/R injury, a model that closely mimics acute myocardial infarction in humans, is still unknown. Methods: The myocardial I/R injury rat model was created with troxerutin preconditioning. Myocardial infarct size was evaluated by the Evans blue-TTC method. Hemodynamic parameters, including the heart rate (HR, left ventricular end-diastolic pressure (LVEDP, left ventricular systolic pressure (LVSP, maximal rate of rise in blood pressure in the ventricular chamber (+dp/dt max, and maximal rate of decline in blood pressure in the ventricular chamber (-dp/dt max were monitored. Serum TNF-α and IL-10 were determined by ELISA kit. Cell apoptosis was detected by MTT method. Results: Troxerutin preconditioning significantly reduced myocardial infarct size, improved cardiac function, and decreased the levels of creatine kinase (CK, aspartate aminotransferase (AST and lactate dehydrogenase (LDH in the I/R injury rat model. The serum and mRNA levels of TNF-α and IL-10 as well as some apoptosis markers (Bax, Caspase 3 also decreased. Moreover, troxerutin pretreatment markedly increased the phosphorylation of Akt, and blocking PI3K activity by LY294002 abolished the protective effect of troxerutin on I/R injury. Conclusion: Troxerutin preconditioning protected against myocardial I/R injury via the PI3K/Akt pathway.

  15. Neutrophil accumulation in experimental myocardial infarcts: relation with extent of injury and effect of reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Chatelain, P.; Latour, J.G.; Tran, D.; de Lorgeril, M.; Dupras, G.; Bourassa, M.

    1987-05-01

    The effects of reperfusion on the myocardial accumulation of neutrophils and their role in the extent of injury were investigated in a canine preparation with a 3 hr coronary occlusion followed by 21 hr of reperfusion. The left anterior descending coronary artery (LAD) was permanently occluded in group 1 and reperfused after 3 hr in four others (groups 2 to 5). All but group 5 received lidocaine (1 mg/min over 8 hr). A critical stenosis was produced and left in place at reperfusion only in group 2. In groups 1 and 2, /sup 111/In-labeled autologous neutrophils were injected at the time of coronary occlusion. Group 4 animals were rendered leukopenic 2 hr before the coronary ligature and throughout the experiment by injection of an antineutrophil rabbit serum. Quantification of the radioactivity by digitized scintigraphy of the heart slices revealed an 80% increase in neutrophil accumulation in the infarct region after reperfusion (group 2) as compared with permanent occlusion (group 1). Gamma counting of myocardial tissue samples showed that the neutrophil accumulation ratio in the subendocardial central zone of the infarct was increased five times by reperfusion, whereas no difference was evident in the subepicardium. Infarct size and myocardial area at risk were not statistically different among the five groups. However LAD flow in the leukopenic group (group 4) was significantly higher 30 min after reperfusion (40.0 +/- 5 ml/min) when compared with the preocclusion value (21.7 +/- 4 ml/min). In contrast, in a parallel experiment without leukopenia (group 3), LAD flow after reperfusion did not differ from the preocclusion value.

  16. Fibroblast growth factor-1 improves cardiac functional recovery and enhances cell survival after ischemia and reperfusion: a fibroblast growth factor receptor, protein kinase C, and tyrosine kinase-dependent mechanism

    NARCIS (Netherlands)

    Palmen, Meindert; Daemen, Mat J. A. P.; de Windt, Leon J.; Willems, Jodil; Dassen, Willem R. M.; Heeneman, Sylvia; Zimmermann, Rene; van Bilsen, Marc; Doevendans, Pieter A.

    2004-01-01

    We sought to investigate the role of fibroblast growth factor (FGF)-1 during acute myocardial ischemia and reperfusion. The FGFs display cardioprotective effects during ischemia and reperfusion. We investigated FGF-1-induced cardioprotection during ischemia and reperfusion and the intracellular

  17. Allogeneic adipose stem cell therapy in acute myocardial infarction.

    Science.gov (United States)

    Rigol, Montserrat; Solanes, Núria; Roura, Santiago; Roqué, Mercè; Novensà, Laura; Dantas, Ana Paula; Martorell, Jaume; Sitges, Marta; Ramírez, José; Bayés-Genís, Antoni; Heras, Magda

    2014-01-01

    Stem cell therapy offers a promising approach to reduce the long-term mortality rate associated with heart failure after acute myocardial infarction (AMI). To date, in vivo translational studies have not yet fully studied the immune response to allogeneic adipose tissue-derived mesenchymal stem cells (ATMSCs). We analysed the immune response and the histological and functional effects of allogeneic ATMSCs in a porcine model of reperfused AMI and determine the effect of administration timing. Pigs that survived AMI (24/26) received intracoronary administration of culture medium after reperfusion (n = 6), ATMSCs after reperfusion (n = 6), culture medium 7 days after AMI (n = 6) or ATMSCs 7 days after AMI (n = 6). At 3-week follow-up, cardiac function, alloantibodies and histological analysis were evaluated. Administration of ATMSCs after reperfusion and 7 days after AMI resulted in similar rates of cell engraftment; some of those cells expressed endothelial, smooth muscle and cardiomyogenic cell lineage markers. Delivery of ATMSCs after reperfusion compared with that performed at 7 days was more effective in increasing: vascular density (249 ± 64 vs. 161 ± 37 vessels/mm2; P < 0.01), T lymphocytes (1 ± 0.4 vs. 0.4 ± 0.3% of area CD3(+) ; P < 0.05) and expression of vascular endothelial growth factor (VEGF; 32 ± 7% vs. 20 ± 4% of area VEGF(+) ; P < 0.01). Allogeneic ATMSC-based therapy did not change ejection fraction but generated alloantibodies. The present study is the first to demonstrate that allogeneic ATMSCs elicit an immune response and, when administered immediately after reperfusion, are more effective in increasing VEGF expression and neovascularization. © 2013 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

  18. Impaired myocardial microcirculation in the flow-glucose metabolism mismatch regions in revascularized acute myocardial infarction.

    Science.gov (United States)

    Fukuoka, Yoshitomo; Nakano, Akira; Tama, Naoto; Hasegawa, Kanae; Ikeda, Hiroyuki; Morishita, Tetsuji; Ishida, Kentaro; Kaseno, Kenichi; Amaya, Naoki; Uzui, Hiroyasu; Okazawa, Hidehiko; Tada, Hiroshi

    2017-10-01

    In successfully revascularized acute myocardial infarction (AMI), microvascular function in a myocardial flow-glucose metabolism mismatch pattern has not been reported. We aimed to elucidate myocardial flow reserve (MFR) and myocardial viability in mismatch segments. 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET) and adenosine stress 13 N-ammonia PET were performed in eighteen AMI patients to evaluate myocardial glucose metabolism, myocardial blood flow (MBF), and MFR. Infarct segments were classified into 3 groups: normal (preserved resting MBF), mismatch (preserved FDG uptake but reduced resting MBF), and match (reduced FDG uptake and resting MBF). Regional wall motion score (WMS) was assessed immediately after reperfusion and recovery periods. MFR in the mismatch group was significantly lower than that in non-infarct-related segments (1.655 ± 0.516 vs 2.282 ± 0.629, P mismatch group was significantly improved (3.07 ± 0.48 vs 2.07 ± 1.14, P = .003); however, in recovery periods, WMS in the mismatch group was significantly higher than that in the normal group (1.05 ± 1.04, P mismatch segments.

  19. Pharmacological postconditioning with atorvastatin calcium attenuates myocardial ischemia/reperfusion injury in diabetic rats by phosphorylating GSK3β.

    Science.gov (United States)

    Chen, Linyan; Cai, Ping; Cheng, Zhendong; Zhang, Zaibao; Fang, Jun

    2017-07-01

    Diabetes is an independent risk factor for myocardial ischemia, and many epidemiological data and laboratory studies have revealed that diabetes significantly exacerbated myocardial ischemia/reperfusion injury and ameliorated protective effects. The present study aimed to determine whether pharmacological postconditioning with atorvastatin calcium lessened diabetic myocardial ischemia/reperfusion injury, and investigated the role of glycogen synthase kinase (GSK3β) in this. A total of 72 streptozotocin-induced diabetic rats were randomly divided into six groups, and 24 age-matched male non-diabetic Sprague-Dawley rats were randomly divided into two groups. Rats all received 40 min myocardial ischemia followed by 180 min reperfusion, except sham-operated groups. Compared with the non-diabetic ischemia/reperfusion model group, the diabetic ischemia/reperfusion group had a comparable myocardial infarct size, but a higher level of serum cardiac troponin I (cTnI) and morphological alterations to their myocardial cells. Compared with the diabetic ischemia/reperfusion group, the group that received pharmacological postconditioning with atorvastatin calcium had smaller myocardial infarct sizes, lower levels of cTnI, reduced morphological alterations to myocardial cells, higher levels of p-GSK3β, heat shock factor (HSF)-1 and heat shock protein (HSP)70. The cardioprotective effect conferred by atorvastatin calcium did not attenuate myocardial ischemia/reperfusion injury following application of TDZD-8, which phosphorylates and inactivates GSK3β. Pharmacological postconditioning with atorvastatin calcium may attenuate diabetic heart ischemia/reperfusion injury in the current context. The phosphorylation of GSK3β serves a critical role during the cardioprotection in diabetic rats, and p-GSK3β may accelerate HSP70 production partially by activating HSF-1 during myocardial ischemic/reperfusion injury.

  20. [Protective effects of endogenous carbon monoxide against myocardial ischemia-reperfusion injury in rats].

    Science.gov (United States)

    Zhou, Zhen; Ma, Shuang; Liu, Jie; Ji, Qiao-Rong; Cao, Cheng-Zhu; Li, Xiao-Na; Tang, Feng; Zhang, Wei

    2018-04-25

    The present study is aimed to explore the effects of endogenous carbon monoxide on the ischemia-reperfusion in rats. Wistar rats were intraperitoneally injected with protoporphyrin cobalt chloride (CoPP, an endogenous carbon monoxide agonist, 5 mg/kg), zinc protoporphyrin (ZnPP, an endogenous carbon monoxide inhibitor, 5 mg/kg) or saline. Twenty-four hours after injection, the myocardial ischemia-reperfusion model was made by Langendorff isolated cardiac perfusion system, and cardiac function parameters were collected. Myocardial cGMP content was measured by ELISA, and the endogenous carbon monoxide in plasma and myocardial enzymes in perfusate at 10 min after reperfusion were measured by colorimetry. The results showed that before ischemia the cardiac functions of CoPP, ZnPP and control groups were stable, and there were no significant differences. After reperfusion, cardiac functions had significant differences among the three groups (P endogenous carbon monoxide can maintain cardiac function, shorten the time of cardiac function recovery, and play a protective role in cardiac ischemia-reperfusion.

  1. Myocardial ischemia and reperfusion injury: Studies using transgenic and knockout mice

    NARCIS (Netherlands)

    Jong, W. M. C.; ten Cate, H.; Reitsma, P. H.; de Winter, R. J.

    2005-01-01

    Transgenic and knockout mice are created and used for a large variety of research objectives. This overview describes the (genetically modified) mouse models that have been used to study the development of myocardial ischemia and reperfusion injury. The role of cytokines, chemokines, leukocytes,

  2. Beneficial effects of sevoflurane and desflurane against myocardial reperfusion injury after cardioplegic arrest

    NARCIS (Netherlands)

    Preckel, B.; Thämer, V.; Schlack, W.

    1999-01-01

    PURPOSE: To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest. METHODS: Isolated rat hearts in a Langendorff-preparation (n = 9) were arrested by infusion

  3. Referral of patients with ST-segment elevation acute myocardial infarction directly to the catheterization suite based on prehospital teletransmission of 12-lead electrocardiogram

    DEFF Research Database (Denmark)

    Sillesen, Martin; Sejersten, Maria; Strange, Søren

    2008-01-01

    BACKGROUND: Time from symptom onset to reperfusion is essential in patients with ST-segment elevation acute myocardial infarction. Prior studies have indicated that prehospital 12-lead electrocardiogram (ECG) transmission can reduce time to reperfusion. PURPOSE: Determine 12-lead ECG transmission...

  4. Relation between reperfusion and hemorrhagic transformation in acute ischemic stroke

    NARCIS (Netherlands)

    Horsch, Alexander D; Dankbaar, Jan Willem; van der Graaf, Yolanda; Niesten, Joris M; van Seeters, Tom; van der Schaaf, Irene C; Kappelle, L Jaap; Velthuis, Birgitta K

    2015-01-01

    INTRODUCTION: Intravenous recombinant tissue plasminogen activator (IV-rtPA) is given in acute ischemic stroke patients to achieve reperfusion. Hemorrhagic transformation (HT) is a serious complication of IV-rtPA treatment and related to blood-brain barrier (BBB) injury. It is unclear whether HT

  5. Relation between reperfusion and hemorrhagic transformation in acute ischemic stroke

    NARCIS (Netherlands)

    Horsch, Alexander D.; Dankbaar, Jan Willem; van der Graaf, Yolanda; Niesten, Joris M.; van Seeters, Tom; van der Schaaf, Irene C.; Kappelle, L. Jaap; Velthuis, Birgitta K.; Majoie, C. B.; Roos, Y. B.; Duijm, L. E.; Keizer, K.; van der Lugt, A.; Dippel, D. W.; Droogh-deGreve, K. E.; van Walderveen, M. A.; Wermer, M. J.; Lycklama à Nijeholt, G. J.; Boiten, J.; Duyndam, D.; Kwa, V. I.; Meijer, F. J.; van Dijk, E. J.; Kesselring, F. O.; Hofmeijer, J.; Vos, J. A.; Schonewille, W. J.; van Rooij, W. J.; de Kort, P. L.; Pleiter, C. C.; Bakker, S. L.; Bot, J.; Visser, M. C.; Velthuis, B. K.; van der Schaaf, I. C.; Dankbaar, J. W.; Mali, W. P.; van Seeters, T.; Horsch, A. D.; Niesten, J. M.; Biessels, G. J.; Kappelle, L. J.; Luitse, M. J.; van der Graaf, Y.

    2015-01-01

    Intravenous recombinant tissue plasminogen activator (IV-rtPA) is given in acute ischemic stroke patients to achieve reperfusion. Hemorrhagic transformation (HT) is a serious complication of IV-rtPA treatment and related to blood-brain barrier (BBB) injury. It is unclear whether HT occurs secondary

  6. [Correction of a reperfusion dysfunction in acute intestinal obstruction].

    Science.gov (United States)

    Bagnenko, S F; Sinenchenko, G I; Kurygin, A A; Chupris, V G

    2008-01-01

    An analysis of experimental investigations carried out in 32 dogs and 30 rabbits and laboratory data of 242 patients has shown that the application of antioxidant and antihypoxic medicines decrease reperfusion lesions and endotoxicosis in operative treatment of acute intestinal obstruction.

  7. EphrinA1-Fc attenuates myocardial ischemia/reperfusion injury in mice.

    Directory of Open Access Journals (Sweden)

    Augustin DuSablon

    Full Text Available EphrinA1, a membrane-bound receptor tyrosine kinase ligand expressed in healthy cardiomyocytes, is lost in injured cells following myocardial infarction. Previously, we have reported that a single intramyocardial injection of chimeric ephrinA1-Fc at the time of ischemia reduced injury in the nonreperfused myocardium by 50% at 4 days post-MI by reducing apoptosis and inflammatory cell infiltration. In a clinically relevant model of acute ischemia (30min/reperfusion (24hr or 4 days injury, we now demonstrate that ephrinA1-Fc reduces infarct size by 46% and completely preserves cardiac function (ejection fraction, fractional shortening, and chamber dimensions in the short-term (24hrs post-MI as well as long-term (4 days. At 24 hours post-MI, diminished serum inflammatory cell chemoattractants in ephrinA1-Fc-treated mice reduces recruitment of neutrophils and leukocytes into the myocardium. Differences in relative expression levels of EphA-Rs are described in the context of their putative role in mediating cardioprotection. Validation by Western blotting of selected targets from mass spectrometry analyses of pooled samples of left ventricular tissue homogenates from mice that underwent 30min ischemia and 24hr of reperfusion (I/R indicates that ephrinA1-Fc administration alters several regulators of signaling pathways that attenuate apoptosis, promote autophagy, and shift from FA metabolism in favor of increased glycolysis to optimize anaerobic ATP production. Taken together, reduced injury is due a combination of adaptive metabolic reprogramming, improved cell survival, and decreased inflammatory cell recruitment, suggesting that ephrinA1-Fc enhances the capacity of the heart to withstand an ischemic insult.

  8. Comparison of Myocardial Remodeling between Cryoinfarction and Reperfused Infarction in Mice

    Directory of Open Access Journals (Sweden)

    Georg D. Duerr

    2011-01-01

    Full Text Available Myocardial infarction is associated with inflammatory reaction leading to tissue remodeling. We compared tissue remodeling between cryoinfarction (cMI and reperfused myocardial infarction (MI in order to better understand the local environment where we apply cell therapies. Models of closed-chest one-hour ischemia/reperfusion MI and cMI were used in C57/Bl6-mice. The reperfused MI showed rapid development of granulation tissue and compacted scar formation after 7 days. In contrast, cMI hearts showed persistent cardiomyocyte debris and cellular infiltration after 7 days and partially compacted scar formation accompanied by persistent macrophages and myofibroblasts after 14 days. The mRNA of proinflammatory mediators was transiently induced in MI and persistently upregulated in cMI. Tenascin C and osteopontin-1 showed delayed induction in cMI. In conclusion, the cryoinfarction was associated with prolonged inflammation and active myocardial remodeling when compared to the reperfused MI. These substantial differences in remodeling may influence cellular engraftment and should be considered in cell therapy studies.

  9. Impairment of endothelial-myocardial interaction increases the susceptibility of cardiomyocytes to ischemia/reperfusion injury.

    Directory of Open Access Journals (Sweden)

    Thorsten M Leucker

    Full Text Available Endothelial-myocardial interactions may be critically important for ischemia/reperfusion injury. Tetrahydrobiopterin (BH4 is a required cofactor for nitric oxide (NO production by endothelial NO synthase (eNOS. Hyperglycemia (HG leads to significant increases in oxidative stress, oxidizing BH4 to enzymatically incompetent dihydrobiopterin. How alterations in endothelial BH4 content impact myocardial ischemia/reperfusion injury remains elusive. The aim of this study was to examine the effect of endothelial-myocardial interaction on ischemia/reperfusion injury, with an emphasis on the role of endothelial BH4 content. Langendorff-perfused mouse hearts were treated by triton X-100 to produce endothelial dysfunction and subsequently subjected to 30 min of ischemia followed by 2 h of reperfusion. The recovery of left ventricular systolic and diastolic function during reperfusion was impaired in triton X-100 treated hearts compared with vehicle-treated hearts. Cardiomyocytes (CMs were co-cultured with endothelial cells (ECs and subsequently subjected to 2 h of hypoxia followed by 2 h of reoxygenation. Addition of ECs to CMs at a ratio of 1∶3 significantly increased NO production and decreased lactate dehydrogenase activity compared with CMs alone. This EC-derived protection was abolished by HG. The addition of 100 µM sepiapterin (a BH4 precursor or overexpression of GTP cyclohydrolase 1 (the rate-limiting enzyme for BH4 biosynthesis in ECs by gene trasfer enhanced endothelial BH4 levels, the ratio of eNOS dimer/monomer, eNOS phosphorylation, and NO production and decreased lactate dehydrogenase activity in the presence of HG. These results demonstrate that increased BH4 content in ECs by either pharmacological or genetic approaches reduces myocardial damage during hypoxia/reoxygenation in the presence of HG. Maintaining sufficient endothelial BH4 is crucial for cardioprotection against hypoxia/reoxygenation injury.

  10. Pharmacological Attenuation of Myocardial Reperfusion Injury in a Closed-Chest Porcine Model

    DEFF Research Database (Denmark)

    Ekeløf, Sarah; Rosenberg, Jacob; Jensen, Jan Skov

    2014-01-01

    effective in clinically relevant experimental studies before initiation of human studies. The closed-chest porcine model is a promising experimental model of ischemia-reperfusion injury. The purpose of this systematic review was to describe the pharmacological treatments evaluated in the closed......Myocardial ischemia-reperfusion injury is a clinical challenge in interventional cardiology, and at the moment, no pharmacological agent is universally accepted in the prevention. In order to prevent inappropriate clinical trials, a potential pharmacological agent should be proved reproducibly...

  11. Myocardial capillary permeability for small hydrophilic indicators during normal physiological conditions and after ischemia and reperfusion

    DEFF Research Database (Denmark)

    Svendsen, Jesper Hastrup

    1991-01-01

    these PdS values Pd values between 1.57.10(-5) and 1.92.10(-5) cm.s-1 were calculated, in accordance with values obtained by other methods. Similar data have been obtained in myocardium of patients undergoing coronary angiography. Oxygen derived free radicals seems to participate in reperfusion injury...... including microvascular alterations. In open chest dogs transitory increases in capillary extraction fraction and PdS for small hydrophilic solutes were seen following 20 minutes of regional myocardial ischemia and reperfusion. This response could be inhibited by treatment directed against superoxide...

  12. Postconditioning attenuates acute intestinal ischemia–reperfusion injury

    Directory of Open Access Journals (Sweden)

    Ilker Sengul

    2013-03-01

    Full Text Available The aim of this study was to test the hypothesis that postconditioning (POC would reduce the detrimental effects of the acute intestinal ischemia–reperfusion (I/R compared to those of the abrupt onset of reperfusion. POC has a protective effect on intestinal I/R injury by inhibiting events in the early minutes of reperfusion in rats. Twenty-four Wistar–Albino rats were subjected to the occlusion of superior mesenteric artery for 30 minutes, then reperfused for 120 minutes, and randomized to the four different modalities of POC: (1 control (no intervention; (2 POC-3 (three cycles of 10 seconds of reperfusion–reocclusion, 1 minute total intervention; (3 POC-6 (six cycles of 10 seconds of reperfusion–reocclusion, 2 minutes total intervention; and (4 sham operation (laparotomy only. The arterial blood samples [0.3 mL total creatine kinase (CK and 0.6 mL malondialdehyde (MDA] and the intestinal mucosal MDA were collected from each after reperfusion. POC, especially POC-6, was effective in attenuating postischemic pathology by decreasing the intestinal tissue MDA levels, serum total CK activity, inflammation, and total histopathological injury scores. POC exerted a protective effect on the intestinal mucosa by reducing the mesenteric oxidant generation, lipid peroxidation, and neutrophil accumulation. The six-cycle algorithm demonstrated the best protection.

  13. Anterior wall myocardial infarction in real world: does reperfusion strategy make any differences?

    Science.gov (United States)

    Solodky, Alejandro; Assali, Abid R; Behar, Solomon; Boyko, Valentina; Battler, Alexander; Kornowski, Ran

    2004-01-01

    Some prospective randomized trials have established the superiority of primary percutaneous coronary intervention (PCI) over fibrinolytic treatment in patients with acute myocardial infarction (MI). These excellent PCI results are not duplicated in smaller hospitals where there may be delays in getting the cardiac catheterization team to the laboratory. This study aimed to compare the outcome of patients with anterior wall MI, without cardiogenic shock on admission, treated with primary PCI or thrombolytic therapy, in everyday practice. The data of all patients with MI hospitalized in all coronary care units operating in Israel during three consecutive national surveys was analyzed. A total of 1,038 patients with anterior wall MI were treated by reperfusion (886 received thrombolytic therapy, 152 primary PCI). Overall, the outcome of patients treated using primary PCI was better compared to patients treated with thrombolysis, with 68% relative risk reduction of 30-day mortality (mortality at 30 days: 2% vs. 6.3%; P = 0.04). A subanalysis of patients according to age showed that the beneficial effect of primary PCI on mortality was mainly clustered among the younger. In our study, patients (especially younger than 75 years) with anterior wall MI allocated to primary PCI have a better clinical outcome. Copyright 2004 Wiley-Liss, Inc.

  14. Leucocyte depletion attenuates the early increase in myocardial capillary permeability to small hydrophilic solutes following ischaemia and reperfusion

    DEFF Research Database (Denmark)

    Svendsen, Jesper Hastrup; Hansen, P R; Ali, S

    1993-01-01

    The aim was to assess the significance of polymorphonuclear leucocytes on the myocardial capillary permeability to a small hydrophilic indicator, on the vascular tone of the resistance vessels, and on contractile function following ischaemia and reperfusion.......The aim was to assess the significance of polymorphonuclear leucocytes on the myocardial capillary permeability to a small hydrophilic indicator, on the vascular tone of the resistance vessels, and on contractile function following ischaemia and reperfusion....

  15. Sodium 4-Phenylbutyrate Attenuates Myocardial Reperfusion Injury by Reducing the Unfolded Protein Response.

    Science.gov (United States)

    Takatori, Osamu; Usui, Soichiro; Okajima, Masaki; Kaneko, Shuichi; Ootsuji, Hiroshi; Takashima, Shin-Ichiro; Kobayashi, Daisuke; Murai, Hisayoshi; Furusho, Hiroshi; Takamura, Masayuki

    2017-05-01

    The unfolded protein response (UPR) plays a pivotal role in ischemia-reperfusion (I/R) injury in various organs such as heart, brain, and liver. Sodium 4-phenylbutyrate (PBA) reportedly acts as a chemical chaperone that reduces UPR. In the present study, we evaluated the effect of PBA on reducing the UPR and protecting against myocardial I/R injury in mice. Male C57BL/6 mice were subjected to 30-minute myocardial I/R, and were treated with phosphate-buffered saline (as a vehicle) or PBA. At 4 hours after reperfusion, mice treated with PBA had reduced serum cardiac troponin I levels and numbers of apoptotic cells in left ventricles (LVs) in myocardial I/R. Infarct size had also reduced in mice treated with PBA at 48 hours after reperfusion. At 2 hours after reperfusion, UPR markers, including eukaryotic initiation of the factor 2α-subunit, activating transcription factor-6, inositol-requiring enzyme-1, glucose-regulated protein 78, CCAAT/enhancer-binding protein (C/EBP) homologous protein, and caspase-12, were significantly increased in mice treated with vehicle compared to sham-operated mice. Administration of PBA significantly reduced the I/R-induced increases of these markers. Cardiac function and dimensions were assessed at 21 days after I/R. Sodium 4-phenylbutyrate dedicated to the improvement of cardiac parameters deterioration including LV end-diastolic diameter and LV fractional shortening. Consistently, PBA reduced messenger RNA expression levels of cardiac remodeling markers such as collagen type 1α1, brain natriuretic peptide, and α skeletal muscle actin in LV at 21 days after I/R. Unfolded protein response mediates myocardial I/R injury. Administration of PBA reduces the UPR, apoptosis, infarct size, and preserved cardiac function. Hence, PBA may be a therapeutic option to attenuate myocardial I/R injury in clinical practice.

  16. The activation of mitochondrial BK potassium channels contributes to the protective effects of naringenin against myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Testai, L; Martelli, A; Marino, A; D'Antongiovanni, V; Ciregia, F; Giusti, L; Lucacchini, A; Chericoni, S; Breschi, M C; Calderone, V

    2013-06-01

    Naringenin (NAR), flavonoid abundant in the genus Citrus, has been reported to interact with the large-conductance calcium-activated potassium channels (BK). Since activators of BK channels expressed in cardiac mitochondria trigger protective effects in several models of myocardial ischemia/reperfusion (I/R), this work aimed to evaluate the potential cardioprotective effects of NAR and the involvement of mitochondrial BK channels. In an in vivo model of acute infarct in rats, NAR (100mg/kg i.p.) significantly reduced the heart injury induced by I/R. This effect was antagonized by the selective BK-blocker paxilline (PAX). The cardioprotective dose of NAR did not cause significant effects on the blood pressure. In Largendorff-perfused rat hearts submitted to ischemia/reperfusion, NAR improved the post-ischemic functional parameters (left ventricle developed pressure and dP/dt) with lower extension of myocardial injury. On isolated rat cardiac mitochondria, NAR caused a concentration-dependent depolarization of mitochondrial membrane and caused a trans-membrane flow of thallium (potassium-mimetic cation). Both these effects were antagonized by selective blockers of BK channels. Furthermore, NAR half-reduced the calcium accumulation into the matrix of cardiac mitochondria exposed to high calcium concentrations. In conclusion, NAR exerts anti-ischemic effects through a "pharmacological preconditioning" that it is likely to be mediated, at least in part, by the activation of mitochondrial BK channels. Copyright © 2013. Published by Elsevier Inc.

  17. Serial change of TL/BMIPP dual SPECT myocardial scintigram in patients with acute myocardial infarction. Meaning of chronic mismatch phenomenon

    International Nuclear Information System (INIS)

    Iwasawa, Hirohito; Abe, Masahiro; Abe, Toshihiro; Nagai, Yoshikazu; Ibukiyama, Chiharu

    1999-01-01

    This study was aimed to elucidate the serial changes and clinical significance of accumulation mismatch with TL and BMIPP dual SPECT myocardial scintigraphy during 6 months in patients with acute myocardial infarction (AMI). The dual SPECT scintigraphy was performed at one, three and six months after onset of AMI in 46 patients who underwent reperfusion therapy. Long axis fractional shortening in infarct-related area and left ventricular end-diastolic volume index (LVEDVI) were measured by left ventriculography performed immediately after reperfusion and at one, six months after onset of AMI. The patients were divided into two groups: those with mismatch (Group (+)) and those without (Group (-)) at one month after reperfusion. Group (+) was subdivided into three groups according to duration of persistence of mismatch; one month persistence (1M), three months (3M) and six months (6M). Improvement of wall motion abnormality (WMA) in infarct-related area was seen at one month after reperfusion in group 1M and group 3M, while group 6M showed no apparent change in WMA throughout the study period. LVEDVI did not change at six months after reperfusion in group 1M and 3M, while significant increase was seen in group 6M. It is concluded that the case with disappearance of mismatch between TL and BMIPP until three months after reperfusion indicates myocardial stunning while in the case with long-standing mismatch left ventricular remodeling is suggested. (author)

  18. NMR studies of myocardial energy metabolism and ionic homeostasis during ischemia and reperfusion

    International Nuclear Information System (INIS)

    Kirkels, J.H.

    1989-01-01

    In this study several aspects of myocardial energy metabolism and ionic homeostasis during ischemia and reperfusion were investigated in isolated perfused rat hearts, regionally ischemic rabbit hearts, and ex vivo human donor hearts during long term hypothermic cardioplegia. Phosphorus-31 nuclear magnetic resonance ( 31 P NMR) spectroscopy was used as a powerful tool to non-destructively follow the time course in changes in intracellular high-energy phosphates, (creatine phosphate and ATP), inorganic phosphate, and pH. In addition, changes in intracellular free magnesium were followed during ischemia and reperfusion. Sodium-23 ( 23 Na) NMR spectroscopy was used to study intracellular sodium during ischemia and reperfusion and during calcium-free perfusion. (author). 495 refs.; 33 figs.; 11 tabs

  19. Quantitative N-linked Glycoproteomics of Myocardial Ischemia and Reperfusion Injury Reveals Early Remodeling in the Extracellular Environment

    DEFF Research Database (Denmark)

    Parker, Benjamin L; Palmisano, Giuseppe; Edwards, Alistair V G

    2011-01-01

    Extracellular and cell surface proteins are generally modified with N-linked glycans and glycopeptide enrichment is an attractive tool to analyze these proteins. The role of N-linked glycoproteins in cardiovascular disease, particularly ischemia and reperfusion injury, is poorly understood...... quantitation (iTRAQ) and validation with dimethyl labeling to analyze changes in glycoproteins from tissue following prolonged ischemia and reperfusion (40 mins ischemia and 20 mins reperfusion) indicative of myocardial infarction. The iTRAQ approach revealed 80 of 437 glycopeptides with altered abundance......-associated proteins. The data suggest that cardiac remodeling is initiated earlier during reperfusion than previously hypothesized....

  20. Cardioprotective Effect of Electroacupuncture Pretreatment on Myocardial Ischemia/Reperfusion Injury via Antiapoptotic Signaling

    Directory of Open Access Journals (Sweden)

    Sheng-feng Lu

    2016-01-01

    Full Text Available Objectives. Our previous study has used RNA-seq technology to show that apoptotic molecules were involved in the myocardial protection of electroacupuncture pretreatment (EAP on the ischemia/reperfusion (I/R animal model. Therefore, this study was designed to investigate how EAP protects myocardium against myocardial I/R injury through antiapoptotic mechanism. Methods. By using rats with myocardial I/R, we ligated the left anterior descending artery (LAD for 30 minutes followed by 4 hr of reperfusion after EAP at the Neiguan (PC6 acupoint for 12 days; we employed arrhythmia scores, serum myocardial enzymes, and cardiac troponin T (cTnT to evaluate the cardioprotective effect. Heart tissues were harvested for western blot analyses for the expressions of pro- and antiapoptotic signaling molecules. Results. Our preliminary findings showed that EAP increased the survival of the animals along with declined arrhythmia scores and decreased CK, LDH, CK-Mb, and cTnT levels. Further analyses with the heart tissues detected reduced myocardial fiber damage, decreased number of apoptotic cells and the protein expressions of Cyt c and cleaved caspase 3, and the elevated level of Endo G and AIF after EAP intervention. At the same time, the protein expressions of antiapoptotic molecules, including Xiap, BclxL, and Bcl2, were obviously increased. Conclusions. The present study suggested that EAP protected the myocardium from I/R injury at least partially through the activation of endogenous antiapoptotic signaling.

  1. [Vasoprotective effect of adaptation to hypoxia in myocardial ischemia and reperfusion injury].

    Science.gov (United States)

    Manukhina, E B; Terekhina, O L; Belkina, L M; Abramochkin, D V; Budanova, O P; Mashina, S Yu; Smirin, B V; Yakunina, E B; Downey, H F

    2013-01-01

    Adaptation to hypoxia is known to be cardioprotective in ischemic and reperfusion (IR) injury of the myocardium. This study was focused on investigating a possibility for prevention of endothelial dysfunction in IR injury of the rat heart using adaptation to intermittent hypoxia, which was performed in a cyclic mode (5-10 min of hypoxia interspersed with 4 min of normoxia, 5-8 cycles daily) for 21 days. Endothelial function of coronary blood vessels was evaluated after the in vitro IR of isolated heart (15 min of ischemia and 10 min of reperfusion) by the increment of coronary flow rate in response to acetylcholine. Endothelium-dependent relaxation of isolated rat aorta was evaluated after the IR myocardial injury in situ (30 min of ischemia and 60 min of reperfusion) by a relaxation response of noradrenaline-precontracted vessel rings to acetylcholine. The following major results were obtained in this study: 1) IR myocardial injury induced endothelial dysfunction of coronary blood vessels and the aorta, a non-coronary blood vessel, remote from the IR injury area; and 2) adaptation to hypoxia prevented the endothelial dysfunction of both coronary and non-coronary blood vessels associated with the IR injury. Therefore, adaptation to hypoxia is not only cardioprotective but also vasoprotective in myocardial IR injury.

  2. Frequency of acute right ventricular myocardial infarction in patients with acute inferior myocardial infarction

    International Nuclear Information System (INIS)

    Iqbal, M.A.; Shah, I.; Rauf, M.A.; Khan, N.; Khan, S.B.; Hafizullah, M.

    2012-01-01

    Objective: To determine the frequency of acute right ventricular myocardial infarction (RVMI) in patients with acute inferior myocardial infarction. Methodology: This prospective case series study was conducted at Cardiology Department in a period from May to October 2009. A total of 174 patients with acute inferior myocardial infarction were evaluated for the presence of acute right ventricular myocardial infarction (RVMI). Results: Male patients were 135 (77.6%) and females 39 (24.4%). Patient's age ranged from 28 to 82 years with majority in the age group 40 to 60 years. Frequency of RVMI was 27% among patients presenting with acute inferior myocardial infarction. Among patients presenting with acute RVMI, 64 % patients received thrombolysis. Overall 65% patients of RVMI had hospital stay of more than 4 days. Conclusion: Frequency of RVMI among inferior MI patients was 27 % with longer hospital stay. (author)

  3. Thallium-201 myocardial imaging in acute-myocardial infarction

    International Nuclear Information System (INIS)

    Wackers, F.J.Th.; Lie, K.I.; Sokole, E.B.; Wellens, H.J.J.; Samson, G.; Schoot, J.B. van der

    1980-01-01

    Thallium-201 scintigraphy has proven to be an early and highly sensitive technique to detect myocardial perfusion abnormalities in patients with acute myocardial infarction. During the early phase of acute myocardial infarction, patients may be hemodynamically and electrically unstable. Therefore, scintigraphy is performed preferably at the bed side in the Coronary Care Unit using a mobile gamma camera. Additionally, in order to shorten imaging time in these often critically ill patients, the authors recommend injecting no less than 2 mCi of 201 Tl. Using this dosage, the imaging time per view will be approximately five minutes. Routinely, three views are taken: the first view is a supine 45 0 left-anterior-oblique view, followed by a supine anterior view and finally a left-lateral view, the latter with the patient turned on the right side. (Auth.)

  4. Intracoronary and systemic melatonin to patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L; Busch, Sarah Ekeløf; Jensen, Svend Eggert

    2014-01-01

    reperfusion. The endogenous hormone, melatonin, works as an antioxidant and could potentially minimise the ischaemia-reperfusion injury. Given intracoronarily, it enables melatonin to work directly at the site of reperfusion. We wish to test if melatonin, as an antioxidant, can minimise the reperfusion injury......-point is the Myocardial Salvage Index assessed by cardiovascular magnetic resonance imaging on day 4 (± 1) after pPCI. The secondary end-points are high-sensitivity troponin, creatinekinase myocardial band and clinical events. CONCLUSION: The aim of the IMPACT trial is to evaluate the effect of melatonin on reperfusion...... injuries following pPCI. Owing to its relatively non-toxic profile, melatonin is an easily implementable drug in the clinical setting, and melatonin has the potential to reduce morbidity in patients with AMI. FUNDING: This study received no financial support from the industry. TRIAL REGISTRATION: www...

  5. The effect of levosimendan on myocardial ischemia–reperfusion injury in streptozotocin-induced diabetic rats

    Science.gov (United States)

    Kiraz, Hasan Ali; Poyraz, Fatih; Kip, Gülay; Erdem, Özlem; Alkan, Metin; Arslan, Mustafa; Özer, Abdullah; Şivgin, Volkan; Çomu, Faruk Metin

    2015-01-01

    Objective Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio protective effects of levosimendan in a diabetic rat model of myocardial I/R injury. Methods A total of 18 streptozotocin-induced diabetic Wistar Albino rats (55 mg/kg) were randomly divided into three equal groups as follows: the diabetic I/R group (DIR) in which myocardial I/R was induced following left thoracotomy, by ligating the left anterior descending coronary artery for 60 min, followed by 2 h of reperfusion; the diabetic I/R levosimendan group (DIRL), which underwent I/R by the same method while taking levosimendan intraperitoneal 12 µg kg−1; and the diabetic control group (DC) which underwent sham operations without tightening of the coronary sutures. As a control group (C), six healthy age-matched Wistar Albino rats underwent sham operations similar to the DC group. Two hours after the operation, the rats were sacrificed and the myocardial tissue samples were examined by light microscopy for evidence of myonecrosis and inflammatory cell infiltration. Results Myonecrosis findings were significantly different among groups (p=0.008). Myonecrosis was more pronounced in the DIR group compared with the C, DC, and DIRL groups (p=0.001, p=0.007 and p=0.037, respectively). Similarly, the degree of inflammatory cell infiltration showed significant difference among groups (p<0.0001). Compared with C, DC, and DIRL groups, the inflammatory cell infiltration was significantly higher among the DIR group (p<0.0001, p<0.0001, and p=0.020, respectively). Also, myocardial tissue edema was significantly different among groups (p=0.006). The light microscopic myocardial tissue edema levels were significantly higher in the DIR group than the C, DC, and DIRL groups (p=0.001, p=0.037, and p=0.014, respectively). Conclusion Taken together, our data indicate that

  6. The effect of levosimendan on myocardial ischemia–reperfusion injury in streptozotocin-induced diabetic rats

    Directory of Open Access Journals (Sweden)

    Hasan Ali Kiraz

    2015-12-01

    Full Text Available Objective: Ischemia/reperfusion (I/R injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio protective effects of levosimendan in a diabetic rat model of myocardial I/R injury. Methods: A total of 18 streptozotocin-induced diabetic Wistar Albino rats (55 mg/kg were randomly divided into three equal groups as follows: the diabetic I/R group (DIR in which myocardial I/R was induced following left thoracotomy, by ligating the left anterior descending coronary artery for 60 min, followed by 2 h of reperfusion; the diabetic I/R levosimendan group (DIRL, which underwent I/R by the same method while taking levosimendan intraperitoneal 12 µg kg−1; and the diabetic control group (DC which underwent sham operations without tightening of the coronary sutures. As a control group (C, six healthy age-matched Wistar Albino rats underwent sham operations similar to the DC group. Two hours after the operation, the rats were sacrificed and the myocardial tissue samples were examined by light microscopy for evidence of myonecrosis and inflammatory cell infiltration. Results: Myonecrosis findings were significantly different among groups (p=0.008. Myonecrosis was more pronounced in the DIR group compared with the C, DC, and DIRL groups (p=0.001, p=0.007 and p=0.037, respectively. Similarly, the degree of inflammatory cell infiltration showed significant difference among groups (p<0.0001. Compared with C, DC, and DIRL groups, the inflammatory cell infiltration was significantly higher among the DIR group (p<0.0001, p<0.0001, and p=0.020, respectively. Also, myocardial tissue edema was significantly different among groups (p=0.006. The light microscopic myocardial tissue edema levels were significantly higher in the DIR group than the C, DC, and DIRL groups (p=0.001, p=0.037, and p=0.014, respectively. Conclusion: Taken together, our data

  7. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion.

    Science.gov (United States)

    Kin, Hajime; Zhao, Zhi-Qing; Sun, He-Ying; Wang, Ning-Ping; Corvera, Joel S; Halkos, Michael E; Kerendi, Faraz; Guyton, Robert A; Vinten-Johansen, Jakob

    2004-04-01

    We previously showed that brief intermittent ischemia applied during the onset of reperfusion (i.e., postconditioning) is cardioprotective in a canine model of ischemia-reperfusion. This study tested the hypothesis that the early minutes of reperfusion (R) during which postconditioning (Post-con) is applied are critical to its cardioprotection. In anesthetized open-chest rats, the left coronary artery (LCA) was occluded for 30 min and reperfused for 3 h. All rats were randomly divided into six groups: Control (n=8): no intervention at R; Ischemic preconditioning (IPC) (n=8): the LCA was occluded for 5 min followed by 10 min of R before the index occlusion; Post-con 1 (n=8): after LCA occlusion, three cycles of 10 s R followed by 10 s LCA re-occlusion were applied during the first minute of R; Post-con 2 (n=8): Six cycles of 10 s R and 10 s re-occlusion were applied during the first 2 min of R; Delayed Post-con (n=8): the ligature was loosened for full reflow for the first minute of R, after which the three-cycle Post-con algorithm was applied; Sham (n=6): the surgical procedure was identical to other groups, but the LCA ligature was not ligated. Infarct size (TTC staining) was 23% smaller in Post-con 1 (40+/-2%*) than in Control (52+/-3%), confirmed by plasma creatine kinase activity (18+/-2* vs. 46+/-6 IU/g protein). There was no further reduction in infarct size with 6 cycles of Post-con (40+/-2.9%, p>0.05 vs. Post-con 1). Meanwhile, infarct size reduction was significantly greater in the IPC group (17+/-3%) than in Post-con1 (pinjury; (2) cardioprotection may be mediated, in part, by inhibiting oxidant generation and oxidant mediated injury; (3) the first minute of R in the rat model is critical to cardioprotection by Post-con; and (4) cardioprotection by Post-con may be independent of neutrophil accumulation in AAR. *p<0.05 Post-con vs. Control.

  8. Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers.

    Science.gov (United States)

    Jin, Jiyang; Chen, Min; Li, Yongjun; Wang, YaLing; Zhang, Shijun; Wang, Zhen; Wang, Lin; Ju, Shenghong

    2016-10-01

    We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) ( P =0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction-identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.

  9. Factors associated with myocardial salvage immediately after emergent percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction

    International Nuclear Information System (INIS)

    Yoshida, Susumu; Nakamura, Seishi; Sugiura, Tetsuro

    2009-01-01

    The amount of myocardial salvage after percutaneous coronary intervention (PCI) is reported to be a major determinant of functional recovery in patients with ST-elevation acute myocardial infarction (MI). However, factors related to the amount of myocardial salvage remain unknown. The goal of this study was to investigate the factors related to the amount of myocardial salvage after emergent PCI in patients with ST-elevation acute MI by incorporating pre- and post-treatment indices and adjunctive treatments. Technetium-99m myocardial imaging was performed before, immediately after, and one month after emergent PCI in 161 patients with ST-elevation acute MI, and the defect score was serially evaluated. A good myocardial salvage was defined as ≥4 change (before minus immediately after PCI) of the defect score. Good myocardial salvage was observed in 89 patients. Based on nine clinical variables, logistic regression analysis was performed to determine the important variables related to myocardial salvage. Multivariate analysis revealed that earlier time from onset to PCI (χ 2 =6.55, P=0.01, odds ratio=2.78), larger defect score before PCI (χ 2 =7.29, P=0.01, odds ratio=1.13) and administration of nicorandil before PCI (χ 2 =9.88, P=0.008, odds ratio=4.42) were independently associated with good myocardial salvage. Thrombolysis In Myocardial Infarction (TIMI) flow grade 2 =4.91, P=0.03, odds ratio=0.36) and TIMI flow grade ≤2 after PCI (χ 2 =4.82, P=0.03, odds ratio=0.31) were independently associated with poor myocardial salvage. In contrast, the number of asynergic segments before PCI, infarct-related artery, adequate collaterals before PCI and stent implantation were not determinants of myocardial salvage. This study demonstrated that patients with a greater improvement of 99 mTc tetrofosmin myocardial uptake immediately after PCI had better recovery of left ventricular function and smaller final infarct size. Reperfusion time and TIMI flow grade ≤2 after

  10. Effects and Mechanisms of Chinese Herbal Medicine in Ameliorating Myocardial Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Qing Liu

    2013-01-01

    Full Text Available Myocardial ischemia-reperfusion (MIR injury is a major contributor to the morbidity and mortality associated with coronary artery disease, which accounts for approximately 450,000 deaths a year in the United States alone. Chinese herbal medicine, especially combined herbal formulations, has been widely used in traditional Chinese medicine for the treatment of myocardial infarction for hundreds of years. While the efficacy of Chinese herbal medicine is well documented, the underlying molecular mechanisms remain elusive. In this review, we highlight recent studies which are focused on elucidating the cellular and molecular mechanisms using extracted compounds, single herbs, or herbal formulations in experimental settings. These studies represent recent efforts to bridge the gap between the enigma of ancient Chinese herbal medicine and the concepts of modern cell and molecular biology in the treatment of myocardial infarction.

  11. Update on intravenous fibrinolytic therapy for acute myocardial infarction.

    Science.gov (United States)

    Wright, R S; Kopecky, S L; Reeder, G S

    2000-11-01

    Intravenous fibrinolytic therapy is used widely in the treatment of ST-elevation acute myocardial infarction. Advances in this therapeutic modality during the past 5 years include new third-generation fibrinolytic agents and creative strategies to enhance administration and efficacy of fibrinolytic therapy. Several of the new agents allow for single- or double-bolus injection. A number of ongoing large randomized trials are attempting to determine whether the combination of fibrinolytic therapy with low-molecular-weight heparin or a glycoprotein IIb/IIIa antagonist enhances coronary reperfusion and reduces mortality and late reocclusion. One large prospective trial is investigating the potential benefit of prehospital administration of fibrinolytic therapy. This article summarizes recent safety and efficacy data on fibrinolytic therapy, with particular emphasis on the new third-generation fibrin-specific agents; reviews the preliminary data on facilitated fibrinolysis; and discusses the rationale for prehospital administration of fibrinolytic therapy.

  12. Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents.

    Science.gov (United States)

    Eisenmann, Eric D; Rorabaugh, Boyd R; Zoladz, Phillip R

    2016-01-01

    Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia-reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions.

  13. Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents

    Science.gov (United States)

    Eisenmann, Eric D.; Rorabaugh, Boyd R.; Zoladz, Phillip R.

    2016-01-01

    Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia–reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions. PMID:27199778

  14. Circulating NOS3 modulates left ventricular remodeling following reperfused myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Simone Gorressen

    Full Text Available Nitric oxide (NO is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3. We have shown that NO protects against myocardial ischemia/reperfusion (I/R injury and that depletion of circulating NOS3 increases within 24 h of ischemia/reperfusion the size of myocardial infarction (MI in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI.To analyze the role of circulating NOS3 we transplanted bone marrow of NOS3-/- and wild type (WT mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC-/EC+ or in both, blood cells and vascular endothelium (BC+/EC+. Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24 h, 4 d, 1 w, 2 w and 3 w by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori's One-step trichrome staining.Three weeks post MI, LV end-systolic (53.2±5.9 μl; ***p≤0.001; n = 5 and end-diastolic volumes (82.7±5.6 μl; *p<0.05; n = 5 were significantly increased in BC-/EC+, along with decreased LV developed pressure (67.5±1.8 mm Hg; n = 18; ***p≤0.001 and increased scar size/left ventricle (19.5±1.5%; n = 13; **p≤0.01 compared to BC+/EC+ (ESV: 35.6±2.2 μl; EDV: 69.1±2.6 μl n = 8; LVDP: 83.2±3.2 mm Hg; n = 24; scar size/LV13.8±0.7%; n = 16. Myocardial scar of BC-/EC+ was characterized by increased total collagen content (20.2±0.8%; n = 13; ***p≤0.001 compared to BC+/EC+ (15.9±0.5; n = 16, and increased collagen type I and III subtypes

  15. Influence of acute glycaemic level on measures of myocardial infarction in non-diabetic pigs.

    Science.gov (United States)

    Diemar, Sarah S; Sejling, Anne-Sophie; Iversen, Kasper K; Engstrøm, Thomas; Honge, Jesper L; Tønder, Niels; Vejlstrup, Niels; Idorn, Manja; Ekström, Kathrine; Pedersen-Bjergaard, Ulrik; Thorsteinsson, Birger; Dalsgaard, Morten

    2015-01-01

    Patients with diabetes are at increased risk of experiencing myocardial infarction. The influence of the prevailing plasma glucose level on infarction and mortality after acute ischaemia is however unknown. The aim was to study the effect of the acute plasma glucose level on the myocardial infarction size in a closed-chest pig model. 38 non-diabetic pigs were randomised to hypoglycaemic (1.8-2.2 mmol/l; n = 15), normoglycaemic (5-7 mmol/l; n = 12) or hyperglycaemic glucose clamping (22-23 mmol/l; n = 11). After 30 min within glucose target myocardial infarction was induced for 30 min followed by reperfusion for 120 min. Hereafter the heart was double-stained to delineate infarction from viable tissue within the area at risk. Mean infarction size was 201 ± 35 mm(2) (mean ± SEM) in the hypoglycaemic group, 154 ± 40 mm(2) in the normoglycaemic group and 134 ± 40 mm(2) in the hyperglycaemic group, with no differences in infarction size, infarct/area at risk ratio or troponin T levels between the groups. There was no difference in incidence of ventricular fibrillation or mortality between the groups. No statistically significant associations were observed between the acute glycaemic level and measures of myocardial infarction, rates of ventricular fibrillation and subsequent premature death in the setting of acute ischaemia and reperfusion.

  16. Inhibition of KV7 channels protects against myocardial ischemia and reperfusion injury

    DEFF Research Database (Denmark)

    Hedegaard, Elise Røge; Johnsen, Jacob; Povlsen, Jonas Agerlund

    2015-01-01

    Aims: KV7 channel are activated by ischemia and mediate hypoxic vasodilatation. We investigated the effect of KV7 channel modulation on cardiac ischemia and reperfusion (IR) injury and the interaction with cardioprotection by ischemic preconditioning (IPC). Methods and Results: We investigated....... In isolated coronary arteries XE991 inhibited relaxation during both hypoxia and reoxygenation. Conclusion: KV7 channel are active during hypoxia and KV7 channel inhibition is cardioprotective. These findings suggest a potential for KV7 blockers in the treatment of ischemia-reperfusion injury although safety...... the expression of the KV7 channels in rat hearts by reverse transcriptse PCR. The effect of the KV7 channel inhibitors, XE991 and linopirdine, and the KV7 channel opener, flupirtine on myocardial IR injury in isolated hearts and coronary arteries from Wistar rats was examined. Hearts were subjected to no...

  17. LOX-1 inhibition in myocardial ischemia-reperfusion injury: modulation of MMP-1 and inflammation.

    Science.gov (United States)

    Li, Dayuan; Williams, Victor; Liu, Ling; Chen, Hongjiang; Sawamura, Tatsuya; Antakli, Tamim; Mehta, Jawahar L

    2002-11-01

    A recently identified lectin-like oxidized low-density lipoprotein receptor (LOX-1) mediates endothelial cell injury and facilitates inflammatory cell adhesion. We studied the role of LOX-1 in myocardial ischemia-reperfusion (I/R) injury. Anesthetized Sprague-Dawley rats were subjected to 60 min of left coronary artery (LCA) ligation, followed by 60 min of reperfusion. Rats were treated with saline, LOX-1 blocking antibody JXT21 (10 mg/kg), or nonspecific anti-goat IgG (10 mg/kg) before I/R. Ten other rats underwent surgery without LCA ligation and served as a sham control group. LOX-1 expression was markedly increased during I/R (P injury.

  18. Effect of monoamine oxidase inhibitors on ischaemia/reperfusion-induced acute kidney injury in rats.

    Science.gov (United States)

    Tsutsui, Hidenobu; Shimokawa, Takaomi; Miura, Takeshi; Takama, Masashi; Nishinaka, Toru; Terada, Tomoyuki; Yamagata, Masayo; Yukimura, Tokihito

    2018-01-05

    Increases in renal sympathetic nerve activity during ischaemia and renal venous norepinephrine levels after reperfusion play important roles in the development of ischaemia/reperfusion-induced acute kidney injury. In the present study, we examined the effect of isatin, an endogenous monoamine oxidase inhibitor, on renal venous norepinephrine levels, superoxide production after reperfusion, and ischaemia/reperfusion-induced acute kidney injury. Ischaemia/reperfusion-induced acute kidney injury was accomplished by clamping the left renal artery and vein for 45min, followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal superoxide production and norepinephrine overflow were elevated and significant renal tissue damage was observed following ischaemia/reperfusion injury. Intravenous injection of isatin (10mg/kg) at 5min before ischaemia increased the renal venous plasma norepinephrine level after reperfusion and aggravated ischaemia/reperfusion-induced renal dysfunction and histological damage. The excessive superoxide production after reperfusion was significantly suppressed by isatin administration, indicating that the inhibition of oxidative deamination effectively suppressed superoxide production. These data suggest that the exacerbation effect of isatin is associated, at least in part, with increased norepinephrine levels but not with superoxide production. To the best of our knowledge, this is the first report of isatin involvement in the pathogenesis and/or development of acute kidney injury. Copyright © 2017 Elsevier B.V. All rights reserved.

  19. β2-adrenoceptor agonist clenbuterol reduces infarct size and myocardial apoptosis after myocardial ischaemia/reperfusion in anaesthetized rats

    Science.gov (United States)

    Zhang, Qiufang; Xiang, Jizhou; Wang, Xuanbin; Liu, Hui; Hu, Benrong; Feng, Mei; Fu, Qin

    2010-01-01

    Background and purpose: Considerable evidence indicates that the β2-adrenoceptor agonist clenbuterol decreases apoptosis in a rodent model of ischaemic cardiomyopathy. In this study, we investigated the effects of clenbuterol on infarct size caused by myocardial ischaemia/reperfusion (I/R) in anaesthetized rats. Experimental approach: Rats were randomly assigned to the following groups: (i) sham (ii) I/R (iii) clenbuterol + I/R (iv) ICI 118551 + clenbuterol + I/R (v) metoprolol + clenbuterol + I/R (vi) metoprolol + I/R (vii) pertussis toxin + clenbuterol + I/R. Under anaesthesia, left anterior descending coronary artery was occluded for 30 min followed by reperfusion for 2 h. Key results: Compared with the control I/R group,the clenbuterol (0.5 mg·kg−1, i.p.) group had reduced infarct size, improved diastolic function and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) activity, increased superoxide dismutase activity, and decreased malondialdehyde (MDA) level and LDH, CK release. Clenbuterol increased the phosphorylation of ERK1/2, which resulted in inhibition of myocardial apoptosis as indicated by the reduction of terminal deoxynucleotidyltransferase end labelling-positive staining, Bax/Bcl-2 mRNA and caspase-3 protein expression. The Gi-protein inhibitor pertussis toxin blocked the clenbuterol-induced improvement in cardiac function and infarct size. Pretreatment with ICI 118551(a selective β2-adrenoceptor antagonist) inhibited the effects of clenbuterol mentioned above. The β1-adrenoceptor agonist metoprolol had similar effects to clenbuterol but failed to reduce MDA and improve SERCA activity. When administered together, metoprolol and clenbuterol did not induce synergistic effects. Conclusions and implications: Clenbuterol pretreatment provides significant cardioprotection against ischaemia/reperfusion injury and this is mediated by the β2-adrenoceptor–Gi-protein signalling. A combination of the β2-adrenoceptor agonist clenbuterol and the

  20. Hypercholesterolemia aggravates myocardial ischemia reperfusion injury via activating endoplasmic reticulum stress-mediated apoptosis.

    Science.gov (United States)

    Wu, Nan; Zhang, Xiaowen; Jia, Pengyu; Jia, Dalin

    2015-12-01

    The effect of hypercholesterolemia on myocardial ischemia reperfusion injury (MIRI) is in controversy and the underlying mechanism is still not well understood. In the present study, we firstly detected the effects of hypercholesterolemia on MIRI and the role of endoplasmic reticulum (ER) stress-mediated apoptosis pathway in this process. The infarct size was determined by TTC staining, and apoptosis was measured by the TUNEL method. The marker proteins of ER stress response and ER stress-mediated apoptosis pathway were detected by Western blot. The results showed that high cholesterol diet-induced hypercholesterolemia significantly increased the myocardial infarct size, the release of myocardium enzyme and the ratio of apoptosis, but did not affect the recovery of cardiac function. Moreover, hypercholesterolemia also remarkably up-regulated the expressions of ER stress markers (glucose-regulated protein 78 and calreticulin) and critical molecules in ER stress-mediated apoptosis pathway (CHOP, caspase 12, phospho-JNK). In conclusion, our study demonstrated that hypercholesterolemia enhanced myocardial vulnerability/sensitivity to ischemia reperfusion injury involved in aggravation the ER stress and activation of ER stress-mediated apoptosis pathway and it gave us a new insight into the underlying mechanisms associated with hypercholesterolemia-induced exaggerated MIRI and also provided a novel target for preventing MIRI in the presence of hypercholesterolemia. Copyright © 2015 Elsevier Inc. All rights reserved.

  1. Reperfusion therapy with recombinant human relaxin-2 (Serelaxin) attenuates myocardial infarct size and NLRP3 inflammasome following ischemia/reperfusion injury via eNOS-dependent mechanism.

    Science.gov (United States)

    Valle Raleigh, Juan; Mauro, Adolfo G; Devarakonda, Teja; Marchetti, Carlo; He, Jun; Kim, Erica; Filippone, Scott; Das, Anindita; Toldo, Stefano; Abbate, Antonio; Salloum, Fadi N

    2017-05-01

    The preconditioning-like infarct-sparing and anti-inflammatory effects of the peptide hormone relaxin following ischemic injury have been studied in the heart. Whether reperfusion therapy with recombinant human relaxin-2, serelaxin, reduces myocardial infarct size and attenuates the subsequent NLRP3 inflammasome activation leading to further loss of functional myocardium following ischemia/reperfusion (I/R) injury is unknown. After baseline echocardiography, adult male wild-type C57BL or eNOS knockout mice underwent myocardial infarction (MI) by coronary artery ligation for 30 min followed by 24 h reperfusion. Mice were treated with either serelaxin (10 µg/kg; sc) or saline 1 h prior to ischemia or 5 min before reperfusion. In both pre-treatment and reperfusion therapy arms, serelaxin improved survival at 24 h post MI in wild-type mice (79% and 82%) as compared with controls (46% and 50%, P = 0.01), whereas there was no difference in survival between serelaxin- and saline-treated eNOS knockout mice. Moreover, serelaxin significantly reduced infarct size (64% and 67% reduction, P injury and the subsequent caspase-1 activation via eNOS-dependent mechanism. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com.

  2. The effect of cloricromene, a coumarine derivative, on leukocyte accumulation, myocardial necrosis and TNF-alpha production in myocardial ischaemia-reperfusion injury.

    Science.gov (United States)

    Squadrito, F; Altavilla, D; Zingarelli, B; Ioculano, M; Calapai, G; Campo, G M; Miceli, A; Prosdocimi, M; Caputi, A P

    1993-01-01

    The effects of cloricromene, a coumarine derivative, were studied in an anaesthetized rat model of coronary artery ligation (60 min) followed by reperfusion (60 min; MI/R). Sham operated rats were used as controls (Sham MI/R). Myocardial ischaemia-reperfusion injury produced a marked myocardial injury (necrotic area/area-at-risk = 68 +/- 4%; necrotic area/total area = 48 +/- 3%) high serum creatinphosphokinase activity (Sham MI/R = 29 +/- 8 U/ml; MI/R = 205 +/- 11 U/ml) and elevated myocardial myeloperoxidase activity (investigated as an index of leukocyte adhesion and accumulation), in the area-at-risk (6.3 +/- 0.2 U x 10(-3)/g tissue) and in necrotic area (6.5 +/- 0.5 U x 10(-3)/g tissue). Furthermore, serum TNF-alpha was undetectable during the occlusion period, but upon the release of the coronary artery significantly increased. At the end of reperfusion, macrophage TNF-alpha was also enhanced. The administration of cloricromene (2 mg/kg, 5 minutes after the onset of reperfusion) significantly reduced myocardial injury (necrotic area/area-at-risk 30 +/- 1.3%; necrotic area/total area = 25 +/- 1.5) blunted the increase in serum creatinphosphokinase activity (92 +/- 5 U/ml) and lowered myeloperoxidase activity in area-at-risk (2.5 +/- 0.2 U x 10(-3)/g tissue) and in necrotic area (2.2 +/- 0.3 U x 10(-3)/g tissue) and decreased the serum and macrophage levels of TNF-alpha. These data indicate that cloricromene exerts beneficial effects on myocardial ischaemia/reperfusion injury. Finally, since we measured increased serum levels of TNF-alpha that were blunted by the cloricromene treatment, our data are consistent with an involvement of TNF-alpha in the reperfusion injury induced by myocardial ischaemia.

  3. High-Resolution Imaging with 99mTc-Glucarate for Assessing Myocardial Injury in Rat Heart Models Exposed to Different Durations of Ischemia with Reperfusion

    Science.gov (United States)

    Liu, Zhonglin; Barrett, Harrison H.; Stevenson, Gail D.; Kastis, George A.; Bettan, Michael; Furenlid, Lars R.; Wilson, Donald W.; Pak, Koon Yan

    2008-01-01

    99mTc-Glucarate (99mTc-GLA) is a novel infarct-avid imaging agent. The aim of this study was to evaluate the role of 99mTc-GLA for assessing the severity of myocardial ischemia—reperfusion injury in rat heart models exposed to varied durations of left coronary artery (LCA) occlusion with reperfusion using a high-resolution SPECT system, FASTSPECT. We also wanted to clarify whether a rapid sequence of 3-dimensional imaging with FASTSPECT can quantify uptake and washout kinetics of cardiovascular imaging agents in small-animal heart models. Methods The ischemic—reperfused rat heart models were created by ligating the LCA for 30 min (IR30, n = 12) or 90 min (IR90, n = 6) (IR = ischemia—reperfusion) and releasing the ligature for 30 min. Dynamic images were acquired over a 2-h period after 99mTc-GLA was intravenously injected. The ischemic area at risk (IAR) was determined by Evans blue staining. Necrosis was assessed with triphenyltetrazolium chloride (TTC) staining and a transmission electron microscope (TEM). Results The infarct size of the left ventricle (% IAR) on TTC staining was smaller in IR30 (49.2 ± 4.3) than in IR90 (73.4 ± 4.7, P < 0.05), which exhibited evidence of more severe irreversible injury than the IR30 heart on TEM. FASTSPECT images demonstrated hot spot accumulations of 99mTc-GLA in all hearts. The washout of 99mTc-GLA from the ischemic—reperfused area in IR90 was significantly slower than that in IR30. The ratio of the hot spot to normal myocardial activity was 4.1 ± 0.3 in IR30 and 7.1 ± 1.1 in IR90 (P < 0.05). The hot spot size (% IAR) (58.4 ± 2.7 in IR30 vs. 75.9 ± 2.7 in IR90, P < 0.05) related significantly to the infarct size. Conclusion The severity of myocardial injury induced by ischemia—reperfusion can be assessed by FASTSPECT imaging with 99mTc-GLA. The results suggest that 99mTc-GLA will be clinically useful in detecting and quantifying acute necrotic myocardium. The FASTSPECT imaging with the rat heart models provides

  4. Determinants and impact of microvascular obstruction in successfully reperfused ST-segment elevation myocardial infarction. Assessment by magnetic resonance imaging

    Energy Technology Data Exchange (ETDEWEB)

    Bogaert, Jan; Kalantzi, Maria; Dymarkowski, Steven [Gasthuisberg University Hospital, Department of Radiology, Leuven (Belgium); Rademakers, Frank E.; Janssens, Stefan [Gasthuisberg University Hospital, Department of Cardiology, Leuven (Belgium)

    2007-10-15

    Microvascular obstruction (MVO) is an important and independent determinant of post-infarct remodeling. Fifty-two patients with a successfully reperfused ST-segment elevation acute myocardial infarction (MI) were studied with MRI in the first week and at 4 months post-infarction. On early (i.e., 2-5 min) post-contrast MRI, MVO was detected in 32 patients with an MVO to infarct ratio of 36.3 {+-} 24.9%. On late (i.e., 10-25 min) post-contrast MRI, MVO was detected in only 27 patients, with an MVO to infarct ratio of 15.9 {+-} 13.9%. MVO infarcts (n = 32) were associated with higher cardiac enzymes (troponin I, P = 0.016), and lower pre-revascularization thrombolysis in myocardial infarction (TIMI) flow (P = 0.018) than non-MVO infarcts (n = 20). Infarct size was larger in MVO infarcts (25.0 {+-} 14.3 g) than non-MVO infarcts (12.5 {+-} 7.9 g), P = 0.0007. Systolic wall thickening in the infarct and peri-infarct area, and left ventricular (LV) ejection fraction (EF) were worse in MVO (46.1 {+-} 7.2%) than non-MVO infarcts (50.5 {+-} 6.6%, P = 0.038). At 4 months, MVO infarcts showed more adverse remodeling and lack of functional improvement, whereas non-MVO infarcts improved significantly (LV EF at 4 months, MVO, 47.5 {+-} 7.8%, P = 0.31; non-MVO, 55.2 {+-} 10.3%, P = 0.0028). In the majority of patients with successfully reperfused ST-segment elevation MI, MVO is observed, whose present and maximal extent can be best evaluated on early post-contrast MRI. Presence of MVO is associated with more extensive infarctions, and characterized by greater adverse LV remodeling and lack of functional recovery. (orig.)

  5. Suv39h1 Protects from Myocardial Ischemia-Reperfusion Injury in Diabetic Rats

    Directory of Open Access Journals (Sweden)

    Bo Yang

    2014-04-01

    Full Text Available Background: Patients with diabetes are at increased risk of ischemic events. Suv39h1 is a histone methyltransferase that catalyzes the methylation of histone 3 lysine 9, which is associated with the suppression of inflammatory genes in diabetes. However, the role of Suv39h1 in myocardial ischemia/reperfusion (I/R injury under diabetic condition has not been evaluated. Methods: To generate diabetic model, male SD rats were fed with 60% fat diet followed by intraperitoneal injection with 40mg/kg streptozotocin. Adenovirus encoding Suv39h1 gene was used for Suv39h1 overexpression. Each rat received injections of adenovirus at five myocardial sites. Three days after gene transfection, each rat was subjected to left main coronary artery occlusion and reperfusion. After 30 min ischemia and reperfusion for 4 h, the rats were euthanized for real-time PCR, Western blot, immunohistochemical staining, and morphometric analysis. Results: Delivery of Ad-Suv39h1 into the hearts of diabetic rats could markedly increase Suv39h1 expression. Up-regulation of Suv39h1 significantly reduced infarct size and tissue damage after I/R injury, which was associated with protection from apoptosis of cardiac myocytes and reduction of inflammatory response. In addition, compared with injury group, Ad-Suv39h1 led to a decreased activity of mitogen-activated protein kinase family and its down-steam transcriptional factor NF-κB. Conclusion: Overexpression of Suv39h1 results in the de-activation of proinflammatory pathways and reduced apoptosis and myocardial injury. Therefore, Suv39h1 might represent a novel therapeutic strategy to reduce I/R injury under diabetic condition.

  6. Reperfusion of myocardial infarction in India: Notions for México.

    Science.gov (United States)

    Araiza-Garaygordobil, Diego; Arias-Mendoza, Alexandra; Martínez-Sánchez, Carlos; Martínez-Ríos, Marco Antonio; Ajit, Mullasari S

    2017-11-25

    In India and México, cardiovascular diseases are the first cause of death and potential years of life lost. Close similarities exist between these two countries when facing the difficulties to establish a universal reperfusion program for ST elevation myocardial infarction (STEMI). This paper describes the situation of STEMI treatment in both countries, and examines the lessons that Mexico's health care system could adopt from the recent advances accomplished by the STEMI initiative in India. Copyright © 2017 Instituto Nacional de Cardiología Ignacio Chávez. Publicado por Masson Doyma México S.A. All rights reserved.

  7. Effect of Curcuma longa and Ocimum sanctum on myocardial apoptosis in experimentally induced myocardial ischemic-reperfusion injury

    Science.gov (United States)

    Mohanty, Ipseeta; Arya, Dharamvir Singh; Gupta, Suresh Kumar

    2006-01-01

    Background In the present investigation, the effect of Curcuma longa (Cl) and Ocimum sanctum (Os) on myocardial apoptosis and cardiac function was studied in an ischemia and reperfusion (I-R) model of myocardial injury. Methods Wistar albino rats were divided into four groups and orally fed saline once daily (sham, control IR) or Cl (100 mg/kg; Cl-IR) or Os (75 mg/kg; Os-IR) respectively for 1 month. On the 31st day, in the rats of the control IR, Cl-IR and Os-IR groups LAD occlusion was undertaken for 45 min, and reperfusion was allowed for 1 h. The hemodynamic parameters{mean arterial pressure (MAP), heart rate (HR), left ventricular end-diastolic pressure (LVEDP), left ventricular peak positive (+) LVdP/dt (rate of pressure development) and negative (-) LVdP/dt (rate of pressure decline)} were monitored at pre-set points throughout the experimental duration and subsequently, the animals were sacrificed for immunohistopathological (Bax, Bcl-2 protein expression & TUNEL positivity) and histopathological studies. Results Chronic treatment with Cl significantly reduced TUNEL positivity (p < 0.05), Bax protein (p < 0.001) and upregulated Bcl-2 (p < 0.001) expression in comparison to control IR group. In addition, Cl demonstrated mitigating effects on several myocardial injury induced hemodynamic {(+)LVdP/dt, (-) LVdP/dt & LVEDP} and histopathological perturbations. Chronic Os treatment resulted in modest modulation of the hemodynamic alterations (MAP, LVEDP) but failed to demonstrate any significant antiapoptotic effects and prevent the histopathological alterations as compared to control IR group. Conclusion In the present study, significant cardioprotection and functional recovery demonstrated by Cl may be attributed to its anti-apoptotic property. In contrast to Os, Cl may attenuate cell death due to apoptosis and prevent the impairment of cardiac performance. PMID:16504000

  8. Blood PGC-1α Concentration Predicts Myocardial Salvage and Ventricular Remodeling After ST-segment Elevation Acute Myocardial Infarction.

    Science.gov (United States)

    Fabregat-Andrés, Óscar; Ridocci-Soriano, Francisco; Estornell-Erill, Jordi; Corbí-Pascual, Miguel; Valle-Muñoz, Alfonso; Berenguer-Jofresa, Alberto; Barrabés, José A; Mata, Manuel; Monsalve, María

    2015-05-01

    Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is a metabolic regulator induced during ischemia that prevents cardiac remodeling in animal models. The activity of PGC-1α can be estimated in patients with ST-segment elevation acute myocardial infarction. The aim of the present study was to evaluate the value of blood PGC-1α levels in predicting the extent of necrosis and ventricular remodeling after infarction. In this prospective study of 31 patients with a first myocardial infarction in an anterior location and successful reperfusion, PGC-1α expression in peripheral blood on admission and at 72 hours was correlated with myocardial injury, ventricular volume, and systolic function at 6 months. Edema and myocardial necrosis were estimated using cardiac magnetic resonance imaging during the first week. At 6 months, infarct size and ventricular remodeling, defined as an increase > 10% of the left ventricular end-diastolic volume, was evaluated by follow-up magnetic resonance imaging. Myocardial salvage was defined as the difference between the edema and necrosis areas. Greater myocardial salvage was seen in patients with detectable PGC-1α levels at admission (mean [standard deviation (SD)], 18.3% [5.3%] vs 4.5% [3.9%]; P = .04). Induction of PGC-1α at 72 hours correlated with greater ventricular remodeling (change in left ventricular end-diastolic volume at 6 months, 29.7% [11.2%] vs 1.2% [5.8%]; P = .04). Baseline PGC-1α expression and an attenuated systemic response after acute myocardial infarction are associated with greater myocardial salvage and predict less ventricular remodeling. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  9. Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow: therapeutic potential of DNase-based reperfusion strategy.

    Science.gov (United States)

    Ge, Lan; Zhou, Xin; Ji, Wen-Jie; Lu, Rui-Yi; Zhang, Yan; Zhang, Yi-Dan; Ma, Yong-Qiang; Zhao, Ji-Hong; Li, Yu-Ming

    2015-03-01

    Emerging evidence suggests a potential role of neutrophil extracellular traps (NETs) in linking sterile inflammation and thrombosis. We hypothesized that NETs would be induced during myocardial ischemia-reperfusion (I/R), and NET-mediated microthrombosis may contribute to myocardial "no-reflow". Male Wistar rats were randomly divided into I/R control, DNase (DNase I, 20 μg/rat), recombinant tissue-type plasminogen activator (rt-PA, 420 μg/rat), DNase + rt-PA, and sham control groups after 45-min myocardial ischemia. In situ NET formation, the anatomic "no re-flow" area, and infarct size were evaluated immediately after 3 h of reperfusion. Long-term left ventricular (LV) functional and histological analyses were performed 45 days after operation. Compared with the I/R controls, the DNase + rt-PA group exhibited reduced NET density [8.38 ± 1.98 vs. 26.86 ± 3.07 (per 200 × field), P injury-induced LV remodeling (LV ejection fraction: 64.22 ± 3.37 vs. 33.81 ± 2.98%, P reperfusion strategy (DNase I + rt-PA), which might be a promising option for the treatment of myocardial I/R injury and coronary no-reflow. Copyright © 2015 the American Physiological Society.

  10. Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux.

    Science.gov (United States)

    Ling, Yuanna; Chen, Guiming; Deng, Yi; Tang, Huixiong; Ling, Long; Zhou, Xiaoming; Song, Xudong; Yang, Pingzhen; Liu, Yingfeng; Li, Zhiliang; Zhao, Cong; Yang, Yufei; Wang, Xianbao; Kitakaze, Masafumi; Liao, Yulin; Chen, Aihua

    2016-09-01

    Polydatin (PD), a resveratrol (RES) glycoside, has a stronger antioxidative effect than RES. It is known that RES is an autophagic enhancer and exerts a cardioprotective effect against ischaemia/reperfusion (I/R) injury. However, the effect of PD post-treatment on myocardial I/R injury remains unclear. In the present study, we investigated the influences of PD post-treatment on myocardial I/R injury and autophagy. C57BL/6 mice underwent left coronary artery (LCA) occlusion and cultured neonatal rat cardiomyocytes (NRCs) subjected to hypoxia were treated with vehicle or PD during reperfusion or re-oxygenation. We noted that PD enhanced autophagy and decreased apoptosis during I/R or hypoxia/reoxygenation (H/R), and this effect was antagonized by co-treatment with adenovirus carrying short hairpin RNA for Beclin 1 and 3-methyladenine (3-MA), an autophagic inhibitor. Compared with vehicle-treated mice, PD-treated mice had a significantly smaller myocardial infarct size (IS) and a higher left ventricular fractional shortening (LVFS) and ejection fraction (EF), whereas these effects were partly reversed by 3-MA. Furthermore, in the PD-treated NRCs, tandem fluorescent mRFP-GFP-LC3 assay showed abundant clearance of autophagosomes with an enhanced autophagic flux, and co-treatment with Bafilomycin A1 (Baf), a lysosomal inhibitor, indicated that PD promoted the degradation of autolysosome. In addition, PD post-treatment reduced mitochondrial membrane potential and cellular reactive oxygen species (ROS) production in NRCs, and these effects were partially blocked by Baf. These findings indicate that PD post-treatment limits myocardial I/R injury by promoting autophagic flux to clear damaged mitochondria to reduce ROS and cell death. © 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.

  11. Thrombolytic therapy of acute myocardial infarction alters collagen metabolism

    DEFF Research Database (Denmark)

    Høst, N B; Hansen, S S; Jensen, L T

    1994-01-01

    infarction and receiving thrombolytic therapy. Regardless of whether acute myocardial infarction was confirmed or not, S-PIIINP increased (94-120%) 4 h after streptokinase therapy (p ....02). With confirmed acute myocardial infarction, S-PIIINP increased from 24 h towards a plateau reached at day 2-3 (p acute myocardial infarction had S-PICP above baseline at 1, 2, and 6 months (p ....05). A less pronounced S-PIIINP increase was noted with tissue-plasminogen activator than with streptokinase. Thrombolytic therapy induces collagen breakdown regardless of whether acute myocardial infarction is confirmed or not. With confirmed acute myocardial infarction collagen metabolism is altered...

  12. Gender specific effect of progesterone on myocardial ischemia/reperfusion injury in rats.

    Science.gov (United States)

    Dhote, Vipin V; Balaraman, R

    2007-06-27

    The study was designed to investigate the effect of progesterone and its gender based variation on myocardial ischemia/reperfusion (I/R) injury in rats. Adult Sprague Dawley rats were divided into vehicle treated reperfusion injury group male (I/R-M), female (I/R-F), ovariectomised (I/R-OVR) and progesterone treatment (I/R-M+PG, I/R-F+PG, I/R-OVR+PG) groups, respectively. I/R injury was produced by occluding the left descending coronary artery (LCA) for 1 h and followed by re-opening for 1 h. Progesterone (2 mg kg(-1) i.p.) was administered 30 min after induction of ischemia. Hemodynamic parameters (+/-dp/dt, MAP), heart rate, ST-segment elevation and occurrence of ventricular tachycardia (VT) were measured during the I/R period. The myocardial infarct area, oxidative stress markers, activities of myeloperoxidase (MPO) and creatine kinase (CK) were determined after the experiment along with the assessment of the effect on apoptotic activity by using DNA fragmentation analysis. Histological observations were carried out on heart tissue. Treatment with progesterone significantly (Pinjury induced damage is based on gender of the animal. The protective effect could be mediated by attenuation of inflammation and its possible interaction with endogenous estrogen.

  13. Effects of Phikud Navakot Extract on Myocardial Ischemia/Reperfusion Injury in Rats.

    Science.gov (United States)

    Kengkoom, Kanchana; Sirimontaporn, Aunchalee; Sotanaphun, Uthai; Gerdprasert, Orapin; Nusuetrong, Punnee

    2015-10-01

    Phikud Navakot (PN) is a set of nine medicinal plants and the main ingredient of "Yahom Navakot", a traditional Thai herbal formula for treatment of cardiovascular symptoms. To investigate the cardioprotective effects of PN on myocardial ischemia/reperfusion (IR) in male Sprague Dawley rats. Rats were randomly divided into 7 groups: sham, IR, and IR orally pretreated with PN (10, 50, 100, 200, and 400 mg/kg B W)for 7 days. After treatment, IR induction was performed by left coronary artery (LCA) ligation for 30 min, followed by reperfusion for 24 h. At the end of the experiment, blood was collected for hematological and biochemical parameters, and hearts were immediately removed for histopathological examination and Western blot analysis. IR induction caused ST elevation in the electrocardiogram and an increase in serum troponin I (TnI), confirming myocardial damage. In addition, histopathological changes of ischemic myocardium showed inflammation, infiltration, and edema. Oral administration of PN (10, 50, 100, 200, and 400 mg/kg BW) for 7 days prior to IR simulation showed no change on serum TnI and histopathology ofcardiac tissues, when compared to IR group. However Western blot analysis showed that IR rats pretreated with PN (10 mg/kg BW) significantly increased (p injury induced by LCA ligation. Investigation at molecular level found however that PN up-regulated the expression of protective proteins pERK/ERK ratio and HO-1 in cardiac tissues, suggesting molecular mechanism of PN in cardioprotection against IR injury.

  14. High-resolution imaging with (99m)Tc-glucarate for assessing myocardial injury in rat heart models exposed to different durations of ischemia with reperfusion.

    Science.gov (United States)

    Liu, Zhonglin; Barrett, Harrison H; Stevenson, Gail D; Kastis, George A; Bettan, Michael; Furenlid, Lars R; Wilson, Donald W; Pak, Koon Yan

    2004-07-01

    (99m)Tc-Glucarate ((99m)Tc-GLA) is a novel infarct-avid imaging agent. The aim of this study was to evaluate the role of (99m)Tc-GLA for assessing the severity of myocardial ischemia-reperfusion injury in rat heart models exposed to varied durations of left coronary artery (LCA) occlusion with reperfusion using a high-resolution SPECT system, FASTSPECT. We also wanted to clarify whether a rapid sequence of 3-dimensional imaging with FASTSPECT can quantify uptake and washout kinetics of cardiovascular imaging agents in small-animal heart models. The ischemic-reperfused rat heart models were created by ligating the LCA for 30 min (IR30, n = 12) or 90 min (IR90, n = 6) (IR = ischemia-reperfusion) and releasing the ligature for 30 min. Dynamic images were acquired over a 2-h period after (99m)Tc-GLA was intravenously injected. The ischemic area at risk (IAR) was determined by Evans blue staining. Necrosis was assessed with triphenyltetrazolium chloride (TTC) staining and a transmission electron microscope (TEM). The infarct size of the left ventricle (% IAR) on TTC staining was smaller in IR30 (49.2 +/- 4.3) than in IR90 (73.4 +/- 4.7, P injury than the IR30 heart on TEM. FASTSPECT images demonstrated hot spot accumulations of (99m)Tc-GLA in all hearts. The washout of (99m)Tc-GLA from the ischemic-reperfused area in IR90 was significantly slower than that in IR30. The ratio of the hot spot to normal myocardial activity was 4.1 +/- 0.3 in IR30 and 7.1 +/- 1.1 in IR90 (P injury induced by ischemia-reperfusion can be assessed by FASTSPECT imaging with (99m)Tc-GLA. The results suggest that (99m)Tc-GLA will be clinically useful in detecting and quantifying acute necrotic myocardium. The FASTSPECT imaging with the rat heart models provides a solution-specific approach with high-resolution and fast dynamic acquisition for kinetic studies of new myocardial imaging agents.

  15. Melatonin ameliorates myocardial ischemia reperfusion injury through SIRT3-dependent regulation of oxidative stress and apoptosis.

    Science.gov (United States)

    Zhai, Mengen; Li, Buying; Duan, Weixun; Jing, Lin; Zhang, Bin; Zhang, Meng; Yu, Liming; Liu, Zhenhua; Yu, Bo; Ren, Kai; Gao, Erhe; Yang, Yang; Liang, Hongliang; Jin, Zhenxiao; Yu, Shiqiang

    2017-09-01

    Sirtuins are a family of highly evolutionarily conserved nicotinamide adenine nucleotide-dependent histone deacetylases. Sirtuin-3 (SIRT3) is a member of the sirtuin family that is localized primarily to the mitochondria and protects against oxidative stress-related diseases, including myocardial ischemia/reperfusion (MI/R) injury. Melatonin has a favorable effect in ameliorating MI/R injury. We hypothesized that melatonin protects against MI/R injury by activating the SIRT3 signaling pathway. In this study, mice were pretreated with or without a selective SIRT3 inhibitor and then subjected to MI/R operation. Melatonin was administered intraperitoneally (20 mg/kg) 10 minutes before reperfusion. Melatonin treatment improved postischemic cardiac contractile function, decreased infarct size, diminished lactate dehydrogenase release, reduced the apoptotic index, and ameliorated oxidative damage. Notably, MI/R induced a significant decrease in myocardial SIRT3 expression and activity, whereas the melatonin treatment upregulated SIRT3 expression and activity, and thus decreased the acetylation of superoxide dismutase 2 (SOD2). In addition, melatonin increased Bcl-2 expression and decreased Bax, Caspase-3, and cleaved Caspase-3 levels in response to MI/R. However, the cardioprotective effects of melatonin were largely abolished by the selective SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl)pyridine (3-TYP), suggesting that SIRT3 plays an essential role in mediating the cardioprotective effects of melatonin. In vitro studies confirmed that melatonin also protected H9c2 cells against simulated ischemia/reperfusion injury (SIR) by attenuating oxidative stress and apoptosis, while SIRT3-targeted siRNA diminished these effects. Taken together, our results demonstrate for the first time that melatonin treatment ameliorates MI/R injury by reducing oxidative stress and apoptosis via activating the SIRT3 signaling pathway. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons

  16. Comparison of blood biochemics between acute myocardial infarction models with blood stasis and simple acute myocardial infarction models in rats

    International Nuclear Information System (INIS)

    Qu Shaochun; Yu Xiaofeng; Wang Jia; Zhou Jinying; Xie Haolin; Sui Dayun

    2010-01-01

    Objective: To construct the acute myocardial infarction models in rats with blood stasis and study the difference on blood biochemics between the acute myocardial infarction models with blood stasis and the simple acute myocardial infarction models. Methods: Wistar rats were randomly divided into control group, acute blood stasis model group, acute myocardial infarction sham operation group, acute myocardial infarction model group and of acute myocardial infarction model with blood stasis group. The acute myocardial infarction models under the status of the acute blood stasis in rats were set up. The serum malondialdehyde (MDA), nitric oxide (NO), free fatty acid (FFA), tumor necrosis factor-α (TNF-α) levels were detected, the activities of serum superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of prostacycline (PGI2), thromboxane A 2 (TXA 2 ) and endothelin (ET) in plasma were determined. Results: There were not obvious differences in MDA, SOD, GSH-Px and FFA between the acute myocardial infarction models with blood stasis in rats and the simple acute myocardial infarction models (P 2 and NO, and the increase extents of TXA 2 , ET and TNF-α in the acute myocardial infarction models in rats with blood stasis were higher than those in the simple acute myocardial infarction models (P 2 and NO, are significant when the acute myocardial infarction models in rats with blood stasis and the simple acute myocardial infarction models are compared. The results show that it is defective to evaluate pharmacodynamics of traditional Chinese drug with only simple acute myocardial infarction models. (authors)

  17. Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms.

    Science.gov (United States)

    Shi, Zhenwei; Fu, Feng; Yu, Liming; Xing, Wenjuan; Su, Feifei; Liang, Xiangyan; Tie, Ru; Ji, Lele; Zhu, Miaozhang; Yu, Jun; Zhang, Haifeng

    2015-02-15

    Diabetes mellitus increases morbidity/mortality of ischemic heart disease. Although atrial natriuretic peptide and C-type natriuretic peptide reduce the myocardial ischemia-reperfusion damage in nondiabetic rats, whether vasonatrin peptide (VNP), the artificial synthetic chimera of atrial natriuretic peptide and C-type natriuretic peptide, confers cardioprotective effects against ischemia-reperfusion injury, especially in diabetic patients, is still unclear. This study was designed to investigate the effects of VNP on ischemia-reperfusion injury in diabetic rats and to further elucidate its mechanisms. The high-fat diet-fed streptozotocin-induced diabetic Sprague-Dawley rats were subjected to ischemia-reperfusion operation. VNP treatment (100 μg/kg iv, 10 min before reperfusion) significantly improved the instantaneous first derivation of left ventricle pressure (±LV dP/dtmax) and LV systolic pressure and reduced LV end-diastolic pressure, apoptosis index, caspase-3 activity, plasma creatine kinase (CK), and lactate dehydrogenase (LDH) activities. Moreover, VNP inhibited endoplasmic reticulum (ER) stress by suppressing glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP). These effects were mimicked by 8-bromine-cyclic guanosinemonophosphate (8-Br-cGMP), a cGMP analog, whereas they were inhibited by KT-5823, the selective inhibitor of PKG. In addition, pretreatment with tauroursodeoxycholic acid (TUDCA), a specific inhibitor of ER stress, could not further promote the VNP's cardioprotective effect in diabetic rats. In vitro H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation and incubated with or without VNP (10(-8) mol/l). Gene knockdown of PKG1α with siRNA blunted VNP inhibition of ER stress and apoptosis, while overexpression of PKG1α resulted in significant decreased ER stress and apoptosis. VNP protects the diabetic heart against ischemia-reperfusion injury by inhibiting ER stress via the cGMP-PKG signaling pathway. These

  18. Kaempferol Attenuates Myocardial Ischemic Injury via Inhibition of MAPK Signaling Pathway in Experimental Model of Myocardial Ischemia-Reperfusion Injury

    Science.gov (United States)

    Suchal, Kapil; Malik, Salma; Gamad, Nanda; Malhotra, Rajiv Kumar; Goyal, Sameer N.; Chaudhary, Uma; Bhatia, Jagriti; Ojha, Shreesh; Arya, Dharamvir Singh

    2016-01-01

    Kaempferol (KMP), a dietary flavonoid, has antioxidant, anti-inflammatory, and antiapoptotic effects. Hence, we investigated the effect of KMP in ischemia-reperfusion (IR) model of myocardial injury in rats. We studied male albino Wistar rats that were divided into sham, IR-control, KMP-20 + IR, and KMP 20 per se groups. KMP (20 mg/kg; i.p.) was administered daily to rats for the period of 15 days, and, on the 15th day, ischemia was produced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. After completion of surgery, rats were sacrificed; heart was removed and processed for biochemical, morphological, and molecular studies. KMP pretreatment significantly ameliorated IR injury by maintaining cardiac function, normalizing oxidative stress, and preserving morphological alterations. Furthermore, there was a decrease in the level of inflammatory markers (TNF-α, IL-6, and NFκB), inhibition of active JNK and p38 proteins, and activation of ERK1/ERK2, a prosurvival kinase. Additionally, it also attenuated apoptosis by reducing the expression of proapoptotic proteins (Bax and Caspase-3), TUNEL positive cells, and increased level of antiapoptotic proteins (Bcl-2). In conclusion, KMP protected against IR injury by attenuating inflammation and apoptosis through the modulation of MAPK pathway. PMID:27087891

  19. Kaempferol Attenuates Myocardial Ischemic Injury via Inhibition of MAPK Signaling Pathway in Experimental Model of Myocardial Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Kapil Suchal

    2016-01-01

    Full Text Available Kaempferol (KMP, a dietary flavonoid, has antioxidant, anti-inflammatory, and antiapoptotic effects. Hence, we investigated the effect of KMP in ischemia-reperfusion (IR model of myocardial injury in rats. We studied male albino Wistar rats that were divided into sham, IR-control, KMP-20 + IR, and KMP 20 per se groups. KMP (20 mg/kg; i.p. was administered daily to rats for the period of 15 days, and, on the 15th day, ischemia was produced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. After completion of surgery, rats were sacrificed; heart was removed and processed for biochemical, morphological, and molecular studies. KMP pretreatment significantly ameliorated IR injury by maintaining cardiac function, normalizing oxidative stress, and preserving morphological alterations. Furthermore, there was a decrease in the level of inflammatory markers (TNF-α, IL-6, and NFκB, inhibition of active JNK and p38 proteins, and activation of ERK1/ERK2, a prosurvival kinase. Additionally, it also attenuated apoptosis by reducing the expression of proapoptotic proteins (Bax and Caspase-3, TUNEL positive cells, and increased level of antiapoptotic proteins (Bcl-2. In conclusion, KMP protected against IR injury by attenuating inflammation and apoptosis through the modulation of MAPK pathway.

  20. Clinical value of delayed thallium-201 myocardial imaging in suspected acute myocardial infarction.

    Science.gov (United States)

    McKillop, J H; Turner, J G; Gray, H W; Bessent, R G; Greig, W R

    1978-01-01

    Fifty patients with acute chest pain had thallium-201 myocardial imaging performed three to six days after emergency admission to hospital. The image was abnormal in 20 out of 22 patients with acute transmural myocardial infarcts but in only 1 of 5 with acute subendocardial infarcts. Indistinguishable scan abnormalities caused by old infarcts were seen in 7 patients, and caused by myocardial ischaemia in 1 patient. A single thallium-201 myocardial scan some days after the onset of symptoms appears to be of little value in the clinical assessment of patients with suspected acute myocardial infarction. Images PMID:687488

  1. Acute myocardial infarction as a result of stress

    OpenAIRE

    Bakusová, Tereza

    2007-01-01

    This thesis aims to describe acute myocardial infarction as a psychosomatic disease. Represents acute myocardial infarction as a result of stress and type A behavior. Research part reveals number of respondents, affected by stresss at the time of myocardial infarction and respondents with type A behavior.

  2. Confronting the issues of patient safety and investigator conflict of interest in an international clinical trial of myocardial reperfusion

    NARCIS (Netherlands)

    E.J. Topol (Eric); N.S. Kleiman (Neal); K.L. Lee (Kerry); D. Morris; M.L. Simoons (Maarten); H.D. White (Harvey); R.M. Califf (Robert); F.J.J. van de Werf (Frans); P.W. Armstrong (Paul); G.I. Barbash

    1992-01-01

    textabstractThe Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) trial is a large scale international trial of new myocardial reperfusion strategies. The primary hypothesis is that early and sustained coronary artery recanalization will be

  3. Primary Percutaneous Coronary Intervention as a National Reperfusion Strategy in Patients With ST-Segment Elevation Myocardial Infarction

    DEFF Research Database (Denmark)

    Terkelsen, Christian Juhl; Jensen, Lisette O; Hansen, Hans-Henrik Tilsted

    2011-01-01

    In Denmark, primary percutaneous coronary intervention (PPCI) was chosen as a national reperfusion strategy for patients with ST-segment elevation myocardial infarction in 2003. This study describes the temporal implementation of PPCI in Western Denmark, the gradual introduction of field triage...

  4. Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart

    NARCIS (Netherlands)

    Schlack, W.; Preckel, B.; Stunneck, D.; Thämer, V.

    1998-01-01

    A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation

  5. Soluble epoxide hydrolase inhibition and gene deletion are protective against myocardial ischemia-reperfusion injury in vivo.

    Science.gov (United States)

    Motoki, Atsuko; Merkel, Matthias J; Packwood, William H; Cao, Zhiping; Liu, Lijuan; Iliff, Jeffrey; Alkayed, Nabil J; Van Winkle, Donna M

    2008-11-01

    Soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids. EETs are formed from arachidonic acid during myocardial ischemia and play a protective role against ischemic cell death. Deletion of sEH has been shown to be protective against myocardial ischemia in the isolated heart preparation. We tested the hypothesis that sEH inactivation by targeted gene deletion or pharmacological inhibition reduces infarct size (I) after regional myocardial ischemia-reperfusion injury in vivo. Male C57BL\\6J wild-type or sEH knockout mice were subjected to 40 min of left coronary artery (LCA) occlusion and 2 h of reperfusion. Wild-type mice were injected intraperitoneally with 12-(3-adamantan-1-yl-ureido)-dodecanoic acid butyl ester (AUDA-BE), a sEH inhibitor, 30 min before LCA occlusion or during ischemia 10 min before reperfusion. 14,15-EET, the main substrate for sEH, was administered intravenously 15 min before LCA occlusion or during ischemia 5 min before reperfusion. The EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE) was given intravenously 15 min before reperfusion. Area at risk (AAR) and I were assessed using fluorescent microspheres and triphenyltetrazolium chloride, and I was expressed as I/AAR. I was significantly reduced in animals treated with AUDA-BE or 14,15-EET, independent of the time of administration. The cardioprotective effect of AUDA-BE was abolished by the EET antagonist 14,15-EEZE. Immunohistochemistry revealed abundant sEH protein expression in left ventricular tissue. Strategies to increase 14,15-EET, including sEH inactivation, may represent a novel therapeutic approach for cardioprotection against myocardial ischemia-reperfusion injury.

  6. Inhibition of Fas-associated death domain-containing protein (FADD protects against myocardial ischemia/reperfusion injury in a heart failure mouse model.

    Directory of Open Access Journals (Sweden)

    Qian Fan

    Full Text Available As technological interventions treating acute myocardial infarction (MI improve, post-ischemic heart failure increasingly threatens patient health. The aim of the current study was to test whether FADD could be a potential target of gene therapy in the treatment of heart failure.Cardiomyocyte-specific FADD knockout mice along with non-transgenic littermates (NLC were subjected to 30 minutes myocardial ischemia followed by 7 days of reperfusion or 6 weeks of permanent myocardial ischemia via the ligation of left main descending coronary artery. Cardiac function were evaluated by echocardiography and left ventricular (LV catheterization and cardiomyocyte death was measured by Evans blue-TTC staining, TUNEL staining, and caspase-3, -8, and -9 activities. In vitro, H9C2 cells transfected with ether scramble siRNA or FADD siRNA were stressed with chelerythrin for 30 min and cleaved caspase-3 was assessed.FADD expression was significantly decreased in FADD knockout mice compared to NLC. Ischemia/reperfusion (I/R upregulated FADD expression in NLC mice, but not in FADD knockout mice at the early time. FADD deletion significantly attenuated I/R-induced cardiac dysfunction, decreased myocardial necrosis, and inhibited cardiomyocyte apoptosis. Furthermore, in 6 weeks long term permanent ischemia model, FADD deletion significantly reduced the infarct size (from 41.20 ± 3.90% in NLC to 26.83 ± 4.17% in FADD deletion, attenuated myocardial remodeling, improved cardiac function and improved survival. In vitro, FADD knockdown significantly reduced chelerythrin-induced the level of cleaved caspase-3.Taken together, our results suggest FADD plays a critical role in post-ischemic heart failure. Inhibition of FADD retards heart failure progression. Our data supports the further investigation of FADD as a potential target for genetic manipulation in the treatment of heart failure.

  7. Cardiovascular magnetic resonance imaging of myocardial oedema following acute myocardial infarction

    DEFF Research Database (Denmark)

    Hamshere, Stephen; Jones, A Daniel; Pellaton, Cyril

    2016-01-01

    Background: AAR measurement is useful when assessing the efficacy of reperfusion therapy and novel cardioprotective agents after myocardial infarction. Multi-slice (Typically 10-12) T2-STIR has been used widely for its measurement, typically with a short axis stack (SAX) covering the entire left ...

  8. Acute myocardial infarction after mediastinal radiotherapy

    International Nuclear Information System (INIS)

    Gagliardi, Juan; Tezanos Pinto, Miguel; Avalos, Adolfo; Sarubbi, Augusto; Padilla, Lucio; Espinosa, Daniel

    2004-01-01

    Mediastinal radiotherapy can affect the heart and great vessels to different degrees. It may turn up as coronary heart disease and less frequently as acute myocardial infarction. We report the case of a patient without coronary risk factors and an antecedent of mediastinal radiotherapy for Hodgkin's lymphoma. Considerations about mediastinal radiation as a risk factor for early development of coronary heart diseases are exposed. (author) [es

  9. TGF-beta 1 attenuates myocardial ischemia-reperfusion injury via inhibition of upregulation of MMP-1.

    Science.gov (United States)

    Chen, Hongjiang; Li, Dayuan; Saldeen, Tom; Mehta, Jawahar L

    2003-05-01

    Ischemia-reperfusion (I/R) is thought to upregulate the expression and activity of matrix metalloproteinases (MMPs), which regulate myocardial and vascular remodeling. Previous studies have shown that transforming growth factor-beta(1) (TGF-beta(1)) can attenuate myocardial injury induced by I/R. TGF-beta(1) is also reported to suppress the release of MMPs. To study the modulation of MMP-1 by TGF-beta(1) in I/R myocardium, Sprague-Dawley rats were given saline and subjected to 1 h of myocardial ischemia [total left coronary artery (LCA) ligation] followed by 1 h of reperfusion (n = 9). Parallel groups of rats were pretreated with recombinant TGF-beta(1) (rTGF-beta(1), 1 mg/rat, n = 9) before reperfusion or exposure to sham I/R (control group). I/R caused myocardial necrosis and dysfunction, indicated by decreased first derivative of left ventricular pressure, mean arterial blood pressure, and heart rate (all P injury and death of cultured myocytes, measured as lactate dehydrogenase release and trypan blue staining, in a dose- and time-dependent manner (P injury and death induced by active MMP-1. The present study for the first time shows that MMP-1 can directly cause myocyte injury or death and that attenuation of myocardial I/R injury by TGF-beta(1) may, at least partly, be mediated by the inhibition of upregulation of MMP-1.

  10. Gaseous hydrogen sulfide protects against myocardial ischemia-reperfusion injury in mice partially independent from hypometabolism.

    Directory of Open Access Journals (Sweden)

    Pauline M Snijder

    Full Text Available BACKGROUND: Ischemia-reperfusion injury (IRI is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H2S is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant properties. We investigated whether gaseous H2S administration is protective in cardiac IRI and whether non-hypometabolic concentrations of H2S have similar protective properties. METHODS: Male C57BL/6 mice received a 0, 10, or 100 ppm H2S-N2 mixture starting 30 minutes prior to ischemia until 5 minutes pre-reperfusion. IRI was inflicted by temporary ligation of the left coronary artery for 30 minutes. High-resolution respirometry equipment was used to assess CO2-production and blood pressure was measured using internal transmitters. The effects of H2S were assessed by histological and molecular analysis. RESULTS: Treatment with 100 ppm H2S decreased CO2-production by 72%, blood pressure by 14% and heart rate by 25%, while treatment with 10 ppm H2S had no effects. At day 1 of reperfusion 10 ppm H2S showed no effect on necrosis, while treatment with 100 ppm H2S reduced necrosis by 62% (p<0.05. Seven days post-reperfusion, both 10 ppm (p<0.01 and 100 ppm (p<0.05 H2S showed a reduction in fibrosis compared to IRI animals. Both 10 ppm and 100 ppm H2S reduced granulocyte-influx by 43% (p<0.05 and 60% (p<0.001, respectively. At 7 days post-reperfusion both 10 and 100 ppm H2S reduced expression of fibronectin by 63% (p<0.05 and 67% (p<0.01 and ANP by 84% and 63% (p<0.05, respectively. CONCLUSIONS: Gaseous administration of H2S is protective when administered during a cardiac ischemic insult. Although hypometabolism is restricted to small animals, we now showed that low non-hypometabolic concentrations of H2S also have protective properties in IRI. Since IRI is a frequent cause of myocardial damage during percutaneous coronary intervention and cardiac

  11. Total flavonoid extract from Coreopsis tinctoria Nutt. protects rats against myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Zhang, Ya; Yuan, Changsheng; Fang, He; Li, Jia; Su, Shanshan; Chen, Wen

    2016-09-01

    This study aimed to evaluate the protective effects of total flavonoid extract from Coreopsis tinctoria Nutt. (CTF) against myocardial ischemia/reperfusion injury (MIRI) using an isolated Langendorff rat heart model. Left ventricular developed pressure (LVDP) and the maximum rate of rise and fall of LV pressure (±dp/dtmax) were recorded. Cardiac injury was assessed by analyzing lactate dehydrogenase (LDH) and creatine kinase (CK) released in the coronary effluent. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels were determined. Myocardial inflammation was assessed by monitoring tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), interleukin-8 (IL-8), and interleukin-6 (IL-6) levels. Myocardial infarct size was estimated. Cell morphology was assessed by 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin (HE) staining. Cardiomyocyte apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Pretreatment with CTF significantly increased the heart rate and increased LVDP, as well as SOD and GSH-Px levels. In addition, CTF pretreatment decreased the TUNEL-positive cell ratio, infarct size, and levels of CK, LDH, MDA, TNF-α, CRP, IL-6, and IL-8. These results suggest that CTF exerts cardio-protective effects against MIRI via anti-oxidant, anti-inflammatory, and anti-apoptotic activities.

  12. The role of glycogen synthase kinase 3 beta in brain injury induced by myocardial ischemia/reperfusion injury in a rat model of diabetes mellitus.

    Science.gov (United States)

    Zhao, Bo; Gao, Wen-Wei; Liu, Ya-Jing; Jiang, Meng; Liu, Lian; Yuan, Quan; Hou, Jia-Bao; Xia, Zhong-Yuan

    2017-10-01

    Myocardial ischemia/reperfusion injury can lead to severe brain injury. Glycogen synthase kinase 3 beta is known to be involved in myo-cardial ischemia/reperfusion injury and diabetes mellitus. However, the precise role of glycogen synthase kinase 3 beta in myocardial ischemia/reperfusion injury-induced brain injury is unclear. In this study, we observed the effects of glycogen synthase kinase 3 beta on brain injury induced by myocardial ischemia/reperfusion injury in diabetic rats. Rat models of diabetes mellitus were generated via intraperitoneal injection of streptozotocin. Models of myocardial ischemia/reperfusion injury were generated by occluding the anterior descending branch of the left coronary artery. Post-conditioning comprised three cycles of ischemia/reperfusion. Immunohistochemical staining and western blot assays demonstrated that after 48 hours of reperfusion, the structure of the brain was seriously damaged in the experimental rats compared with normal controls. Expression of Bax, interleukin-6, interleukin-8, terminal deoxynucleotidyl transferase dUTP nick end labeling, and cleaved caspase-3 in the brain was significantly increased, while expression of Bcl-2, interleukin-10, and phospho-glycogen synthase kinase 3 beta was decreased. Diabetes mellitus can aggravate inflammatory reactions and apoptosis. Ischemic post-conditioning with glycogen synthase kinase 3 beta inhibitor lithium chloride can effectively reverse these changes. Our results showed that myocardial ischemic post-conditioning attenuated myocardial ischemia/reperfusion injury-induced brain injury by activating glyco-gen synthase kinase 3 beta. According to these results, glycogen synthase kinase 3 beta appears to be an important factor in brain injury induced by myocardial ischemia/reperfusion injury.

  13. Cardiac progenitor-derived exosomes protect ischemic myocardium from acute ischemia/reperfusion injury

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Lijuan [Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Cardiovascular Disease, Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States); Wang, Yingjie [Cardiovascular Disease, Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States); Internal Medicine of Traditional Chinese Medicine, Shuguang Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 201203 (China); Pan, Yaohua; Zhang, Lan [Cardiovascular Disease, Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States); Shen, Chengxing [Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University, Shanghai (China); Qin, Gangjian [Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 (United States); Ashraf, Muhammad [Pathology and Lab Med, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States); Weintraub, Neal [Cardiovascular Disease, Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States); Ma, Genshan, E-mail: magenshan@hotmail.com [Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Tang, Yaoliang, E-mail: tangyg@ucmail.uc.edu [Cardiovascular Disease, Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267 (United States)

    2013-02-15

    Highlights: ► Cardiac progenitor-derived (CPC) Exosomes protect H9C2 from apoptosis in vitro. ► CPC-exosomes protect cardiomyoyctes from MI/R induced apoptosis in vivo. ► CPC-exosomes were taken up by H9C2 with high efficiency using PKH26 labeling. ► miR-451, one of GATA4-responsive miRNA cluster, is enriched in CPC-exosomes. -- Abstract: Background: Cardiac progenitors (CPC) mediate cardioprotection via paracrine effects. To date, most of studies focused on secreted paracrine proteins. Here we investigated the CPC-derived-exosomes on protecting myocardium from acute ischemia/reperfusion (MI/R) injury. Methods and results: CPC were isolated from mouse heart using two-step protocol. Exosomes were purified from conditional medium, and confirmed by electron micrograph and Western blot using CD63 as a marker. qRT-PCR shows that CPC-exosomes have high level expression of GATA4-responsive-miR-451. Exosomes were ex vivo labeled with PKH26, We observed exosomes can be uptaken by H9C2 cardiomyoblasts with high efficiency after 12 h incubation. CPC-exosomes protect H9C2 from oxidative stress by inhibiting caspase 3/7 activation invitro. In vivo delivery of CPC-exosomes in an acute mouse myocardial ischemia/reperfusion model inhibited cardiomyocyte apoptosis by about 53% in comparison with PBS control (p < 0.05). Conclusion: Our results suggest, for the first time, the CPC-exosomes can be used as a therapeutic vehicle for cardioprotection, and highlights a new perspective for using non-cell exosomes for cardiac disease.

  14. Acute perimyocarditis mimicking transmural myocardial infarction

    Directory of Open Access Journals (Sweden)

    Omar Hesham R

    2009-12-01

    Full Text Available Abstract Although acute pericarditis has charachteristic electrocardiographic (ECG findings that differentiate it from acute ST segment elevation myocardial infarction (MI; in certain cases diagnosis is somewhat difficult especially when the ECG reveals focal instead of diffuse changes and moreover when pericarditis is associated with an underlying myocarditis causing elevation of the cardiac biomarkers therefore increasing the difficulty in differentiating between both enteties. This is especially important because adverse lethal side effect can occur if thrombolytic therapy is administered for a patient with acute pericarditis, or if a diagnosis of transmural MI is missed. In this case report we are describing an 18 year old male patient who presented with an acute onset of severe chest pain associated with focal ECG changes and elevated cardiac enzymes mimicking transmural MI. This report aims to sensitize readers to this debate and create awareness among cardiologists and intensivists with both presentations and how to reach an accurate diagnosis.

  15. Remote Ischemic Postconditioning Protects against Myocardial Ischemia-Reperfusion Injury by Inhibition of the RAGE-HMGB1 Pathway

    Directory of Open Access Journals (Sweden)

    Xiangming Wang

    2018-01-01

    Full Text Available Background. The aim of the present study was to observe the effect of RAGE-HMGB1 signal pathway on remote ischemic postconditioning in mice with myocardial ischemia reperfusion injury. Methods. Mice model of MIRI was established and randomly divided into three groups: control group, ischemia reperfusion group, and remote ischemic postconditioning group. Infarction size was detected by Evans blue and TTC staining. Cardiac function was detected by echocardiography measurement. The protein levels of RAGE, HMGB1, P-AKT, and ERK1/2 were detected by Western blot 120 min following reperfusion. Results. RIPostC could decrease the infarct size and increase LVEF and FS compared with I/R group. Two hours after myocardial ischemia reperfusion, the levels of RAGE and HMGB1 were significantly decreased in RIPostC group compared with those in I/R group. The level of p-AKT was significantly higher in the RIPostC group than in the I/R group. LY294002 significantly attenuated RIPostC-increased levels of Akt phosphorylation. Conclusion. RIPostC may inhibit the expression of RAGE and HMGB1 and activate PI3K/Akt signaling pathway to extenuate ischemic reperfusion injury in mice. It could further suppress the oxidative stress, have antiapoptosis effect, and reduce inflammatory reaction, but this effect has certain timeliness.

  16. Acute myocardial infarction in young adults with Antiphospholipid ...

    African Journals Online (AJOL)

    Abstract Acute myocardial infarction (AMI) is rarely associated with antiphospholipid syndrome. The treatment of these patients is a clinical challenge. We report the observations of 2 young adults (1 woman and 1 man), admitted in our acute care unit for acute myocardial infarction (AMI). A coagulopathy work-up concludes ...

  17. Gaseous hydrogen sulfide protects against myocardial ischemia-reperfusion injury in mice partially independent from hypometabolism.

    Science.gov (United States)

    Snijder, Pauline M; de Boer, Rudolf A; Bos, Eelke M; van den Born, Joost C; Ruifrok, Willem-Peter T; Vreeswijk-Baudoin, Inge; van Dijk, Marcory C R F; Hillebrands, Jan-Luuk; Leuvenink, Henri G D; van Goor, Harry

    2013-01-01

    Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H2S) is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant properties. We investigated whether gaseous H2S administration is protective in cardiac IRI and whether non-hypometabolic concentrations of H2S have similar protective properties. Male C57BL/6 mice received a 0, 10, or 100 ppm H2S-N2 mixture starting 30 minutes prior to ischemia until 5 minutes pre-reperfusion. IRI was inflicted by temporary ligation of the left coronary artery for 30 minutes. High-resolution respirometry equipment was used to assess CO2-production and blood pressure was measured using internal transmitters. The effects of H2S were assessed by histological and molecular analysis. Treatment with 100 ppm H2S decreased CO2-production by 72%, blood pressure by 14% and heart rate by 25%, while treatment with 10 ppm H2S had no effects. At day 1 of reperfusion 10 ppm H2S showed no effect on necrosis, while treatment with 100 ppm H2S reduced necrosis by 62% (pcardiac ischemic insult. Although hypometabolism is restricted to small animals, we now showed that low non-hypometabolic concentrations of H2S also have protective properties in IRI. Since IRI is a frequent cause of myocardial damage during percutaneous coronary intervention and cardiac transplantation, H2S treatment might lead to novel therapeutical modalities.

  18. Activity Exerted by a Testosterone Derivative on Myocardial Injury Using an Ischemia/Reperfusion Model

    Science.gov (United States)

    Lauro, Figueroa-Valverde; Francisco, Díaz-Cedillo; Elodia, García-Cervera; Eduardo, Pool-Gómez; Maria, López-Ramos; Marcela, Rosas-Nexticapa; Lenin, Hau-Heredia; Betty, Sarabia-Alcocer; Monica, Velázquez-Sarabia Betty

    2014-01-01

    Some reports indicate that several steroid derivatives have activity at cardiovascular level; nevertheless, there is scarce information about the activity exerted by the testosterone derivatives on cardiac injury caused by ischemia/reperfusion (I/R). Analyzing these data, in this study, a new testosterone derivative was synthetized with the objective of evaluating its effect on myocardial injury using an ischemia/reperfusion model. In addition, perfusion pressure and coronary resistance were evaluated in isolated rat hearts using the Langendorff technique. Additionally, molecular mechanism involved in the activity exerted by the testosterone derivative on perfusion pressure and coronary resistance was evaluated by measuring left ventricular pressure in the absence or presence of the following compounds: flutamide, prazosin, metoprolol, nifedipine, indomethacin, and PINANE TXA2. The results showed that the testosterone derivative significantly increases (P = 0.05) the perfusion pressure and coronary resistance in isolated heart. Other data indicate that the testosterone derivative increases left ventricular pressure in a dose-dependent manner (0.001–100 nM); however, this phenomenon was significantly inhibited (P = 0.06) by indomethacin and PINANE-TXA2  (P = 0.05) at a dose of 1 nM. In conclusion, these data suggest that testosterone derivative induces changes in the left ventricular pressure levels through thromboxane receptor activation. PMID:24839599

  19. Nursing Care in Patient with Acute Myocardial Infarction

    OpenAIRE

    Němec, Pavel

    2016-01-01

    This thesis deals with the issue of acute myocardial infarction in context of prehospital, and hospital care. Specific clinical symptoms, diagnostic procedures, and treatment of acute myocardial infarction are described in the theoretical part. The part is also devoted to nursing care. Emphasis is put especially on prevention of cardiovascular diseases development. The goal is to evaluate nursing care of patients with acute myocardial infarction in prehospital, and later on, hospital care. Th...

  20. Transient metabolic alkalosis during early reperfusion abolishes helium preconditioning against myocardial infarction: restoration of cardioprotection by cyclosporin A in rabbits.

    Science.gov (United States)

    Pagel, Paul S; Krolikowski, John G

    2009-04-01

    Intracellular acidosis during early reperfusion after coronary artery occlusion was recently linked to cardioprotection resulting from myocardial ischemic postconditioning. We tested the hypotheses that transient alkalosis during early reperfusion abolishes helium preconditioning and that the mitochondrial permeability transition pore inhibitor cyclosporin A (CsA) restores the cardioprotective effects of helium during alkalosis in vivo. Rabbits (n = 36) instrumented for hemodynamics measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3-h reperfusion. The rabbits received 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of transient alkalosis (pH = 7.5) produced by administration of IV sodium bicarbonate (10 mEq) 2 min before reperfusion. Other rabbits preconditioned with helium received CsA (5 mg/kg) in the presence of alkalosis or CsA alone. Helium reduced myocardial infarct size (25% +/- 4% of left ventricular area at risk; P Alkalosis during early reperfusion did not alter infarct size alone (46% +/- 2%), but this intervention abolished helium-induced cardioprotection (45% +/- 3%). CsA restored reductions in infarct size produced by helium preconditioning in the presence of alkalosis (28% +/- 6%; P alkalosis during early reperfusion abolishes helium preconditioning in rabbits. CsA restored helium-induced cardioprotection during alkalosis, suggesting that helium preconditioning inhibits mitochondrial permeability transition pore formation by maintaining intracellular acidosis during early reperfusion.

  1. Effects of Nitrate Intake on Myocardial Ischemia-Reperfusion Injury in Diabetic Rats

    Directory of Open Access Journals (Sweden)

    Sajad Jeddi

    Full Text Available Abstract Background: Coronary artery disease is 2-3 times more common in diabetic individuals. Dietary nitrate/nitrite has beneficial effects in both diabetes and cardiovascular disease. It also has protective effects against myocardial ischemia-reperfusion (IR injury in healthy animals. However, the effects of nitrate on myocardial IR injury in diabetic rats have not yet been investigated. Objective: We examined the effects of dietary nitrate on myocardial IR injury in streptozotocin-nicotinamide-induced diabetic rats. Method: Rats were divided into four groups (n=7 in each group: control, control+nitrate, diabetes, and diabetes+nitrate. Type 2 diabetes was induced by injection of streptozotocin and nicotinamide. Nitrate (sodium nitrate was added to drinking water (100 mg/L for 2 months. The hearts were perfused in a Langendorff apparatus at 2 months and assessed before (baseline and after myocardial IR for the following parameters: left ventricular developed pressure (LVDP, minimum and maximum rates of pressure change in the left ventricle (±dP/dt, endothelial nitric oxide (NO synthase (eNOS and inducible NO synthase (iNOS mRNA expression, and levels of malondialdehyde (MDA and NO metabolites (NOx. Results: Recovery of LVDP and ±dP/dt was lower in diabetic rats versus controls, but almost normalized after nitrate intake. Diabetic rats had lower eNOS and higher iNOS expression both at baseline and after IR, and dietary nitrate restored these parameters to normal values after IR. Compared with controls, heart NOx level was lower in diabetic rats at baseline but was higher after IR. Diabetic rats had higher MDA levels both at baseline and after IR, which along with heart NOx levels decreased following nitrate intake. Conclusion: Dietary nitrate in diabetic rats provides cardioprotection against IR injury by regulating eNOS and iNOS expression and inhibiting lipid peroxidation in the heart.

  2. How reliable is myocardial imaging in the diagnosis of acute myocardial infarction

    International Nuclear Information System (INIS)

    Willerson, J.T.

    1983-01-01

    Myocardial scintigraphic techniques available presently allow a sensitive and relatively specific diagnosis of acute myocardial infarction when they are used correctly, although every technique has definite limitations. Small myocardial infarcts (less than 3 gm.) may be missed, and there are temporal limitations in the usefulness of the scintigraphic techniques. The development of tomographic methodology that may be used with single-photon radionuclide emitters (including technetium and 201 Tl will allow the detection of relatively small abnormalities in myocardial perfusion and regions of myocardial infarction and will help to provide a more objective interpretation of the myocardial scintigrams. The use of overlay techniques allowing simultaneous assessment of myocardial perfusion, infarct-avid imaging, and radionuclide ventriculograms will provide insight into the relevant aspects of the extent of myocardial damage, the relationship of damage to myocardial perfusion, and the functional impact of myocardial infarction on ventricular performance

  3. The Cardioprotective Effects of Citric Acid and L-Malic Acid on Myocardial Ischemia/Reperfusion Injury

    Science.gov (United States)

    Tang, Xilan; Liu, Jianxun; Dong, Wei; Li, Peng; Li, Lei; Lin, Chengren; Zheng, Yongqiu; Hou, Jincai; Li, Dan

    2013-01-01

    Organic acids in Chinese herbs, the long-neglected components, have been reported to possess antioxidant, anti-inflammatory, and antiplatelet aggregation activities; thus they may have potentially protective effect on ischemic heart disease. Therefore, this study aims to investigate the protective effects of two organic acids, that is, citric acid and L-malic acid, which are the main components of Fructus Choerospondiatis, on myocardial ischemia/reperfusion injury and the underlying mechanisms. In in vivo rat model of myocardial ischemia/reperfusion injury, we found that treatments with citric acid and L-malic acid significantly reduced myocardial infarct size, serum levels of TNF-α, and platelet aggregation. In vitro experiments revealed that both citric acid and L-malic acid significantly reduced LDH release, decreased apoptotic rate, downregulated the expression of cleaved caspase-3, and upregulated the expression of phosphorylated Akt in primary neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation injury. These results suggest that both citric acid and L-malic acid have protective effects on myocardial ischemia/reperfusion injury; the underlying mechanism may be related to their anti-inflammatory, antiplatelet aggregation and direct cardiomyocyte protective effects. These results also demonstrate that organic acids, besides flavonoids, may also be the major active ingredient of Fructus Choerospondiatis responsible for its cardioprotective effects and should be attached great importance in the therapy of ischemic heart disease. PMID:23737849

  4. Captopril Pretreatment Produces an Additive Cardioprotection to Isoflurane Preconditioning in Attenuating Myocardial Ischemia Reperfusion Injury in Rabbits and in Humans.

    Science.gov (United States)

    Tian, Yi; Li, Haobo; Liu, Peiyu; Xu, Jun-mei; Irwin, Michael G; Xia, Zhengyuan; Tian, Guogang

    2015-01-01

    Pretreatment with the angiotensin-converting inhibitor captopril or volatile anesthetic isoflurane has, respectively, been shown to attenuate myocardial ischemia reperfusion (MI/R) injury in rodents and in patients. It is unknown whether or not captopril pretreatment and isoflurane preconditioning (Iso) may additively or synergistically attenuate MI/R injury. Patients selected for heart valve replacement surgery were randomly assigned to five groups: untreated control (Control), captopril pretreatment for 3 days (Cap3d), or single dose captopril (Cap1hr, 1 hour) before surgery with or without Iso (Cap3d+Iso and Cap1hr+Iso). Rabbit MI/R model was induced by occluding coronary artery for 30 min followed by 2-hour reperfusion. Rabbits were randomized to receive sham operation (Sham), MI/R (I/R), captopril (Cap, 24 hours before MI/R), Iso, or the combination of captopril and Iso (Iso+Cap). In patients, Cap3d+Iso but not Cap1hr+Iso additively reduced postischemic myocardial injury and attenuated postischemic myocardial inflammation. In rabbits, Cap or Iso significantly reduced postischemic myocardial infarction. Iso+Cap additively reduced cellular injury that was associated with improved postischemic myocardial functional recovery and reduced myocardial apoptosis and attenuated oxidative stress. A joint use of 3-day captopril treatment and isoflurane preconditioning additively attenuated MI/R by reducing oxidative stress and inflammation.

  5. Cardioprotective Effect of Aloe vera Biomacromolecules Conjugated with Selenium Trace Element on Myocardial Ischemia-Reperfusion Injury in Rats.

    Science.gov (United States)

    Yang, Yang; Yang, Ming; Ai, Fen; Huang, Congxin

    2017-06-01

    The present study was undertaken to evaluate the cardioprotection potential and underlying molecular mechanism afforded by a selenium (Se) polysaccharide (Se-AVP) from Aloe vera in the ischemia-reperfusion (I/R) model of rats in vivo. Myocardial I/R injury was induced by occluding the left anterior descending coronary artery (LAD) for 30 min followed by 2-h continuous reperfusion. Pretreatment with Se-AVP (100, 200, and 400 mg/kg) attenuated myocardial damage, as evidenced by reduction of the infarct sizes, increase in serum and myocardial endogenous antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT)), and decrease in the malondialdehyde (MDA) level in the rats suffering I/R injury. This cardioprotective activity afforded by Se-AVP is further supported by the decreased levels of cardiac marker enzymes creatine kinase (CK) and lactate dehydrogenase (LDH), as well as the rise of myocardial Na + -K + -ATPase and Ca 2+ -Mg 2+ -ATPase activities in I/R rats. Additionally, cardiomyocytic apoptosis was measured by terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining and the result showed that the percent of TUNEL-positive cells in myocardium of Se-AVP-treated groups was lower than I/R rats. In conclusion, we clearly demonstrated that Se-AVP had a protective effect against myocardial I/R injury in rats by augmenting endogenous antioxidants and protecting rat hearts from oxidative stress-induced myocardial apoptosis.

  6. Interest of colchicine in the treatment of acute myocardial infarct responsible for heart failure in a mouse model.

    Science.gov (United States)

    Akodad, Mariama; Fauconnier, Jérémy; Sicard, Pierre; Huet, Fabien; Blandel, Florence; Bourret, Annick; de Santa Barbara, Pascal; Aguilhon, Sylvain; LeGall, Marion; Hugon, Gérald; Lacampagne, Alain; Roubille, François

    2017-08-01

    Inflammation is deeply involved in the pathophysiology of ischemia-reperfusion (I/R) lesions and ventricular remodeling due to an acute myocardial infarction (AMI). Colchicine as a pleiotropic anti-inflammatory molecule may exert cardioprotective effects under acute ischemia. Here, we aimed to evaluate the impact of colchicine on reperfusion injury in a mouse model. Myocardial ischemia/reperfusion (I/R) injury was induced in C57BL/6 male mice, after 45min ligation of the left coronary artery followed by reperfusion. 400μg/kg of colchicine or the vehicle was administrated intraperitoneally (i.p.) 25min before the reperfusion (blinded administration). Mice were sacrificed at 24h after the acute myocardial ischemia (AMI) and the infarct size was determined. Circulating level of troponin and cytokines profile were assessed 4h after the AMI. An echocardiography was performed in a follow-up group mice, 48h and 8weeks after the AMI. The infarct size was reduced in colchicine treated mice (39.8±3.5% versus 52.9±3.2%, pcolchicine treated mice (7015.7±1423.7pg/mL, n=5 vs 30,723.7±7959.9pg/mL in the placebo group, n=6; pColchicine group (24.51±3.13% vs 11.38±2.46%, p=0.03). In the follow-up group mice (n=8), there were no differences between mice treated with placebo (n=9) and mice treated with colchicine (n=9) regarding to cardiac remodeling parameters but outflow approximated by the ITV was higher in the colchicine group. In conclusion, colchicine allowed a significant reduction of infarct size in mice, improves hemodynamic parameters and decrease cardiac fibrosis. Copyright © 2017 Elsevier B.V. All rights reserved.

  7. Lipoxin A4 Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

    Directory of Open Access Journals (Sweden)

    Qifeng Zhao

    2013-01-01

    Full Text Available This study aims to investigate the pre- and postconditioning effects of lipoxin A4 (LXA4 on myocardial damage caused by ischemia/reperfusion (I/R injury. Seventy-two rats were divided into 6 groups: sham groups (C1 and C2, I/R groups (I/R1 and I/R2, and I/R plus LXA4 preconditioning and postconditioning groups (LX1 and LX2. The serum levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and cardiac troponin I (cTnI were measured. The content and the activity of Na+-K+-ATPase as well as the superoxide dismutase (SOD, and malondialdehyde (MDA levels were determined. Along with the examination of myocardium ultrastructure and ventricular arrhythmia scores (VAS, connexin 43 (Cx43 expression were also detected. Lower levels of IL-1β, IL-6, IL-8, TNF-α, cTnI, MDA content, and VAS and higher levels of IL-10, SOD activity, Na+-K+-ATPase content and activity, and Cx43 expression appeared in LX groups than I/R groups. Besides, H&E staining, TEM examination as well as analysis of gene, and protein confirmed that LXA4 preconditioning was more effective than postconditioning in preventing arrhythmogenesis via the upregulation of Cx43. That is, LXA4 postconditioning had better protective effect on Na+-K+-ATPase and myocardial ultrastructure.

  8. Metformin attenuates myocardial ischemia-reperfusion injury via up-regulation of antioxidant enzymes.

    Directory of Open Access Journals (Sweden)

    Xiaoling Wang

    Full Text Available The objective was to examine the protective effect of metformin (Met on myocardial ischemia-reperfusion (IR injury and whether the mechanism was related to the AMPK/ antioxidant enzymes signaling pathway. Rat Langendorff test and H2O2-treated rat cardiomyocytes (H9c2 were used in this study. Met treatment significantly improved left ventricular (LV function, reduced infarct size and CK-MB release in comparison with IR group. Decreased TUNEL staining positive cells were also observed in IR+Met group ex vivo. Met treatment markedly inhibited IR inducing cell death and significantly decreased apoptosis with few generations of reactive oxygen species (ROS in H9c2 cells in comparison with IR group. Up-regulated expressions of phosphorylated LKB1/AMPK/ACC, as well as down-regulated expressions of apoptotic proteins (Bax and cleaved caspase 3 were found in IR+Met group when compared to the IR group. Importantly, Met significantly up-regulated the expression of antioxidant enzymes (MnSOD and catalase during IR procedure either ex vivo or in vitro. Compound C, a conventional inhibitor of AMPK, abolished the promoting effect of Met on antioxidant enzymes, and then attenuated the protective effect of Met on IR injury in vitro. In conclusion, Met exerted protective effect on myocardial IR injury, and this effect was AMPK/ antioxidant enzymes dependent.

  9. Acute Anterior Myocardial Infarction Accompanied by Acute Inferior Myocardial Infarction: A Very Rare Coronary Artery Anomaly

    Directory of Open Access Journals (Sweden)

    Y. Alsancak

    2015-01-01

    Full Text Available Coronary artery anomalies are rare and mostly silent in clinical practice. First manifestation of this congenital abnormality can be devastating as syncope, acute coronary syndrome, and sudden cardiac death. Herein we report a case with coronary artery anomaly complicated with ST segment myocardial infarction in both inferior and anterior walls simultaneously diagnosed during primary percutaneous coronary intervention.

  10. Understanding prehospital delay behavior in acute myocardial infarction in women.

    Science.gov (United States)

    Waller, Cynthia G

    2006-12-01

    Studies demonstrate that acute myocardial infarction (AMI) mortality can be reduced if reperfusion therapy is initiated within 1 hour of AMI symptom onset. However, a considerable number of men and women arrive at the emergency department outside of the time frame for thrombolytic and angioplasty effectiveness. This is especially true for women who have been shown to delay longer than men due to their prehospital decision-making process utilized. With a mean total delay time greater than 4 hours, the time interval from symptom onset to transport activation to the hospital consumes the majority of the prehospital phase of emergency cardiac care. The health belief model, self-regulation model, theory of reasoned action, and theory of planned behavior have all been used to describe the prehospital decision-making process of both men and women with an AMI and the variables that impact that process. These models have identified the importance of symptom attribution to cardiac-related causes as a target variable for research and interventions related to care-seeking behavior.

  11. Acute myocardial infarct imaging with indium-111-labeled monoclonal antimyosin Fab

    International Nuclear Information System (INIS)

    Khaw, B.A.; Yasuda, T.; Gold, H.K.; Leinbach, R.C.; Johns, J.A.; Kanke, M.; Barlai-Kovach, M.; Strauss, H.W.; Haber, E.

    1987-01-01

    Indium-111 monoclonal antimyosin Fab scintigraphy was used to detect myocardial necrosis in 52 of 54 patients (96.3%) with acute myocardial infarction. Infarcts were visualized when coronary arteries were persistently occluded (n = 10), became patent after thrombolysis (n = 33), or became patent after spontaneous reperfusion (n = 7). Posteroinferolateral visualizations were obtained in two patients with clinical and enzymatic evidence of infarction but normal electrocardiograms. Of the two patients in whom no infarcts were visualized, one had an anterior myocardial infarct. This patient underwent successful thrombolytic therapy, with attendant minimization of creatine kinase release. The other patient had a small, nonreperfused inferior myocardial infarct. Five patients with a history of remote infarction and acute necrosis showed antimyosin uptake only in regions concordant with the acute episodes of infarction, and radiolabeled antimyosin Fab localized in neither old infarcts nor normal, noninfarcted myocardium. Antimyosin Fab scintigraphy, thus, appears to be a highly specific means of delineating necrotic myocardium, at least in this limited and selected group of patients

  12. Lack of effect of prolonged treatment with liraglutide on cardiac remodeling in rats after acute myocardial infarction

    DEFF Research Database (Denmark)

    Kyhl, Kasper; Lønborg, Jacob; Hartmann, Bolette

    2017-01-01

    Following the acute phase of a myocardial infarction, a set of structural and functional changes evolves in the myocardium, collectively referred to as cardiac remodeling. This complex set of processes, including interstitial fibrosis, inflammation, myocyte hypertrophy and apoptosis may progress...... to heart failure. Analogs of the incretin hormone glucagon-like peptide 1 (GLP-1) have shown some promise as cardioprotective agents. We hypothesized that a long-acting GLP-1 analog liraglutide would ameliorate cardiac remodeling over the course of 4 weeks in a rat model of non-reperfused myocardial...

  13. Myocardial capillary permeability after regional ischemia and reperfusion in the in vivo canine heart. Effect of superoxide dismutase

    DEFF Research Database (Denmark)

    Svendsen, Jesper Hastrup; Bjerrum, P J; Haunsø, S

    1991-01-01

    coronary artery followed by 1 hour of reperfusion. Myocardial plasma flow rate and capillary extraction of chromium 51-labeled EDTA or technetium 99m-labeled diethylenetriaminepentaacetic acid were measured by the single-injection, residue-detection method before ischemia and 5 and 60 minutes after...... fibrillation in contrast to none in the superoxide dismutase group. Before ischemia, plasma flow rate, myocardial capillary extraction fraction, and PS values were similar in the two groups. Five minutes after the start of reperfusion, plasma flow rate increased significantly (p less than 0.01) in both groups....... In the control group, capillary extraction fraction increased by 12% (p = NS) in spite of the higher plasma flow; these increases in capillary extraction fraction and plasma flow induced a 69% increase in PS (p less than 0.01). In the superoxide dismutase-treated group, capillary extraction fraction decreased...

  14. 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...

  15. Effect of thyroid hormone on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass

    OpenAIRE

    Qing-Bin Wei; Fei Xie; Shi-Li Wang; Gang Li

    2017-01-01

    Objective: To study the effect of thyroid hormone (euthyrox) on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass. Methods: A total of 76 patients who received valve replacement under cardiopulmonary bypass in our hospital between January 2013 and December 2016 were collected and divided into control group (n=38) and observation group (n=38) according to random number table. Observation group took euthyrox orally 1 week before...

  16. Short-term fasting reduces the extent of myocardial infarction and incidence of reperfusion arrhythmias in rats

    Czech Academy of Sciences Publication Activity Database

    Šnorek, M.; Hodyc, D.; Šedivý, V.; Ďurišová, J.; Skoumalová, A.; Wilhelm, J.; Neckář, Jan; Kolář, František; Herget, J.

    2012-01-01

    Roč. 61, č. 6 (2012), s. 567-574 ISSN 0862-8408 R&D Projects: GA MŠk(CZ) 1M0510; GA ČR(CZ) GA305/08/0108 Institutional research plan: CEZ:AV0Z5011922 Keywords : myocardial ischemia/reperfusion * arrhythmias * infarction * fasting * ketone bodies Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery Impact factor: 1.531, year: 2012

  17. Cardioprotective effect of the Hibiscus rosa sinensis flowers in an oxidative stress model of myocardial ischemic reperfusion injury in rat

    Science.gov (United States)

    Gauthaman, Karunakaran K; Saleem, Mohamed TS; Thanislas, Peter T; Prabhu, Vinoth V; Krishnamoorthy, Karthikeyan K; Devaraj, Niranjali S; Somasundaram, Jayaprakash S

    2006-01-01

    Background The present study investigates the cardioprotective effects of Hibiscus rosa sinensis in myocardial ischemic reperfusion injury, particularly in terms of its antioxidant effects. Methods The medicinal values of the flowers of Hibiscus rosa sinensis (Chinese rose) have been mentioned in ancient literature as useful in disorders of the heart. Dried pulverized flower of Hibiscus rosa sinensis was administered orally to Wistar albino rats (150–200 gms) in three different doses [125, 250 and 500 mg/kg in 2% carboxy methyl cellulose (CMC)], 6 days per week for 4 weeks. Thereafter, rats were sacrificed; either for the determination of baseline changes in cardiac endogenous antioxidants [superoxide dismutase, reduced glutathione and catalase] or the hearts were subjected to isoproterenol induced myocardial necrosis. Results There was significant increase in the baseline contents of thiobarbituric acid reactive substances (TBARS) [a measure of lipid per oxidation] with both doses of Hibiscus Rosa sinensis. In the 250 mg/kg treated group, there was significant increase in superoxide dismutase, reduced glutathione, and catalase levels but not in the 125 and 500 mg/kg treated groups. Significant rise in myocardial thiobarbituric acid reactive substances and loss of superoxide dismutase, catalase and reduced glutathione (suggestive of increased oxidative stress) occurred in the vehicle treated hearts subjected to in vivo myocardial ischemic reperfusion injury. Conclusion It may be concluded that flower of Hibiscus rosa sinensis (250 mg/kg) augments endogenous antioxidant compounds of rat heart and also prevents the myocardium from isoproterenol induced myocardial injury. PMID:16987414

  18. Effect of thyroid hormone on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass

    Directory of Open Access Journals (Sweden)

    Qing-Bin Wei

    2017-07-01

    Full Text Available Objective: To study the effect of thyroid hormone (euthyrox on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass. Methods: A total of 76 patients who received valve replacement under cardiopulmonary bypass in our hospital between January 2013 and December 2016 were collected and divided into control group (n=38 and observation group (n=38 according to random number table. Observation group took euthyrox orally 1 week before surgery, control group took vitamin C tablets orally at the same point in time, and both therapies lasted for 1 week. Before taking medicine and after cardiopulmonary bypass (before end of surgery, serum levels of myocardial enzyme spectrum indexes and nerve injury indexes were compared between the two groups of patients. Results: Before taking medicine, differences in the serum levels of myocardial enzyme spectrum indexes and nerve injury indexes were not statistically significant between the two groups of patients. After cardiopulmonary bypass, serum myocardial enzyme spectrum indexes cTnT, CK-MB, α-HBD and LDH levels in observation group were lower than those in control group; serum nerve injury indexes NSE, S100B and GFAP levels were lower than those in control group while bFGF level was higher than that in control group. Conclusion: Euthyrox intervention in valve replacement under cardiopulmonary bypass can effectively reduce the myocardial and cerebral ischemia reperfusion injury.

  19. Benefits and risks of thrombolysis for acute myocardial infarction

    NARCIS (Netherlands)

    A.E.R. Arnold (Alfred); M.L. Simoons (Maarten)

    1990-01-01

    textabstractThrombolytic therapy is a major step forward in the treatment of acute myocardial infarction and may result in up to 50% mortality reduction, provided that it is administered early (chapter 1). In 80 to 85% of patients with suspected acute myocardial infarction, a coronary artery is

  20. Prognostic importance of complete atrioventricular block complicating acute myocardial infarction

    DEFF Research Database (Denmark)

    Aplin, Mark; Engstrøm, Thomas; Vejlstrup, Niels G

    2003-01-01

    Third-degree atrioventricular block after acute myocardial infarction is considered to have prognostic importance. However, its importance in conjunction with thrombolytic therapy and its relation to left ventricular function remains uncertain. This report also outlines an important distinction...... between atrioventricular block in the setting of anterior and inferior wall acute myocardial infarction, with profound clinical and prognostic implications....

  1. Myocardial energy metabolism during global ischemia and reperfusion in SHR hypertrophic rat heart assessed by 31P-NMR

    International Nuclear Information System (INIS)

    Shirotani, Hitoshi; Oka, Hiroshi; Katayama, Osamu; Nishioka, Takazumi; Oku, Hidetaka

    1983-01-01

    An experiment regarding myocardial ischemia and reperfusion was performed under various conditions in SHR hypertrophic and WKY non-hypertrophic rat hearts. An effect of cardioplegia was evaluated in the following 4 conditions, that is, Group 1: hypothermia only, Group 2: hypothermia with intermittent infusion of GIK solution, Group 3: hypothermia with intermittent infusion of cold blood cardioplegia, Group 4: hypothermia with intermittent infusion of cold blood cardioplegia and administration of coenzyme Q 10 prior to isolation of the heart. 1) In WKY heart, ATP contents after 90 minutes myocardial ischemia at 15 0 C decreased to 25% in Group 1,42% in Group 2,52% in Group 3 and 62% in Group 4, and the contents after 30 minutes reperfusion increased to 42, 50, 60 and 75%, respectively. On the other hand, in SHR heart, ATP contents decreased to 22, 38, 40 and 41% but no trend of recovery was present. 2) Creatine phosphate content in SHR heart was 50% of that in WKY heart during isolated perfusion. Creatine phosphate decreased to zero after 30 minutes myocardial ischemia. In WKY heart, the content was recovered to over 100% by 30 minutes reperfusion after 90 minutes myocardial ischemia in all groups. On the contrary, in SHR heart, the contents increased to only 10, 15, 22 and 41%, in 4 groups, respectively. 3) In WKY heart, pH fell to 6.2, 6.7, 6.8 and 6.8, in 4 groups, respectively, a fter 90 minutes myocardial ischemia, and returned to the preischemic value of 7.2 after 30 minutes reperfusion in all groups. In SHR heart, pH fell to 6.1 in group 1, 6.3 in group 2, 6.4 in group 3 and 6.7 in group 4 after 90 minutes myocardial ischemia and the values returned to 6.5, 6.6, 6.7 and 6.8, respectively, after 30 minutes reperfusion. The latter values were lower than preischemic value of 7.0. (J.P.N.)

  2. Correlation of QRS complex after percutaneous coronary intervention with myocardial ischemia reperfusion injury and apoptosis molecule contents

    Directory of Open Access Journals (Sweden)

    Ming-Min Jiang

    2017-11-01

    Full Text Available Objective: To study the correlation of QRS complex after percutaneous coronary intervention (PCI with myocardial ischemia reperfusion injury and apoptosis molecule contents. Methods: Patients with non-ST-segment elevation myocardial infarction who were treated in Nanchong Central Hospital between June 2014 and August 2016 were selected and divided into the PCI group who received emergency PCI surgery and the control group who accepted selective PCI or refused emergency PCI after the medical data were retrospectively analyzed. The fQRS as well as the contents of ischemia reperfusion injury indexes and apoptosis molecules was determined after 1 week of treatment. Results: The incidence of fQRS in PCI group was significantly lower than that in control group; serum MDA, cTnI, H-FABP, sTWEAK, sFas, sTRAIL and Caspase-3 contents as well as peripheral blood Nrf-2 and HO-1 expression of PCI group were greatly lower than those of control group; serum MDA, cTnI, H-FABP, sTWEAK, sFas, sTRAIL and Caspase-3 contents as well as peripheral blood Nrf-2 and HO-1 expression of PCI group of patients with fQRS complex (+ were greatly higher than those of patients with fQRS complex (-. Conclusion: The occurrence of fQRS after PCI is closely related to myocardial ischemia reperfusion injury and apoptosis.

  3. Distribution of carbon flux within fatty acid utilization during myocardial ischemia and reperfusion

    International Nuclear Information System (INIS)

    Nellis, S.H.; Liedtke, A.J.; Renstrom, B.

    1991-01-01

    Twenty-nine intact, working pig hearts were extracorporeally perfused and divided into two study groups (16 Aerobic and 13 Ischemic/Reflow hearts). Step function, equilibrium labeling with [14C]palmitate was used to develop uptake and washout curves of radioactive fatty acid products contained in coronary effluent during either aerobic perfusion or reperfusion after ischemia (60% reduction in left anterior descending coronary flow for 30 minutes). Left anterior descending control flows were slightly overperfused in Aerobic hearts (18% higher than in Ischemic/Reflow hearts); otherwise, circumflex and right coronary flows, left ventricular pressure, and serum fatty acids and blood sugar levels were comparable between groups. As expected in Ischemic/Reflow hearts, recovery of regional systolic shortening and myocardial oxygen consumption in reperfusion was only modestly impaired (-20% and -19%, respectively, not significant and p less than 0.011 compared with preischemic values, not significant from Aerobic hearts). The only significant metabolized product to be released from labeled fatty acid utilization in either group was 14CO2. A smaller fatty acid pool also was measured and accounted for by that contained in the coronary intravascular volume. The authors could determine no significant back diffusion of fatty acids from myocardium in either perfusion condition. Uptake time constants of the early phase of 14CO2 production also were virtually identical in both groups (19.9 ± 3.2 versus 16.7 ± 3.2 minutes in Aerobic and Ischemic/Reflow hearts, respectively) and strongly correlated with hemodynamics as described by heart rate. In washout studies, tissue radioactivity in the aqueous soluble and fatty acid pools declined in both study groups, and counts in complex lipids and cholesterol/cholesteryl esters remained steady, whereas those in triacylglycerols varied

  4. Aldose reductase modulates acute activation of mesenchymal markers via the β-catenin pathway during cardiac ischemia-reperfusion.

    Directory of Open Access Journals (Sweden)

    Devi Thiagarajan

    Full Text Available Aldose reductase (AR: human, AKR1B1; mouse, AKR1B3, the first enzyme in the polyol pathway, plays a key role in mediating myocardial ischemia/reperfusion (I/R injury. In earlier studies, using transgenic mice broadly expressing human AKR1B1 to human-relevant levels, mice devoid of Akr1b3, and pharmacological inhibitors of AR, we demonstrated that AR is an important component of myocardial I/R injury and that inhibition of this enzyme protects the heart from I/R injury. In this study, our objective was to investigate if AR modulates the β-catenin pathway and consequent activation of mesenchymal markers during I/R in the heart. To test this premise, we used two different experimental models: in vivo, Akr1b3 null mice and wild type C57BL/6 mice (WT were exposed to acute occlusion of the left anterior descending coronary artery (LAD followed by recovery for 48 hours or 28 days, and ex-vivo, WT and Akr1b3 null murine hearts were perfused using the Langendorff technique (LT and subjected to 30 min of global (zero-flow ischemia followed by 60 min of reperfusion. Our in vivo results reveal reduced infarct size and improved functional recovery at 48 hours in mice devoid of Akr1b3 compared to WT mice. We demonstrate that the cardioprotection observed in Akr1b3 null mice was linked to acute activation of the β-catenin pathway and consequent activation of mesenchymal markers and genes linked to fibrotic remodeling. The increased activity of the β-catenin pathway at 48 hours of recovery post-LAD was not observed at 28 days post-infarction, thus indicating that the observed increase in β-catenin activity was transient in the mice hearts devoid of Akr1b3. In ex vivo studies, inhibition of β-catenin blocked the cardioprotection observed in Akr1b3 null mice hearts. Taken together, these data indicate that AR suppresses acute activation of β-catenin and, thereby, blocks consequent induction of mesenchymal markers during early reperfusion after myocardial

  5. 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

  6. 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

  7. Reperfusion ventricular arrhythmia bursts identify larger infarct size in spite of optimal epicardial and microvascular reperfusion using cardiac magnetic resonance imaging

    NARCIS (Netherlands)

    van der Weg, Kirian; Kuijt, Wichert J.; Bekkers, Sebastiaan C. A. M.; Tijssen, Jan G. P.; Green, Cynthia L.; Lemmert, Miguel E.; Krucoff, Mitchell W.; Gorgels, Anton P. M.

    2017-01-01

    Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardial infarction (STEMI) are related to larger infarct size (IS). Inadequate microvascular reperfusion, as determined by microvascular obstruction (MVO) using cardiac magnetic resonance imaging (CMR), is also

  8. Risk factors for acute myocardial infarction during the postoperative period of myocardial revascularization

    Directory of Open Access Journals (Sweden)

    José Ribamar Costa Jr.

    2003-03-01

    Full Text Available OBJECTIVE: To identify risk factors for acute myocardial infarction during the postoperative period after myocardial revascularization. METHODS: This was a case-control study paired for sex, age, number, type of graft used, coronary endarterectomy, type of myocardial protection, and use of extracorporeal circulation. We assessed 178 patients (89 patients in each group undergoing myocardial revascularization, and the following variables were considered: dyslipidemia, systemic hypertension, smoking, diabetes mellitus, previous myocardial revascularization surgery, previous coronary angioplasty, and acute myocardial infarction. RESULTS: Baseline clinical characteristics did not differ in the groups, except for previous myocardial revascularization surgery, prevalent in the case group (34 patients vs. 12 patients; p = 0.0002. This was the only independent predictor of risk for acute myocardial infarction in the postoperative period, based on a multivariate logistic regression analysis (p=0.0001. Mortality and the time of hospital stay of the case group were significantly higher (19.1% vs. 1.1%; p<0.001 and 15.7 days vs. 10.6 days; p<0.05 respectively than those of the control. CONCLUSION: Only previous myocardial revascularization was an independent predictor of acute myocardial infarction in the postoperative period, based on multivariate logistic regression analysis.

  9. Intracoronary and systemic melatonin to patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L; Busch, Sarah Ekeløf; Jensen, Svend Eggert

    2014-01-01

    -point is the Myocardial Salvage Index assessed by cardiovascular magnetic resonance imaging on day 4 (± 1) after pPCI. The secondary end-points are high-sensitivity troponin, creatinekinase myocardial band and clinical events. CONCLUSION: The aim of the IMPACT trial is to evaluate the effect of melatonin on reperfusion...... injuries following pPCI. Owing to its relatively non-toxic profile, melatonin is an easily implementable drug in the clinical setting, and melatonin has the potential to reduce morbidity in patients with AMI. FUNDING: This study received no financial support from the industry. TRIAL REGISTRATION: www...

  10. Novel curcumin analogue 14p protects against myocardial ischemia reperfusion injury through Nrf2-activating anti-oxidative activity

    Energy Technology Data Exchange (ETDEWEB)

    Li, Weixin [Department of Cardiology, The 5th Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang (China); Chemical Biology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang (China); Wu, Mingchai [Department of Pharmacy, The Third Affiliated Hospital of Wenzhou Medical University, Wenzou, Zhejiang (China); Tang, Longguang; Pan, Yong; Liu, Zhiguo [Chemical Biology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang (China); Zeng, Chunlai [Department of Cardiology, The 5th Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang (China); Wang, Jingying [Chemical Biology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang (China); Wei, Tiemin, E-mail: lswtm@sina.com [Department of Cardiology, The 5th Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang (China); Liang, Guang, E-mail: wzmcliangguang@163.com [Chemical Biology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang (China)

    2015-01-15

    Background: Alleviating the oxidant stress associated with myocardial ischemia reperfusion has been demonstrated as a potential therapeutic approach to limit ischemia reperfusion (I/R)-induced cardiac damage. Curcumin, a natural compound with anti-oxidative activity, exerts beneficial effect against cardiac I/R injury, but poor chemical and metabolic stability. Previously, we have designed and synthesized a series of mono-carbonyl analogues of curcumin (MACs) with high stability. This study aims to find new anti-oxidant MACs and to demonstrate their effects and mechanisms against I/R-induced heart injury. Methods: H9c2 cells challenged with H{sub 2}O{sub 2} or TBHP were used for in vitro bio-screening and mechanistic studies. The MDA, H{sub 2}O{sub 2} and SOD levels in H9C2 cells were determined, and the cell viability was assessed by MTT assay. Myocardial I/R mouse models administrated with or without the compound were used for in vivo studies. Results: The in vitro cell-based screening showed that curcumin analogues 8d and 14p exhibited strong anti-oxidative effects. Pre-treatment of H9c2 cells with 14p activated Nrf2 signaling pathway, attenuated H{sub 2}O{sub 2}-increased MDA and SOD level, followed by the inhibition of TBHP-induced cell death and Bax/Bcl-2–caspase-3 pathway activation. Silencing Nrf2 significantly reversed the protective effects of 14p. In in vivo animal model of myocardial I/R, administration of low dose 14p (10 mg/kg) reduced infarct size and myocardial apoptosis to the same extent as the high dose curcumin (100 mg/kg). Conclusion: These data support the novel curcumin analogue 14p as a promising antioxidant to decrease oxidative stress and limit myocardial ischemia reperfusion injury via activating Nrf2. - Highlights: • Mono-carbonyl analogue of curcumin, 14p, exhibited better chemical stability. • Compound 14p inhibited TBHP-induced apoptosis through activating Nrf2 in vitro. • Compound 14p limited myocardial ischemia/reperfusion

  11. Moving Beyond SHOCK: New Paradigms in the Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock.

    Science.gov (United States)

    Kalavrouziotis, Dimitri; Rodés-Cabau, Josep; Mohammadi, Siamak

    2017-01-01

    The current management of patients with acute myocardial infarction complicated by cardiogenic shock (AMI-CS) is associated with a high rate of mortality, despite widespread regional implementation of rapid transfer to percutaneous coronary intervention-capable centres for prompt infarct-related artery reperfusion. The limited clinical effectiveness of early revascularization in patients with AMI-CS might be secondary to the extent of coronary artery disease in these patients and the risk of incomplete revascularization, as well as the lower probability of achieving successful reperfusion compared with acute myocardial infarction without hemodynamic instability. Also, the severity of end-organ injury is a critical determinant of outcome. We review adjunctive therapies to early revascularization in AMI-CS, specifically with a focus on the role of short-term mechanical circulatory support. In selected patients with AMI-CS, there might be a benefit associated with early institution of mechanical circulatory support before revascularization. Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

  12. Thrombolysis significantly reduces transient myocardial ischaemia following first acute myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H; Pless, P; Nielsen, J R

    1992-01-01

    In order to investigate whether thrombolysis affects residual myocardial ischaemia, we prospectively performed a predischarge maximal exercise test and early out-of-hospital ambulatory ST segment monitoring in 123 consecutive men surviving a first acute myocardial infarction (AMI). Seventy...... less than 0.02). Thrombolysis resulted in a non-significant reduction in exercise-induced ST segment depression: prevalence 43% vs 62% in controls. However, during ambulatory monitoring the duration of transient myocardial ischaemia was significantly reduced in thrombolysed patients: 322 min vs 1144...... myocardial ischaemia. This may explain the improvement in myocardial function during physical activities, which was also observed in this study....

  13. CASE OF EFFECTIVE REPERFUSION THERAPY IN PATIENTS WITH ACUTE CEREBROVASCULAR ACCIDENT AND ACUTE CORONARY SYNDROME

    Directory of Open Access Journals (Sweden)

    L. V. Timchenko

    2015-01-01

    Full Text Available ABSTRACT. Currently, acute cerebrovascular accident is an extremely important medical and social issue. Stroke is a major cause of disability in the population and takes a leading place among the causes of death.Modern high­tech endovascular treatment of the ischemic stroke (IS and acute coronary syndrome (ACS includes effective methods of reperfusion of the brain and myocardium within first hours of the disease.In this paper, we report two clinical examples of high­tech reperfusion endovascular treatment in the same patient at an intervals of 1 year and 6 months in the development of clinical picture of the stroke and ACS in Regional Clinical hospital № 1 n.a. Prof. S.V. Ochapovsky.In the first case, intra­aortic TLT of two cerebral arteries (ACA and MCA was performed simultaneously with delayed recanalization and complete regression of focal neurological symptoms. And in the second case, selective thrombolytic therapy was performed in the acute phase of stroke, which developed few hours after PTCA RCA in ACS, with a good clinical effect. 

  14. Adiponectin and ischemia-reperfusion injury in ST segment elevation myocardial infarction.

    Science.gov (United States)

    De Roeck, Lynn; Vandamme, Sarah; Everaert, Bert R; Hoymans, Vicky; Haine, Steven; Vandendriessche, Tom; Bosmans, Johan; Ronsyn, Mark W; Miljoen, Hielko; Van Berendoncks, An; De Meyer, Guido; Vrints, Christiaan; Claeys, Marc J

    2016-02-01

    Models of experimental ischemia-reperfusion (IR) in adiponectin knockout animals have shown that adiponectin mediates protection against the development of IR injury. However, the role of adiponectin in IR injury in humans is largely unknown. In a total of 234 ST segment elevation myocardial infarction (STEMI) patients, baseline circulating total adiponectin concentration was correlated with IR injury after primary percutaneous coronary intervention (pPCI) and with major adverse cardiac events (MACE, death and cardiac hospitalization) during one year of follow up. IR injury was defined by serial electrocardiography (ECG) as >30% persistent ST segment elevation despite successful restoration of vessel patency and by angiography as thrombolysis in myocardial infarction (TIMI) blush gradeinjury was present in 31% of patients according to ECG criteria and in 28% of patients according to angiographic criteria. The median adiponectin level was 6.8 µg/ml in patients with ECG signs of IR injury and 6.5 µg/ml in patients without ECG signs of IR (p=0.26). When the angiographic criteria of IR were used, the median adiponectin level was 6.9 µg/ml for patients with IR versus 6.3 µg/ml for patients without IR (p=0.06). MACE occurred in 27% of the patients. Median adiponectin levels were similar in patients with MACE and in those without MACE: 6.3 vs. 6.4 µg/ml (p=0.24). In a multivariate model, no significant relation between circulating adiponectin levels and IR injury or MACE was evident. In the current era of pPCI, IR injury still occurs in almost one third of STEMI patients. Our findings do not support a major protective role of adiponectin in the prevention or attenuation of IR injury in these patients. © The European Society of Cardiology 2015.

  15. Acute myocardial infarction in infectious endocarditis. Report of one case

    International Nuclear Information System (INIS)

    Parietti, G; Artucio, C.; Fernandez, A; Areco, D.; Mallo, D; Lluberas, R.

    2012-01-01

    The acute myocardial infarction is a rare complication in the course of an acute endocarditis. It takes place in the first weeks infection. Although is not associated with any particular microorganism it has been associated with virulent microorganism and is common in aortic valve endocarditis insufficiency. This report is a case of a patient who suffered a myocardial infarction during a acute endocarditis of native valve

  16. Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST-Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications.

    Science.gov (United States)

    Carrick, David; Haig, Caroline; Ahmed, Nadeem; Rauhalammi, Samuli; Clerfond, Guillaume; Carberry, Jaclyn; Mordi, Ify; McEntegart, Margaret; Petrie, Mark C; Eteiba, Hany; Hood, Stuart; Watkins, Stuart; Lindsay, M Mitchell; Mahrous, Ahmed; Welsh, Paul; Sattar, Naveed; Ford, Ian; Oldroyd, Keith G; Radjenovic, Aleksandra; Berry, Colin

    2016-02-23

    The time course and relationships of myocardial hemorrhage and edema in patients after acute ST-segment elevation myocardial infarction (STEMI) are uncertain. Patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention underwent cardiac magnetic resonance imaging on 4 occasions: at 4 to 12 hours, 3 days, 10 days, and 7 months after reperfusion. Myocardial edema (native T2) and hemorrhage (T2*) were measured in regions of interest in remote and injured myocardium. Myocardial hemorrhage was taken to represent a hypointense infarct core with a T2* value myocardial infarction (mean age 54 years; 25 [83%] male) gave informed consent. Myocardial hemorrhage occurred in 7 (23%), 13 (43%), 11 (33%), and 4 (13%) patients at 4 to 12 hours, 3 days, 10 days, and 7 months, respectively, consistent with a unimodal pattern. The corresponding median amounts of myocardial hemorrhage (percentage of left ventricular mass) during the first 10 days after myocardial infarction were 2.7% (interquartile range [IQR] 0.0-5.6%), 7.0% (IQR 4.9-7.5%), and 4.1% (IQR 2.6-5.5%; Pmyocardial edema (percentage of left ventricular mass) in all patients (P=0.001) and for infarct zone edema (T2, in ms: 62.1 [SD 2.9], 64.4 [SD 4.9], 65.9 [SD 5.3]; Pmyocardial hemorrhage. Alternatively, in patients with myocardial hemorrhage, infarct zone edema was reduced at day 3 (T2, in ms: 51.8 [SD 4.6]; Pmyocardial hemorrhage (P=0.001) but not in patients without hemorrhage (P=0.377). The temporal evolutions of myocardial hemorrhage and edema are unimodal, whereas infarct zone edema (T2 value) has a bimodal pattern. Myocardial hemorrhage is prognostically important and represents a target for therapeutic interventions that are designed to preserve vascular integrity following coronary reperfusion. URL: https://clinicaltrials.gov/. Unique identifier: NCT02072850. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  17. Acute myocardial infarction and infarct size: do circadian variations play a role?

    Directory of Open Access Journals (Sweden)

    Ibáñez B

    2012-08-01

    Full Text Available Aída Suárez-Barrientos,1 Borja Ibáñez1,21Cardiovascular Institute, Hospital Clínico San Carlos, 2Centro Nacional de Investigaciones Cardiovasculares, Madrid, SpainAbstract: The circadian rhythm influences cardiovascular system physiology, inducing diurnal variations in blood pressure, heart rate, cardiac output, endothelial functions, platelet aggregation, and coronary arterial flow, among other physiological parameters. Indeed, an internal circadian network modulates cardiovascular physiology by regulating heart rate, metabolism, and even myocyte growth and repair ability. Consequently, cardiovascular pathology is also controlled by circadian oscillations, with increased morning incidence of cardiovascular events. The potential circadian influence on the human tolerance to ischemia/reperfusion has not been systematically scrutinized until recently. It has since been proven, in both animals and humans, that infarct size varies during the day depending on the symptom onset time, while circadian fluctuations in spontaneous cardioprotection in humans with ST-segment elevation myocardial infarction (STEMI have also been demonstrated. Furthermore, several studies have proposed that the time of day at which revascularization occurs in patients with STEMI may also influence infarct size and reperfusion outcomes. The potential association of the circadian clock with infarct size advocates the acknowledgment of time of day as a new prognostic factor in patients suffering acute myocardial infarction, which would open up a new field for chronotherapeutic targets and lead to the inclusion of time of day as a variable in clinical trials that test novel cardioprotective strategies.Keywords: cardioprotection, circadian rhythm, reperfusion injury, ST-segment elevation myocardial infarction

  18. Randomized controlled trial of TY-51924, a novel hydrophilic NHE inhibitor, in acute myocardial infarction.

    Science.gov (United States)

    Kimura, Kazuo; Nakao, Koichi; Shibata, Yoshisato; Sone, Takahito; Takayama, Tadateru; Fukuzawa, Shigeru; Nakama, Yasuharu; Hirayama, Haruo; Matsumoto, Naoya; Kosuge, Masami; Hiro, Takafumi; Sakuma, Hajime; Ishihara, Masaharu; Asakura, Masanori; Hamada, Chikuma; Kaneko, Akira; Yokoi, Toshiaki; Hirayama, Atsushi

    2016-04-01

    In patients with ST-elevation acute myocardial infarction (STEMI), reperfusion therapy limits infarct size, but can directly evoke myocardial reperfusion injury. Activation of the Na(+)/H(+) exchanger (NHE) plays an important role in reperfusion injury. TY-51924, a novel NHE inhibitor, significantly reduced infarct size in animal studies and was well tolerated in early-phase clinical trials. This study aim was to evaluate the efficacy and safety of TY-51924 in patients with STEMI. In this multicenter, randomized, double-blind, placebo-controlled Phase II trial, 105 patients with first anterior STEMI undergoing primary percutaneous coronary intervention (pPCI) were randomly assigned to receive an intravenous infusion of either TY-51924 or placebo. Primary endpoints were myocardial salvage index (MSI) as determined by single photon emission computed tomography (SPECT) 3-5 days after pPCI and safety up to 7 days. Baseline characteristics were similar in the two groups. MSI 3-5 days after pPCI (0.200 vs. 0.290, p=0.56), 3 months after pPCI (0.470 vs. 0.500, p=0.76), and the incidences of side effects did not differ between the two groups as a whole. However, on post hoc analysis of 52 patients with a large area at risk (AAR) (≥38%) and no antegrade coronary flow, MSI by SPECT at 3 months after pPCI was significantly higher in TY-51924 group (0.450 vs. 0.320, p=0.03). TY-51924 did not adversely influence hemodynamics. TY-51924 did not improve MSI or increase side effects as a whole. However, TY-51924 is potentially cardioprotective in the presence of a large AAR and no antegrade coronary flow. Copyright © 2015 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

  19. Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Arslan, Fatih; Lai, Ruenn Chai; Smeets, Mirjam B; Akeroyd, Lars; Choo, Andre; Aguor, Eissa N E; Timmers, Leo; van Rijen, Harold V; Doevendans, Pieter A; Pasterkamp, Gerard; Lim, Sai Kiang; de Kleijn, Dominique P

    2013-05-01

    We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myocardium, and could be ameliorated by proteins in exosomes. To test this hypothesis in vivo, mice (C57Bl6/J) underwent 30 min ischemia, followed by reperfusion (I/R injury). Purified exosomes or saline was administered 5 min before reperfusion. Exosomes reduced infarct size by 45% compared to saline treatment. Langendorff experiments revealed that intact but not lysed exosomes enhanced viability of the ischemic/reperfused myocardium. Exosome treated animals exhibited significant preservation of left ventricular geometry and contractile performance during 28 days follow-up. Within an hour after reperfusion, exosome treatment increased levels of ATP and NADH, decreased oxidative stress, increased phosphorylated-Akt and phosphorylated-GSK-3β, and reduced phosphorylated-c-JNK in ischemic/reperfused hearts. Subsequently, both local and systemic inflammation were significantly reduced 24h after reperfusion. In conclusion, our study shows that intact exosomes restore bioenergetics, reduce oxidative stress and activate pro-survival signaling, thereby enhancing cardiac function and geometry after myocardial I/R injury. Hence, mesenchymal stem cell-derived exosomes are a potential adjuvant to reperfusion therapy for myocardial infarction. Copyright © 2013 Elsevier B.V. All rights reserved.

  20. Intracoronary Poloxamer 188 Prevents Reperfusion Injury in a Porcine Model of ST-Segment Elevation Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Jason A. Bartos, MD, PhD

    2016-06-01

    Full Text Available Poloxamer 188 (P188 is a nonionic triblock copolymer believed to prevent cellular injury after ischemia and reperfusion. This study compared intracoronary (IC infusion of P188 immediately after reperfusion with delayed infusion through a peripheral intravenous catheter in a porcine model of ST-segment elevation myocardial infarction (STEMI. STEMI was induced in 55 pigs using 45 min of endovascular coronary artery occlusion. Pigs were then randomized to 4 groups: control, immediate IC P188, delayed peripheral P188, and polyethylene glycol infusion. Heart tissue was collected after 4 h of reperfusion. Assessment of mitochondrial function or infarct size was performed. Mitochondrial yield improved significantly with IC P188 treatment compared with control animals (0.25% vs. 0.13%, suggesting improved mitochondrial morphology and survival. Mitochondrial respiration and calcium retention were also significantly improved with immediate IC P188 compared with control animals (complex I respiratory control index: 7.4 vs. 3.7; calcium retention: 1,152 nmol vs. 386 nmol. This benefit was only observed with activation of complex I of the mitochondrial respiratory chain, suggesting a specific effect from ischemia and reperfusion on this complex. Infarct size and serum troponin I were significantly reduced by immediate IC P188 infusion (infarct size: 13.9% vs. 41.1%; troponin I: 19.2 μg/l vs. 77.4 μg/l. Delayed P188 and polyethylene glycol infusion did not provide a significant benefit. These results demonstrate that intracoronary infusion of P188 immediately upon reperfusion significantly reduces cellular and mitochondrial injury after ischemia and reperfusion in this clinically relevant porcine model of STEMI. The timing and route of delivery were critical to achieve the benefit.

  1. Effect of acute alloxan diabetes on ischemic and reperfusion arrhythmias in rats with different activity of nitric oxide system.

    Science.gov (United States)

    Belkina, L M; Terekhina, O L; Smirnova, E A; Usacheva, M A; Kruglov, S V; Saltykova, V A

    2011-01-01

    Similar degree of glycemia (28-31 mmol/liter) and similar mortality (37-42%) were revealed in August rats exhibiting enhanced activity of NO system and in Wistar rats 3 weeks after alloxan treatment. Under conditions of myocardial ischemia caused by 10-min coronary artery ligation, the intensity of arrhythmias did not differ from the control in Wistar rats with diabetes mellitus and increased in August rats. Under conditions of reperfusion, diabetes produced an antiarrhythmic effect in Wistar rats and did not affect arrhythmia in August rats. Plasma concentrations of nitrates and nitrites in Wistar and August rats increased by 82 and 143%, respectively, compared to the control. The level of hemoxygenase-1 (hsp32) in the myocardium remained unchanged in Wistar rats and decreased by 26% in August rats. Thus, the absence of antiarrhythmic effect of acute diabetes in August rats is probably related to elevated NO content and reduced antioxidant activity.

  2. Aeromedical transport after acute myocardial infarction

    DEFF Research Database (Denmark)

    Seidelin, Jakob B; Bruun, Niels Eske; Nielsen, Henrik

    2009-01-01

    BACKGROUND: No guidelines exist for the planning of aeromedical repatriation after acute myocardial infarction (AMI). In 2004, we employed a risk evaluation-based decision-making system for repatriation of patients after AMI. The objective was to evaluate the safety of transports during 2005...... managed by this system. METHODS: A total of 116 patients were transported according to the algorithm, 64 unescorted and 52 escorted. The decision-making system was based on the recommendations given by the European Society of Cardiology. Whenever possible, patients were evaluated by coronary angiogram...... of death of any cause during transport or departure from the planned repatriation due to worsening of the condition was registered. RESULTS: No patients reached the end point. Patients who were not risk evaluated more often needed escort (p

  3. Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction.

    Science.gov (United States)

    Hall, A R; Burke, N; Dongworth, R K; Kalkhoran, S B; Dyson, A; Vicencio, J M; Dorn, G W; Yellon, D M; Hausenloy, D J

    2016-05-26

    Mitochondria alter their shape by undergoing cycles of fusion and fission. Changes in mitochondrial morphology impact on the cellular response to stress, and their interactions with other organelles such as the sarcoplasmic reticulum (SR). Inhibiting mitochondrial fission can protect the heart against acute ischemia/reperfusion (I/R) injury. However, the role of the mitochondrial fusion proteins, Mfn1 and Mfn2, in the response of the adult heart to acute I/R injury is not clear, and is investigated in this study. To determine the effect of combined Mfn1/Mfn2 ablation on the susceptibility to acute myocardial I/R injury, cardiac-specific ablation of both Mfn1 and Mfn2 (DKO) was initiated in mice aged 4-6 weeks, leading to knockout of both these proteins in 8-10-week-old animals. This resulted in fragmented mitochondria (electron microscopy), decreased mitochondrial respiratory function (respirometry), and impaired myocardial contractile function (echocardiography). In DKO mice subjected to in vivo regional myocardial ischemia (30 min) followed by 24 h reperfusion, myocardial infarct size (IS, expressed as a % of the area-at-risk) was reduced by 46% compared with wild-type (WT) hearts. In addition, mitochondria from DKO animals had decreased MPTP opening susceptibility (assessed by Ca(2+)-induced mitochondrial swelling), compared with WT hearts. Mfn2 is a key mediator of mitochondrial/SR tethering, and accordingly, the loss of Mfn2 in DKO hearts reduced the number of interactions measured between these organelles (quantified by proximal ligation assay), attenuated mitochondrial calcium overload (Rhod2 confocal microscopy), and decreased reactive oxygen species production (DCF confocal microscopy) in response to acute I/R injury. No differences in isolated mitochondrial ROS emissions (Amplex Red) were detected in response to Ca(2+) and Antimycin A, further implicating disruption of mitochondria/SR tethering as the protective mechanism. In summary, despite apparent

  4. Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway

    Energy Technology Data Exchange (ETDEWEB)

    Wang, Y.; Zhang, Z.Z.; Wu, Y.; Ke, J.J.; He, X.H.; Wang, Y.L. [Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Wuhan (China)

    2013-09-24

    Quercetin (Que), a plant-derived flavonoid, has multiple benefical actions on the cardiovascular system. The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R) injury in vivo and its potential cardioprotective mechanisms. Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group): sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. At the end of reperfusion, myocardial infarct size and biochemical changes were compared. Apoptosis was evaluated by both TUNEL staining and measurement of activated caspase-3 immunoreactivity. The phosphorylation of Akt and protein expression of Bcl-2 and Bax were determined by Western blotting. Que postconditioning significantly reduced infarct size and serum levels of creatine kinase and lactate dehydrogenase compared with the I/R group (all P<0.05). Apoptotic cardiomyocytes and caspase-3 immunoreactivity were also suppressed in the Que postconditioning group compared with the I/R group (both P<0.05). Akt phosphorylation and Bcl-2 expression increased after Que postconditioning, but Bax expression decreased. These effects were inhibited by LY294002. The data indicate that Que postconditioning can induce cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.

  5. Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway

    Directory of Open Access Journals (Sweden)

    Y. Wang

    2013-09-01

    Full Text Available Quercetin (Que, a plant-derived flavonoid, has multiple benefical actions on the cardiovascular system. The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R injury in vivo and its potential cardioprotective mechanisms. Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group: sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. At the end of reperfusion, myocardial infarct size and biochemical changes were compared. Apoptosis was evaluated by both TUNEL staining and measurement of activated caspase-3 immunoreactivity. The phosphorylation of Akt and protein expression of Bcl-2 and Bax were determined by Western blotting. Que postconditioning significantly reduced infarct size and serum levels of creatine kinase and lactate dehydrogenase compared with the I/R group (all P<0.05. Apoptotic cardiomyocytes and caspase-3 immunoreactivity were also suppressed in the Que postconditioning group compared with the I/R group (both P<0.05. Akt phosphorylation and Bcl-2 expression increased after Que postconditioning, but Bax expression decreased. These effects were inhibited by LY294002. The data indicate that Que postconditioning can induce cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.

  6. The effect of collateral flow and myocardial viability on the distribution of technetium-99m sestamibi in a closed-chest model of coronary occlusion and reperfusion

    International Nuclear Information System (INIS)

    Chareonthaitawee, P.; O'Connor, M.K.; Gibbons, R.J.; Christian, T.F.; Ritman, E.L.

    2000-01-01

    The objective of this study was to determine the effect of myocardial viability and the degree of collateral blood flow on the uptake and retention of 99m Tc-sestamibi by examining three animal models of coronary occlusion and reperfusion, each reflecting a different state of viability and collateral blood flow. Three closed-chest animal models were studied: canine (high collateral flow, preserved viability), porcine (low collateral flow, absent viability) and porcine with slowly occlusive coronary stents producing infarction and enhanced collateral blood flow (high collateral flow, absent viability). There were seven dogs, seven pigs and six pigs, respectively, in each animal model. Animals from all three models were subjected to a 40-min total left anterior descending artery (LAD) occlusion followed by 2 h of reperfusion. 99m Tc-sestamibi and radiolabelled microspheres were injected during LAD occlusion 10 min prior to reperfusion. Animals were sacrificed after 2 h of reperfusion flow. Ex situ heart slice imaging to determine risk area was followed by viability staining to determine infarct size. Slices were subsequently sectioned into equally sized radial segments and placed in a gamma well counter. Risk area as determined by ex situ 99m Tc-sestamibi imaging was not significantly different by model. Pathological infarct size differed significantly by model [canine = 1%±1% of the left ventricle (LV); porcine = 13%±8% LV; porcine with stent = 14%±7% LV; P=0.002]. Collateral blood flow by microspheres during occlusion tended to differ among models (overall P=0.08), with the canine and porcine with stent models having relatively high flow rates compared with the acute porcine model. 99m Tc-sestamibi activity correlated with microsphere blood flow in all three models, with r values for individual animals (n=20) ranging from 0.86 to 0.96 (all P 99m Tc-sestamibi uptake with myocardial blood flow. 99m Tc-sestamibi uptake overestimated blood flow to a greater extent

  7. [Significance of acute-phase inflammatory reactants as an indicator of prognosis after acute myocardial infarction: which is the most useful predictor?].

    Science.gov (United States)

    Katayama, Toshiro; Nakashima, Hiroshi; Yonekura, Tsuyoshi; Honda, Yukiharu; Suzuki, Shin; Yano, Katsusuke

    2003-08-01

    To investigate the relationship between representative acute-phase inflammatory reactants [highly sensitive C-reactive protein (hsCRP), serum amyloid A protein (SAA) and interleukin-6 (IL-6)] and the severity of acute myocardial infarction and patient prognosis, and to identify the most useful predictor of the three. This study investigated 132 consecutive patients admitted within 8 hr of onset of first acute myocardial infarction and successfully reperfused with primary percutaneous coronary intervention. Acute-phase (= 24 hr from onset) blood samples were taken for evaluation of inflammatory reactants (hsCRP, SAA and IL-6), and peak creatine phosphokinase levels were measured every 4 hr after admission for 48 hr to assess myocardial infarction infarct size. Left ventriculography was performed in the chronic stage (20 +/- 9 days post-admission) to analyze left ventricular ejection fraction and regional wall motion, using Killip's classification to determine acute myocardial infarction severity. Logistic regression analysis was used to quantify the usefulness of the reactants as predictors of patient prognosis. Both hsCRP and SAA showed significant positive correlations with peak creatine phosphokinase. hsCRP and SAA showed significant inverse correlations with left ventricular ejection fraction and regional wall motion in the chronic stage. Multivariate analysis identified SAA as the best predictor of severe heart failure (Killip's classification III, IV). SAA was the best predictor of a major cardiac event (shock, cardiac death). These results suggest a strong correlation between acute-phase SAA and the clinical course of patient outcomes after acute myocardial infarction, such as cardiac function, heart failure and cardiac death. SAA may be the most useful acute-phase inflammatory reactant for predicting the prognosis after acute myocardial infarction.

  8. Detection of Myocardial Ischemia-Reperfusion Injury Using a Fluorescent Near-Infrared Zinc(II-Dipicolylamine Probe and 99mTc Glucarate

    Directory of Open Access Journals (Sweden)

    Leonie wyffels

    2012-05-01

    Full Text Available A fluorescent zinc 2,2′-dipicolylamine coordination complex PSVue®794 (probe 1 is known to selectively bind to phosphatidylserine exposed on the surface of apoptotic and necrotic cells. In this study, we investigated the cell death targeting properties of probe 1 in myocardial ischemia-reperfusion injury. A rat heart model of ischemia-reperfusion was used. Probe 1, control dye, or 99mTc glucarate was intravenously injected in rats subjected to 30-minute and 5-minute myocardial ischemia followed by 2-hour reperfusion. At 90 minutes or 20 hours postinjection, myocardial uptake was evaluated ex vivo by fluorescence imaging and autoradiography. Hematoxylin-eosin and cleaved caspase-3 staining was performed on myocardial sections to demonstrate the presence of ischemia-reperfusion injury and apoptosis. Selective accumulation of probe 1 could be detected in the area at risk up to 20 hours postinjection. Similar topography and extent of uptake of probe 1 and 99mTc glucarate were observed at 90 minutes postinjection. Histologic analysis demonstrated the presence of necrosis, but only a few apoptotic cells could be detected. Probe 1 selectively accumulates in myocardial ischemia-reperfusion injury and is a promising cell death imaging tool.

  9. Role of β-adrenergic modulation in myocardial ischemia/reperfusion injury. Mechanisms underlying cardioprotection

    OpenAIRE

    García-Prieto Cuesta, Jaime

    2017-01-01

    Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Bioquímica. Fecha de lectura: 18-12-2017 The β-adrenergic system plays an important role in the regulation of heart function. The early intravenous administration of ß1-adrenergic receptor (ADRB1)-antagonist, metoprolol, in patients with ST-segment elevation acute myocardial infarction (AMI) reduces the extent of infarct size. The prevailing view has been that metoprolol act...

  10. Correlation of acute myocardial infarct scintigraphy with postmortem studies

    International Nuclear Information System (INIS)

    Holman, L.; Ehrie, M.; Lesch, M.

    1976-01-01

    Acute myocardial infarct scintigraphy with technetium-99m-pyrophosphate was performed in a patient with an acute massive transmural infarct. The patient died 12 hours later, and postmortem tracer studies demonstrated a tracer concentration ratio of 13:1 between acutely infarcted myocardium and normal myocardium remote from the infarct. The concentration of tracer in tissue bordering on the infarct but without histologic evidence of acute infarction was 1.5 times that in normal tissue remote from the infarct. In vitro scintigraphy of the excised heart revealed a pattern of tracer distribution similar to that of scintiscans obtained before death. The biologic distribution of /sup 99m/Tc-pyrophosphate, with large tracer concentrations only within the acutely infarcted tissued, suggests that acute myocardial infarct scintigraphy can be used to estimate the extent of an acute myocardial infarct

  11. Downregulation of adiponectin induced by tumor necrosis factor α is involved in the aggravation of posttraumatic myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Liu, Shaowei; Yin, Tao; Wei, Xufeng; Yi, Wei; Qu, Yan; Liu, Yi; Wang, Rutao; Lian, Kun; Xia, Chenhai; Pei, Haifeng; Sun, Lu; Ma, Yanzhuo; Lau, Wayne Bond; Gao, Erhe; Koch, Walter J; Wang, Haichang; Tao, Ling

    2011-08-01

    Recent clinical observations have indicated that nonlethal mechanical trauma significantly increases myocardial infarction risk even in the presence of completely normal coronary arteries. We investigated the molecular mechanisms responsible for exacerbation of ischemic myocardial injury after nonlethal mechanical trauma with a special focus on the role of tumor necrosis factor α and its potential downstream effector adiponectin, a novel adipokine with anti-inflammatory and cardioprotective properties. Laboratory study. University research unit. Male adult adiponectin knockout mice and wild-type mice. The animals were subjected to nonlethal mechanical trauma using the Noble-Collip drum (40 rpm ± 5 mins) followed by myocardial ischemia/reperfusion injury 7 days posttrauma. We also investigated the effects of neutralizing tumor necrosis factor α with etanercept and exogenous adiponectin supplementation on ischemic myocardial injury after trauma. Trauma significantly sensitized myocardium to ischemia/reperfusion injury as evidenced by increased apoptosis, enlarged infarct size, and decreased cardiac function. Plasma adiponectin concentrations were reduced after traumatic injury (the nadir occurring 3 days posttrauma), an effect abrogated by etanercept-mediated tumor necrosis factor α blockade. The downregulation of adiponectin was accompanied by increased myocardial superoxide and nitric oxide generation and peroxynitrite formation. Both etanercept and exogenous adiponectin supplementation (on day 3 posttrauma or 10 mins before reperfusion on day 7 posttrauma) markedly inhibited oxidative/nitrative stress and ischemia/reperfusion injury in posttraumatic ischemic/reperfused hearts of wild-type mice, whereas only adiponectin supplementation (but not tumor necrosis factor α inhibition) substantially attenuated posttraumatic ischemia/reperfusion injury in adiponectin knockout mice. Tumor necrosis factor α-induced downregulation of adiponectin and the resultant

  12. Value of the Doppler index of myocardial performance in the early phase of acute myocardial infarction

    DEFF Research Database (Denmark)

    Poulsen, S H; Jensen, S E; Tei, C

    2000-01-01

    Prospective assessment of a nongeometric Doppler-derived index of combined systolic and diastolic myocardial performance was performed in 64 patients with acute myocardial infarction (MI) within 1 hour after their arrival to the hospital and in 39 age-matched healthy subjects. The index is defined...

  13. Effect of thrombolysis (streptokinase) on left ventricular function during acute myocardial infarction.

    Science.gov (United States)

    Valentine, R P; Pitts, D E; Brooks-Brunn, J A; Woods, J; Nyhuis, A; Van Hove, E; Schmidt, P E

    1986-11-01

    One hundred ninety-two consecutive patients with acute myocardial infarction were enrolled in a prospective trial of coronary thrombolysis in which either intracoronary or intravenous streptokinase was administered. First-pass radionuclide ejection fraction (EF) was measured early (within 24 hours of admission) and late (10 to 14 days after admission) to assess changes in left ventricular (LV) function. In 68 patients in whom reperfusion was successful, mean EF increased from 39 +/- 11% early to 47 +/- 13% late. In 36 patients in whom reperfusion was not successful, the mean EF increase was significantly smaller (from 38 +/- 10% to 42 +/- 11%, p less than 0.025). Patients in whom reperfusion was successful were then grouped according to extent of LV functional change. The extent of EF change (delta EF) was not significantly influenced by time to lysis at intervals up to 7 hours (delta EF = 9.1 +/- 10% at 2 to 3 hours, 8.7 +/- 12% at 3 to 4 hours, 10 +/- 10% at 4 to 5 hours, and 7.0 +/- 10% at 5 to 7 hours; difference not significant [NS]), location of the infarct (delta EF = 8.9 +/- 11% for inferior and 5.7 +/- 8.0% for anterior, NS), or presence of Q waves on the initial electrocardiogram (delta EF = 8.8 +/- 11% in patients with and 7.8 +/- 9.9% in patients without Q waves). Only the initial EF was predictive of subsequent EF change.(ABSTRACT TRUNCATED AT 250 WORDS)

  14. Acute myocardial infarction in middle-aged male Nigerian with ...

    African Journals Online (AJOL)

    ... are associated with accelerated atherosclerosis. The relationship between pemphigus vulgaris and myocardial infarction is not clear. This report highlights the presentation and management of myocardial infarction and the possible relationship of acute coronary events with autoimmune disease and chronic steroid use.

  15. ROS-mediated PARP activity undermines mitochondrial function after permeability transition pore opening during myocardial ischemia-reperfusion.

    Science.gov (United States)

    Schriewer, Jacqueline M; Peek, Clara Bien; Bass, Joseph; Schumacker, Paul T

    2013-04-18

    Ischemia-reperfusion (I/R) studies have implicated oxidant stress, the mitochondrial permeability transition pore (mPTP), and poly(ADP-ribose) polymerase (PARP) as contributing factors in myocardial cell death. However, the interdependence of these factors in the intact, blood-perfused heart is not known. We therefore wanted to determine whether oxidant stress, mPTP opening, and PARP activity contribute to the same death pathway after myocardial I/R. A murine left anterior descending coronary artery (LAD) occlusion (30 minutes) and release (1 to 4 hours) model was employed. Experimental groups included controls and antioxidant-treated, mPTP-inhibited, or PARP-inhibited hearts. Antioxidant treatment prevented oxidative damage, mPTP opening, ATP depletion, and PARP activity, placing oxidant stress as the proximal death trigger. Genetic deletion of cyclophilin D (CypD(-/-)) prevented loss of total NAD(+) and PARP activity, and mPTP-mediated loss of mitochondrial function. Control hearts showed progressive mitochondrial depolarization and loss of ATP from 1.5 to 4 hours of reperfusion, but not outer mitochondrial membrane rupture. Neither genetic deletion of PARP-1 nor its pharmacological inhibition prevented the initial mPTP-mediated depolarization or loss of ATP, but PARP ablation did allow mitochondrial recovery by 4 hours of reperfusion. These results indicate that oxidant stress, the mPTP, and PARP activity contribute to a single death pathway after I/R in the heart. PARP activation undermines cell survival by preventing mitochondrial recovery after mPTP opening early in reperfusion. This suggests that PARP-mediated prolongation of mitochondrial depolarization contributes significantly to cell death via an energetic crisis rather than by mitochondrial outer membrane rupture.

  16. Acute aortic dissection mimics acute inferoposterior wall myocardial infarction in a Marfan syndrome patient.

    Science.gov (United States)

    Phowthongkum, Prasit

    2010-01-01

    A 30-year old man with acute chest pain was diagnosed with acute inferoposterior wall myocardial infarction following electrocardiography. After a failed coronary angiography, an echocardiogram revealed an aortic intimal flap after which acute aortic dissection was diagnosed. The patient received a successful Bentall operation without immediate complication. Retrospective examination then confirmed the diagnosis of Marfan syndrome. This case demonstrates acute aortic dissection may mimic acute myocardial infarction.

  17. Pharmacodynamic interaction of green tea extract with hydrochlorothiazide against ischemia-reperfusion injury-induced myocardial infarction

    Directory of Open Access Journals (Sweden)

    Manodeep Chakraborty

    2014-01-01

    Full Text Available Globally, the rate of development of myocardial diseases and hypertension is very common, which is responsible for incremental morbidity and mortality statistics. Treatment of ischemic hypertensive patients with diuretics such as hydrochlorothiazide (HCTZ can precipitate myocardial infarction due to hypokalemia. This study was undertaken to evaluate the pharmacodynamic interaction of green tea extract (GTE with HCTZ against ischemia-reperfusion induced myocardial toxicity. Wistar albino rats of either sex were taken and pretreated with high (500 mg/kg, p.o. and low (100 mg/kg, p.o. dose of GTE for 30 days. Standard, high and low dose of interactive groups received HCTZ (10 mg/kg, p.o. for last 7 days. Ischemia-reperfusion injury was induced by modified Lagendorff apparatus, and the effect of different treatments was evaluated by percentage recovery in terms of heart rate and developed tension, serum biomarkers, and heart tissue antioxidant levels. Prophylactic treatment groups, such as high and low dose of GTE and their interactive groups with HCTZ, exhibited significant percentage recovery in terms of heart rate and developed tension. Apart from that, significant increase in superoxide dismutase and catalase, decrease in thiobarbituric acid reactive species in heart tissue, as well as significant decrease in serum lactate dehydrogenase, creatinine phosphokinase-MB and N-acetylcysteine levels have also been documented. The present findings clearly suggest that GTE dose-dependently reduces myocardial toxicity due to ischemia, and combination with HCTZ can reduce the associated side-effects and exhibits myocardial protection.

  18. [Acute myocardial infarct caused by nicotine-induced erythrocytosis].

    Science.gov (United States)

    Andreas, S; Herrmann, K S; Kreuzer, H; Wiegand, V

    1989-10-02

    A 29-year-old heavy smoker presented with an acute myocardial infarction and hematocrit of 70%. At immediate coronary angiography a complete occlusion of the right coronary artery was found. After intracoronary urokinase the coronary arteries were found to be completely normal. Causes for the erythrocytosis other than smoking could be excluded. We conclude that thrombotic coronary occlusion with acute myocardial infarction was caused by erythrocytosis due to heavy smoking.

  19. The role of muscarinic receptors in the beneficial effects of adenosine against myocardial reperfusion injury in rats.

    Directory of Open Access Journals (Sweden)

    Lei Sun

    Full Text Available Adenosine, a catabolite of ATP, displays a wide variety of effects in the heart including regulation of cardiac response to myocardial ischemia and reperfusion injury. Nonetheless, the precise mechanism of adenosine-induced cardioprotection is still elusive. Isolated Sprague-Dawley rat hearts underwent 30 min global ischemia and 120 min reperfusion using a Langendorff apparatus. Both adenosine and acetylcholine treatment recovered the post-reperfusion cardiac function associated with adenosine and muscarinic receptors activation. Simultaneous administration of adenosine and acetylcholine failed to exert any additive protective effect, suggesting a shared mechanism between the two. Our data further revealed a cross-talk between the adenosine and acetylcholine receptor signaling in reperfused rat hearts. Interestingly, the selective M(2 muscarinic acetylcholine receptor antagonist methoctramine significantly attenuated the cardioprotective effect of adenosine. In addition, treatment with adenosine upregulated the expression and the maximal binding capacity of muscarinic acetylcholine receptor, which were inhibited by the selective A(1 adenosine receptor antagonist 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX and the nitric oxide synthase inhibitor N(ω-nitro-L-arginine methyl ester (L-NAME. These data suggested a possible functional coupling between the adenosine and muscarinic receptors behind the observed cardioprotection. Furthermore, nitric oxide was found involved in triggering the response to each of the two receptor agonist. In summary, there may be a cross-talk between the adenosine and muscarinic receptors in ischemic/reperfused myocardium with nitric oxide synthase might serve as the distal converging point. In addition, adenosine contributes to the invigorating effect of adenosine on muscarinic receptor thereby prompting to regulation of cardiac function. These findings argue for a potentially novel mechanism behind the adenosine

  20. Effect of postconditioning on dynamic expression of tenascin-C and left ventricular remodeling after myocardial ischemia and reperfusion.

    Science.gov (United States)

    Taki, Junichi; Inaki, Anri; Wakabayashi, Hiroshi; Matsunari, Ichiro; Imanaka-Yoshida, Kyoko; Ogawa, Kazuma; Hiroe, Michiaki; Shiba, Kazuhiro; Yoshida, Toshimichi; Kinuya, Seigo

    2015-01-01

    Tenascin-C (TNC), an extracellular matrix glycoprotein, is expressed transiently in distinct areas in association with active tissue remodeling. This study aimed to explore how ischemic postconditioning (PC) affects myocardial expression of TNC and ventricular remodeling using (125)I-labeled anti-TNC antibody ((125)I-TNC-Ab) in a rat model of ischemia and reperfusion. In control rats (n = 27), the left coronary artery (LCA) was occluded for 30 min followed by reperfusion for 1, 3, 7, and 14 days. PC (n = 27) was performed just after the reperfusion. At the time of the study, (125)I-TNC-Ab (1.0 to 2.5 MBq) was injected. Six to 9 h later, to verify the area at risk, (99m)Tc-MIBI (100 to 200 MBq) was injected intravenously just after the LCA reocclusion, with the rats sacrificed 1 min later. Dual tracer autoradiography was performed to assess (125)I-TNC-Ab uptake and area at risk. To examine the ventricular remodeling, echocardiography was performed 2 M after reperfusion in both groups. In control rats, (125)I-TNC-Ab uptake ratio at 1 day after reperfusion was 3.73 ± 0.71 and increased at 3 days (4.65 ± 0.87), followed by a significant reduction at 7 days (2.91 ± 0.55, P injury, the subsequent repair process, and its response to novel therapeutic interventions like PC by visualizing TNC expression.

  1. Evaluation by contrast-enhanced MR imaging of the lateral border zone in reperfused myocardial infarction in a cat model

    International Nuclear Information System (INIS)

    Jeong, Ae Kyung; Choi, Sang Il; Kim, Dong Hun; Park, Sung Bin; Lee, Seoung Soo; Choi, Seong Hoon; Lim, Tae Hwan

    2000-01-01

    To identify and evaluate the lateral border zone by comparing the size and distribution of the abnormal signal area demonstrated by MR imaging with the infarct area revealed by pathological examination in a reperfused myocardial infarction cat model. In eight cats, the left anterior descending coronary artery was occluded for 90 minutes, and this was followed by 90 minutes of reperfusion. ECG-triggered breath-hold turbo spin-echo T2-weighted MR images were initially obtained along the short axis of the heart before the administration of contrast media. After the injection of Gadomer-17 and Gadophrin-2, contrastenhanced T1-weighted MR images were obtained for three hours. The size of the abnormal signal area seen on each image was compared with that of the infarct area after TTC staining. To assess ultrastructural changes in the myocardium at the infarct area, lateral border zone and normal myocardium, electron microscopic examination was performed. The high signal area seen on T2-weighted images and the enhanced area seen on Gadomer-17-enhanced T1WI were larger than the enhanced area on Gadophrin-2-enhanced T1WI and the infarct area revealed by TTC staining; the difference was expressed as a percentage of the size of the total left ventricle mass (T2= 39.2 %; Gadomer-17 =37.25 % vs Gadophrin-2 = 29.6 %; TTC staining = 28.2 %; p < 0.05). The ultrastructural changes seen at the lateral border zone were compatible with reversible myocardial damage. In a reperfused myocardial infarction cat model, the presence and size of the lateral border zone can be determined by means of Gadomer-17- and Gadophrin-2-enhanced MR imaging

  2. Educational Level and Long-term Mortality in Patients With Acute Myocardial Infarction.

    Science.gov (United States)

    Consuegra-Sánchez, Luciano; Melgarejo-Moreno, Antonio; Galcerá-Tomás, José; Alonso-Fernández, Nuria; Díaz-Pastor, Ángela; Escudero-García, Germán; Jaulent-Huertas, Leticia; Vicente-Gilabert, Marta

    2015-11-01

    The value of socioeconomic status as a prognostic marker in acute myocardial infarction is controversial. The aim of this study was to evaluate the impact of educational level, as a marker of socioeconomic status, on the prognosis of long-term survival after acute myocardial infarction. We conducted a prospective, observational study of 5797 patients admitted to hospital with acute myocardial infarction. We studied long-term all-cause mortality (median 8.5 years) using adjusted regression models. We found that 73.1% of patients had primary school education (n=4240), 14.5% had secondary school education (including high school) (n=843), 7.0% was illiterate (n=407), and 5.3% had higher education (n=307). Patients with secondary school or higher education were significantly younger, more were male, and they had fewer risk factors and comorbidity. These patients arrived sooner at hospital and had less severe heart failure. During admission they received more reperfusion therapy and their crude mortality was lower. Their drug treatment in hospital and at discharge followed guideline recommendations more closely. On multivariate analysis, secondary school or higher education was an independent predictor and protective factor for long-term mortality (hazard ratio=0.85; 95% confidence interval, 0.74-0.98). Our study shows an inverse and independent relationship between educational level and long-term mortality in patients with acute myocardial infarction. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  3. Suboptimal medical care of patients with ST-elevation myocardial infarction and renal insufficiency: results from the Korea Acute Myocardial Infarction Registry.

    Science.gov (United States)

    Choi, Joon Seok; Kim, Chang Seong; Bae, Eun Hui; Ma, Seong Kwon; Jeong, Myung Ho; Kim, Young Jo; Cho, Myeong Chan; Kim, Chong Jin; Kim, Soo Wan

    2012-09-11

    The clinical outcomes of ST-segment elevation myocardial infarction (STEMI) are poor in patients with renal insufficiency. This study investigated changes in the likelihood that patients received optimal medical care throughout the entire process of myocardial infarction management, on the basis of their glomerular filtration rate (GFR). This study analyzed 7,679 patients (age, 63 ± 13 years; men 73.6%) who had STEMI and were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR) from November 2005 to August 2008. The study subjects were divided into 5 groups corresponding to strata used to define chronic kidney disease stages. Patients with lower GFR were less likely to present with typical chest pain. The average symptom-to-door time, door-to-balloon time, and symptom-to-balloon time were longer with lower GFR than higher GFR. Primary reperfusion therapy was performed less frequently and the results of reperfusion therapy were poorer in patients with renal insufficiency; these patients were less likely to receive adjunctive medical treatment, such as treatment with aspirin, clopidogrel, β-blocker, angiotensin-converting enzyme (ACE) inhibitor/angiotensin-receptor blocker (ARB), or statin, during hospitalization and at discharge. Patients who received less intense medical therapy had worse clinical outcomes than those who received more intense medical therapy. Patients with STEMI and renal insufficiency had less chance of receiving optimal medical care throughout the entire process of MI management, which may contribute to worse outcomes in these patients.

  4. Hyperintense acute reperfusion marker is associated with higher contrast agent dosage in acute ischaemic stroke

    International Nuclear Information System (INIS)

    Ostwaldt, Ann-Christin; Schaefer, Tabea; Villringer, Kersten; Fiebach, Jochen B.; Rozanski, Michal; Ebinger, Martin; Jungehuelsing, Gerhard J.

    2015-01-01

    The hyperintense acute reperfusion marker (HARM) on fluid-attenuated inversion recovery (FLAIR) images is associated with blood-brain barrier (BBB) permeability changes. The aim of this study was to examine the influence of contrast agent dosage on HARM incidence in acute ischaemic stroke patients. We prospectively included 529 acute ischaemic stroke patients (204 females, median age 71 years). Patients underwent a first stroke-MRI within 24 hours from symptom onset and had a follow-up on day 2. The contrast agent Gadobutrol was administered to the patients for perfusion imaging or MR angiography. The total dosage was calculated as ml/kg body weight and ranged between 0.04 and 0.31 mmol/kg on the first examination. The incidence of HARM was evaluated on day 2 FLAIR images. HARM was detected in 97 patients (18.3 %). HARM incidence increased significantly with increasing dosages of Gadobutrol. Also, HARM positive patients were significantly older. HARM was not an independent predictor of worse clinical outcome, and we did not find an association with increase risk of haemorrhagic transformation. A higher dosage of Gadobutrol in acute stroke patients on initial MRI is associated with increased HARM incidence on follow-up. MRI studies on BBB should therefore standardize contrast agent dosages. (orig.)

  5. Hyperintense acute reperfusion marker is associated with higher contrast agent dosage in acute ischaemic stroke

    Energy Technology Data Exchange (ETDEWEB)

    Ostwaldt, Ann-Christin; Schaefer, Tabea; Villringer, Kersten; Fiebach, Jochen B. [Charite Universitaetsmedizin Berlin, Academic Neuroradiology, Center for Stroke Research Berlin (CSB), Berlin (Germany); Rozanski, Michal; Ebinger, Martin [Charite Universitaetsmedizin Berlin, Academic Neuroradiology, Center for Stroke Research Berlin (CSB), Berlin (Germany); Charite Universitaetsmedizin, Department of Neurology, Berlin (Germany); Jungehuelsing, Gerhard J. [Stiftung des Buergerlichen Rechts, Juedisches Krankenhaus Berlin, Berlin (Germany)

    2015-11-15

    The hyperintense acute reperfusion marker (HARM) on fluid-attenuated inversion recovery (FLAIR) images is associated with blood-brain barrier (BBB) permeability changes. The aim of this study was to examine the influence of contrast agent dosage on HARM incidence in acute ischaemic stroke patients. We prospectively included 529 acute ischaemic stroke patients (204 females, median age 71 years). Patients underwent a first stroke-MRI within 24 hours from symptom onset and had a follow-up on day 2. The contrast agent Gadobutrol was administered to the patients for perfusion imaging or MR angiography. The total dosage was calculated as ml/kg body weight and ranged between 0.04 and 0.31 mmol/kg on the first examination. The incidence of HARM was evaluated on day 2 FLAIR images. HARM was detected in 97 patients (18.3 %). HARM incidence increased significantly with increasing dosages of Gadobutrol. Also, HARM positive patients were significantly older. HARM was not an independent predictor of worse clinical outcome, and we did not find an association with increase risk of haemorrhagic transformation. A higher dosage of Gadobutrol in acute stroke patients on initial MRI is associated with increased HARM incidence on follow-up. MRI studies on BBB should therefore standardize contrast agent dosages. (orig.)

  6. Does overprotection cause cardiac invalidism after acute myocardial infarction?

    Science.gov (United States)

    Riegel, B J; Dracup, K A

    1992-01-01

    To determine if overprotection on the part of the patient's family and friends contributes to the development of cardiac invalidism after acute myocardial infarction. Longitudinal survey. Nine hospitals in the southwestern United States. One hundred eleven patients who had experienced a first acute myocardial infarction. Subjects were predominantly male, older-aged, married, caucasian, and in functional class I. Eighty-one patients characterized themselves as being overprotected (i.e., receiving more social support from family and friends than desired), and 28 reported receiving inadequate support. Only two patients reported receiving as much support as they desired. Self-esteem, emotional distress, health perceptions, interpersonal dependency, return to work. Overprotected patients experienced less anxiety, depression, anger, confusion, more vigor, and higher self-esteem than inadequately supported patients 1 month after myocardial infarction (p Overprotection on the part of family and friends may facilitate psychosocial adjustment in the early months after an acute myocardial infarction rather than lead to cardiac invalidism.

  7. Experimental validation of contrast-enhanced SSFP cine CMR for quantification of myocardium at risk in acute myocardial infarction.

    Science.gov (United States)

    Nordlund, David; Kanski, Mikael; Jablonowski, Robert; Koul, Sasha; Erlinge, David; Carlsson, Marcus; Engblom, Henrik; Aletras, Anthony H; Arheden, Håkan

    2017-01-30

    Accurate assessment of myocardium at risk (MaR) after acute myocardial infarction (AMI) is necessary when assessing myocardial salvage. Contrast-enhanced steady-state free precession (CE-SSFP) is a recently developed cardiovascular magnetic resonance (CMR) method for assessment of MaR up to 1 week after AMI. Our aim was to validate CE-SSFP for determination of MaR in an experimental porcine model using myocardial perfusion single-photon emission computed tomography (MPS) as a reference standard and to test the stability of MaR-quantification over time after injecting gadolinium-based contrast. Eleven pigs were subjected to either 35 or 40 min occlusion of the left anterior descending artery followed by six hours of reperfusion. A technetium-based perfusion tracer was administered intravenously ten minutes before reperfusion. In-vivo and ex-vivo CE-SSFP CMR was performed followed by ex-vivo MPS imaging. MaR was expressed as % of left ventricular mass (LVM). There was good agreement between MaR by ex-vivo CMR and MaR by MPS (bias: 1 ± 3% LVM, r 2  = 0.92, p myocardial salvage in experimental studies.

  8. Activation of ALDH2 with Low Concentration of Ethanol Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetes Rat Model

    Directory of Open Access Journals (Sweden)

    Pin-Fang Kang

    2016-01-01

    Full Text Available The aim of this paper is to observe the change of mitochondrial aldehyde dehydrogenase 2 (ALDH2 when diabetes mellitus (DM rat heart was subjected to ischemia/reperfusion (I/R intervention and analyze its underlying mechanisms. DM rat hearts were subjected to 30 min regional ischemia and 120 min reperfusion in vitro and pretreated with ALDH2 activator ethanol (EtOH; cardiomyocyte in high glucose (HG condition was pretreated with ALDH2 activator Alda-1. In control I/R group, myocardial tissue structure collapse appeared. Compared with control I/R group, left ventricular parameters, SOD activity, the level of Bcl-2/Bax mRNA, ALDH2 mRNA, and protein expressions were decreased and LDH and MDA contents were increased, meanwhile the aggravation of myocardial structure injury in DM I/R group. When DM I/R rats were pretreated with EtOH, left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 expression were increased; LDH, MDA, and myocardial structure injury were attenuated. Compared with DM + EtOH I/R group, cyanamide (ALDH2 nonspecific blocker, atractyloside (mitoPTP opener, and wortmannin (PI3K inhibitor groups all decreased left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 and increased LDH, MDA, and myocardial injury. When cardiomyocyte was under HG condition, CCK-8 activity and ALDH2 protein expression were decreased. Alda-1 increased CCK-8 and ALDH2. Our findings suggested enhanced ALDH2 expression in diabetic I/R rats played the cardioprotective role, maybe through activating PI3K and inhibiting mitoPTP opening.

  9. Obestatin Accelerates the Recovery in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

    Directory of Open Access Journals (Sweden)

    Jakub Bukowczan

    Full Text Available Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of obestatin administration following the onset of experimental acute pancreatitis.The aim of this study was to evaluate the impact of obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of obestatin on daily food intake and pancreatic exocrine secretion.Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8 nmol/kg/dose was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula.Treatment with obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and

  10. Obestatin Accelerates the Recovery in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats

    Science.gov (United States)

    Bukowczan, Jakub; Warzecha, Zygmunt; Ceranowicz, Piotr; Kuśnierz-Cabala, Beata; Tomaszewska, Romana

    2015-01-01

    Objective Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of obestatin administration following the onset of experimental acute pancreatitis. Aim The aim of this study was to evaluate the impact of obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of obestatin on daily food intake and pancreatic exocrine secretion. Methods Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula. Results Treatment with obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food

  11. New Horizons of Acute Myocardial Infarction: From the Korea Acute Myocardial Infarction Registry

    Science.gov (United States)

    Lee, Ki Hong; Ahn, Youngkeun; Cho, Myeong Chan; Kim, Chong Jin; Kim, Young Jo

    2013-01-01

    As the first nationwide Korean prospective multicenter data collection registry, the Korea Acute Myocardial Infarction Registry (KAMIR) launched in November 2005. Through a number of innovative approaches, KAMIR suggested new horizons about acute myocardial infarction (AMI) which contains unique features of Asian patients from baseline characteristics to treatment strategy. Obesity paradox was existed in Korean AMI patients, whereas no gender differences among them. KAMIR score suggested new risk stratifying method with increased convenience and an enhanced accuracy for the prediction of adverse outcomes. Standard loading dose of clopidogrel was enough for Asian AMI patients. Triple antiplatelet therapy with aspirin, clopidogrel and cilostazol could improve clinical outcomes than dual antiplatelet therapy with aspirin and clopidogrel. Statin improved clinical outcomes even in AMI patients with very low LDL-C levels. The rate of percutaneous coronary intervention was higher and door-to-balloon time was shorter than the previous reports. Zotarolimus eluting stents as the 2nd generation drug-eluting stent (DES) was not superior to the 1st generation DES, in contrast to the western AMI studies. KAMIR made a cornerstone in the study of Korean AMI and expected to be new standards of care for AMI with the renewal of KAMIR design to overcome its pitfalls. PMID:23399991

  12. Src tyrosine kinase inhibition prevents pulmonary ischemia-reperfusion-induced acute lung injury.

    Science.gov (United States)

    Oyaizu, Takeshi; Fung, Shan-Yu; Shiozaki, Atsushi; Guan, Zehong; Zhang, Qiao; dos Santos, Claudia C; Han, Bing; Mura, Marco; Keshavjee, Shaf; Liu, Mingyao

    2012-05-01

    Pulmonary ischemia-reperfusion is a pathological process seen in several clinical conditions, including lung transplantation, cardiopulmonary bypass, resuscitation for circulatory arrest, atherosclerosis, and pulmonary embolism. A better understanding of its molecular mechanisms is very important. Rat left lung underwent in situ ischemia for 60 min, followed by 2 h of reperfusion. The gene expression profiles and Src protein tyrosine kinase (PTK) phosphorylation were studied over time, and PP2, an Src PTK inhibitor, was intravenously administered 10 min before lung ischemia to determine the role of Src PTK in lung injury. Reperfusion following ischemia significantly changed the expression of 169 genes, with Mmp8, Mmp9, S100a9, and S100a8 being the most upregulated genes. Ischemia alone only affected expression of 9 genes in the lung. However, Src PTK phosphorylation (activation) was increased in the ischemic lung, mainly on the alveolar wall. Src PTK inhibitor pretreatment decreased phosphorylation of Src PTKs, total protein tyrosine phosphorylation, and STAT3 phosphorylation. It increased phosphorylation of the p85α subunit of PI3 kinase, a signal pathway that can inhibit coagulation and inflammation. PP2 reduced leukocyte infiltration in the lung, apoptotic cell death, fibrin deposition, and severity of acute lung injury after reperfusion. Src inhibition also significantly reduced CXCL1 (GRO/KI) and CCL2 (MCP-1) chemokine levels in the serum. During pulmonary ischemia, Src PTK activation, rather than alteration in gene expression, may play a critical role in reperfusion-induced lung injury. Src PTK inhibition presents a new prophylactic treatment for pulmonary ischemia-reperfusion-induced acute lung injury.

  13. Left ventricular global longitudinal strain in acute myocardial infarction

    DEFF Research Database (Denmark)

    Ersbøll, Mads

    Systolic dysfunction, clinical heart failure and elevated levels of neurohormonal peptides are major predictors of adverse outcome after acute myocardial infarction (MI). In the present thesis we evaluated global longitudinal strain (GLS) in patients with acute MI in relation to neurohormonal...

  14. Effects of Antihypertensive, Hypolipidemic and Reperfusion Therapy on In-Hospital Mortality in Predominantly Hypertensive Patients with the First Myocardial Infarction (Fmi)

    Czech Academy of Sciences Publication Activity Database

    Peleška, Jan; Grünfeldová, H.; Reissigová, Jindra; Tomečková, Marie; Monhart, Z.; Ryšavá, D.; Velimský, T.; Ballek, L.; Hubač, J.

    2010-01-01

    Roč. 28, e-Supplement A (2010), e548 ISSN 0263-6352. [European Meeting on Hypertension /20./. 18.06.2010-21.06.2010, Oslo ] R&D Projects: GA MŠk(CZ) 1M06014 Institutional research plan: CEZ:AV0Z10300504 Keywords : in-hospital mortality for the first myocardial infarction * piloty registry of myocardial infarction * effects of pharmacotherapy and reperfusion therapy Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery

  15. Cardioprotective Effect of Licochalcone D against Myocardial Ischemia/Reperfusion Injury in Langendorff-Perfused Rat Hearts.

    Directory of Open Access Journals (Sweden)

    Xuan Yuan

    Full Text Available Flavonoids are important components of 'functional foods', with beneficial effects on cardiovascular function. The present study was designed to investigate whether licochalcone D (LD could be a cardioprotective agent in ischemia/reperfusion (I/R injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax, dp/dtmin, HR and CR and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size. Moreover, LD treatment reversed the I/R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS and reduced nitric oxide (NO production. The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury.

  16. Nifedipine for angina and acute myocardial ischemia

    NARCIS (Netherlands)

    P.G. Hugenholtz (Paul); J.W. de Jong (Jan Willem); P.D. Verdouw (Pieter); P.W.J.C. Serruys (Patrick)

    1983-01-01

    textabstractThis paper reviews the mechanisms believed to be responsible for myocardial ischaemia and the mode of action of calcium antagonist drugs. The clinical management of patients with myocardial ischaemia is discussed in the context of current knowledge about patho-physiology and drug action.

  17. Modulation of myocardial injury and collagen deposition following ischaemia-reperfusion by linagliptin and liraglutide, and both together.

    Science.gov (United States)

    Wang, Xianwei; Ding, Zufeng; Yang, Fen; Dai, Yao; Chen, Peng; Theus, Sue; Singh, Sharda; Budhiraja, Madhu; Mehta, Jawahar L

    2016-08-01

    Studies have indicated that dipeptidyl peptidase-4 (DPP-4) inhibitors and glucagon-like peptide-1 (GLP-1) agonists reduce infarct size after myocardial ischaemia. Whether these agents modify cardiac remodelling after ischaemia is unclear. Furthermore, it is not known if combination of the two types of drugs is superior to either agent alone. We investigated the modulatory effect of the DPP-4 inhibitor linagliptin alone, the GLP-1 activator liraglutide alone, or the two agents together on myocardial infarct size, left ventricular contractile function and cardiac remodelling signals after a brief period of left coronary artery (LCA) occlusion. C57BL/6 mice were treated with vehicle, the DPP-4 inhibitor linagliptin, the GLP-1 activator liraglutide, or both agents together for 5 days, and then subjected to LCA occlusion (1 h) and reperfusion (3 h). Ischaemia-reperfusion increased reactive oxygen species (ROS) generation and expression of NADPH oxidase (p47(phox), p22(phox) and gp91(phox) subtypes), collagens, fibronectin and proinflammatory cytokines (interleukin 6, tumour necrosis factor α and monocyte chemoattractant protein-1) in the LCA-supplied regions. Pre-treatment with linagliptin or liraglutide reduced infarct size, protected cardiomyocytes from injury and preserved cardiac contractile function in a similar fashion. It is interesting that profibrotic (collagen deposition) signals were expressed soon after ischaemia-reperfusion. Both linagliptin and liraglutide suppressed ROS generation, NADPH oxidase and proinflammatory signals, and reduced collagen deposition. Addition of linagliptin or liraglutide had no significant additive effect above and beyond that of liraglutide and linagliptin given alone. In conclusion, linagliptin and liraglutide can improve cardiac contractile function and indices of cardiac remodelling, which may be related to their role in inhibition of ROS production and proinflammatory cytokines after ischaemia. © 2016 The Author

  18. Present treatment of acute myocardial infarction in patients over 75 years--data from the Berlin Myocardial Infarction Registry (BHIR).

    Science.gov (United States)

    Schuler, Jochen; Maier, Birga; Behrens, Steffen; Thimme, Walter

    2006-07-01

    Guidelines issued by European and German cardiology societies clearly define procedures for treatment of acute myocardial infarction (AMI). These guidelines, however, are based on clinical studies in which older patients are underrepresented. Older patients, on the other hand, represent a large and growing portion of the infarction population. It was our goal in the present paper to analyse the present treatment of AMI patients over 75 years of age in the city of Berlin, Germany, with data gained from the Berlin Myocardial Infarction Registry (BHIR). We prospectively collected data from 5079 patients (3311 men and 1768 women, mean age 65.6) with acute myocardial infarction who were treated in 25 hospitals in Berlin during the period 1999-2003. 1319 patients (25.9%) were older than 75 (mean age 82.5 years). Overall hospital mortality rate was 11.6%. In patients over 75, this rate was 23.9%; among the younger infarction population, it was 7.3%. In contrast to the younger AMI patients, the majority of those over 75 were female (62.5 vs 25.1% for the younger) and demonstrated a significantly higher frequency of all prognostically meaningful comorbidities (heart failure 14.4% vs. 3.5%; renal failure 11.5 vs 3.9%; diabetes 37.3 vs 24.3%). Clinical signs of severe infarction, moreover, were more common among the aged patients (pulmonary congestion 45.4 vs 19.7%; left bundle branch block 12.7 vs 3.6%). Pre-hospital time was prolonged (2.8 vs 2 h) and guideline-recommended therapy was applied significantly less frequently to AMI patients over 75 (reperfusion therapy 39.8 vs 71.7%, beta-blockers 62.8 vs 78.3%, statins 26.5 vs 45.5%). Multivariate analysis revealed the following factors to be independent predictors of hospital mortality in patients over 75: age (OR 1.05 per year), acute heart failure (OR 2.39), pre-hospital resuscitation (OR 10.6), cardiogenic shock (OR 2.73), pre-hospital delay >12 h (OR 1.68), and ST elevation in the first ECG (OR 2.09). Independent

  19. Myocardial uptake of {sup 99m}Tc-annexin-V and {sup 111}In-antimyosin-antibodies after ischemia-reperfusion in rats

    Energy Technology Data Exchange (ETDEWEB)

    Sarda-Mantel, Laure [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); AP-HP, Groupe Hospitalier Bichat-Beaujon, Service de Medecine Nucleaire, Paris (France); INSERM, U773, Paris (France); Hopital Bichat, Service de Medecine Nucleaire, Paris (France); Hervatin, Florence [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); CEA, DSV/DRM/SHFJ, Orsay (France); Michel, Jean-Baptiste; Louedec, Liliane [INSERM, U698, Paris (France); Martet, Genevieve [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); INSERM, U773, Paris (France); Rouzet, Francois; Lebtahi, Rachida; Merlet, Pascal; Le Guludec, Dominique [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); AP-HP, Groupe Hospitalier Bichat-Beaujon, Service de Medecine Nucleaire, Paris (France); INSERM, U773, Paris (France); Khaw, Ban-An [Bouve College of Pharmacy and Health Sciences, Center for Drug Targeting and Analysis, Boston, MA (United States)

    2008-01-15

    Phosphatidylserin exposure on cell surfaces occurs early during apoptosis and is detected in vivo by using {sup 99m}Tc-annexin-V (ANX). Cardiomyocyte membrane disruption is detected in vivo by using {sup 111}In-antimyosin-antibodies (AM). We aimed to determine if ANX and AM allow evaluation of the time-course of these two distinct cell death events after myocardial ischemia-reperfusion. Coronary tying (20 min) followed by reperfusion (IR) was performed in 31 rats. Twelve of the rats were injected with ANX, 11 with AM, and eight with both tracers. Myocardial uptake of tracers was studied 1-2 h, 4 h, or 24 h after IR by scintigraphy (ANX, n = 14) and autoradiography (all cases), and compared to histology and Apostain staining. Scintigraphy was positive in all rats 2 h after IR and in three of five rats at 24 h. On autoradiography, ANX activity was intense in myocardial lesions as early as 1 h post-IR, whereas AM activity was mild at 2 h then increased at 4 h post-IR. ANX and AM uptakes evolved from mid-myocardium to endocardial and epicardial regions from 2 h to 24 h post-IR. Apostain staining was significant in myocardial lesions (p < 10{sup 6} compared to six sham-operated rats). On histology, myocardial lesion was characterized by interstitial oedema, myocytes necrosis, and dramatic thinning at 24 h. These data suggest that ANX and AM allow temporal and regional evaluations of PS exposure and membrane disruption, respectively, during myocytes death after 20-min myocardial ischemia followed by reperfusion. Also, (i) apoptosis starts very early in injured myocardium, (ii) myocyte necrosis occurs later (3-4 h post-reperfusion), and (iii) most dead cells are removed from mid-myocardium between 6 h and 24 h after reperfusion. (orig.)

  20. The effects of pentobarbital, ketamine-pentobarbital and ketamine-xylazine anesthesia in a rat myocardial ischemic reperfusion injury model.

    Science.gov (United States)

    Shekarforoush, Shahnaz; Fatahi, Zahra; Safari, Fatemeh

    2016-06-01

    To achieve reliable experimental data, the side-effects of anesthetics should be eliminated. Since anesthetics exert a variety of effects on hemodynamic data and incidence of arrhythmias, the selection of anesthetic agents in a myocardial ischemic reperfusion injury model is very important. The present study was performed to compare hemodynamic variables, the incidence of ventricular arrhythmias, and infarct size during 30 min of ischemia and 120 min of reperfusion in rats using pentobarbital, ketamine-pentobarbital or ketamine-xylazine anaesthesia. A total of 30 rats were randomly divided into three groups. In group P, pentobarbital (60 mg/kg, intraperitoneally [IP]) was used solely; in group K-P, ketamine and pentobarbital (50 and 30 mg/kg, respectively, IP) were used in combination; and in group K-X, ketamine and xylazine (75 and 5 mg/kg, respectively, IP) were also used in combination. Hemodynamic data and occurrence of ventricular arrhythmias were recorded throughout the experiments. The ischemic area was measured by triphenyltetrazolium chloride staining. The combination of ketamine-xylazine caused bradycardia and hypotension. The greatest reduction in mean arterial blood pressure during ischemia was in the P group. The most stability in hemodynamic parameters during ischemia and reperfusion was in the K-P group. The infarct size was significantly less in the K-X group. Whereas none of the rats anesthetized with ketamine-xylazine fibrillated during ischemia, ventricular fibrillation occurred in 57% of the animals anesthetized with pentobarbital or ketamine-pentobarbital. Because it offers the most stable hemodynamic parameters, it is concluded that the ketamine-pentobarbital anesthesia combination is the best anesthesia in a rat ischemia reperfusion injury model. © The Author(s) 2015.

  1. Melatonin does not affect oxidative/inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L.; Busch, Sarah Victoria Ekeløf; Jensen, Svend Eggert

    2014-01-01

    AIM: To test whether melatonin reduces oxidative and inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction. MATERIALS AND METHODS: Twenty pigs were randomized to receive a total dosage of 200 mg (0.4 mg/ml) of melatonin, or placebo immediately prior to reperfusion....... There was an increase in hs-TnT, but no significant difference between the melatonin-treated and placebo-treated groups. There were no significant differences in development of any of the circulating plasma markers between the two groups. CONCLUSION: Melatonin treatment did not result in reduction of inflammatory...

  2. Melatonin Does Not Affect Oxidative/Inflammatory Biomarkers in a Closed-Chest Porcine Model of Acute Myocardial Infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L.; Ekelof, Sarah; Jensen, Svend Eggert

    2014-01-01

    Aim: To test whether melatonin reduces oxidative and inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction. Materials and Methods: Twenty pigs were randomized to receive a total dosage of 200 mg (0.4 mg/ml) of melatonin, or placebo immediately prior to reperfusion....... There was an increase in hs-TnT, but no significant difference between the melatonin-treated and placebo-treated groups. There were no significant differences in development of any of the circulating plasma markers between the two groups. Conclusion: Melatonin treatment did not result in reduction of inflammatory...

  3. Localization and quantification of acute myocardial infarction by myocardial perfusion tomographic imaging

    International Nuclear Information System (INIS)

    Lin Xiufang; Min Changgeng; Lin Zhihu; Ke Ruoyi

    1994-01-01

    The authors reported the result of the quantification and localization of 30 clinically confirmed acute myocardial infarction patients in comparison with that of ECG. A left ventricle model was used to correct the area calculated by the method of Bull's eye. The result indicated that the infarction area calculated by the corrected Bull's eye method correlated closely with that determined by the ECG QRS scoring method (r = 0.706, P<0.01). Myocardial infarctions of all 30 patients were detected by both ECG and myocardial perfusion tomographic imaging. The accuracy of localization of myocardial infarction by myocardial perfusion imaging was similar to that of ECG in the anterior wall, anterior septum, anterior lateral and inferior wall, but superior to that of ECG in the apex, posterior lateral, posterior septum, and posterior wall

  4. Novel adjunctive treatments of myocardial infarction

    DEFF Research Database (Denmark)

    Schmidt, Michael Rahbek; Pryds, Kasper; Bøtker, Hans Erik

    2014-01-01

    Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve...... by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary...... clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic...

  5. Clinical Manifestation of Acute Myocardial Infarction in the Elderly

    Directory of Open Access Journals (Sweden)

    Miftah Suryadipradja

    2003-12-01

    Full Text Available A retrospective study were performed in patients with acute myocardial infarction (AMI that hospitalized in ICCU Cipto Mangunkusumo hospital, Jakarta during the period of January 1994 until Decmber 1999. There were 513 patients hospitalized with MCI, 227 patients (44.2% were classified as elderly, and 35.2% of them were female. Most of the elderly AMI patients reported typical chest pain just like their younger counterparts. Elderly AMI patients tend to come later to the hospital, and more Q-wave myocardial infarction were identified compared to non- Q-wave myocardial infarction. Risk factors of diabetes mellitus and hypertension were more common among the elderly. The prevalence of atrial fibrillation and the mortality rate were higher among elderly AMI patients. (Med J Indones 2003; 12: 229-35 Keywords: clinical manifestation, acute myocardial infarction, elderly

  6. Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats.

    Science.gov (United States)

    Zhang, Rui-Lin; Guo, Zheng; Wang, Li-Li; Wu, Jie

    2012-09-20

    Evidence indicated an involvement of afferent nerves in the pathology of acute myocardial infarction. This study was undertaken to clarify the role and mechanisms by which the sensory afferent degeneration exacerbates the myocardial injury in acute myocardial infarction in rats. The myocardial injury was assessed by analysis of 1) the differences in the infarct size, myocyte apoptosis, the caspase activity in the myocardium and cardiac troponin I in serum between the denervated and non-denervated rats; 2) the differences in the size of infarctiom with and without antagonisms of endogenous neurokinin 1 receptor or calcitonin gene related peptide receptor in acute myocardial infarction. Degeneration of the afferent nerves resulted in marked increase in the pain threshold and decrease in substance P and calcitonin gene related peptide in dorsal root ganglia, spinal dorsal horn and myocardium. Increases of the infarction size (39% ± 4% vs. 26% ± 4%,), troponin-I (28.4 ± 8.89 ng/ml, vs. 14.6 ± 9.75 ng/ml), apoptosis of myocytes (by 1.8 ± 0.2 folds) and caspase-3 activity (1.6 ± 0.3 vs. 1.05 ± 0.18) were observed in the denervated animals at 6h of myocardial infarction, compared with the non-denervated rats. Antagonisms of the endogenous neurokinin 1 receptor or calcitonin gene related peptide receptor caused increase of the size of infarction in the animals. Degeneration of capsaicin sensitive afferent nerves enhances the myocardial injury of acute myocardial infarction, possibly due to reduction of endogenous calcitonin gene related peptide and substance P. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  7. Role of glycogen synthase kinase following myocardial infarction and ischemia-reperfusion.

    Science.gov (United States)

    Ghaderi, S; Alidadiani, N; Dilaver, N; Heidari, H R; Parvizi, R; Rahbarghazi, R; Soleimani-Rad, J; Baradaran, B

    2017-07-01

    Glycogen synthase kinase-3 beta (GSK3β) is principally is a glycogen synthase phosphorylating enzyme that is well known for its role in muscle metabolism. GSK3β is a serine/threonine protein Kinase, which is responsible for several essential roles in mammalian cells. This enzyme is implicated in the pathophysiology of many conditions involved in homeostasis and cellular immigration. GSK3β is involved in several pathways leading to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Increasing evidence has shown the potential importance of GSK3β in ischemic heart disease and ischemia-reperfusion pathologies. Reperfusion injury may occur in tissues after prolonged ischemia following reperfusion. Reperfusion injury can be life threatening. Reperfusion injury occurs due to a change in ionic homeostasis, excess free radical production, mitochondrial damage and cell death. There are however clear, cardiac-protective signals; although the molecular pathophysiology is not clearly understood. In normal physiology, GSK3β has a critical role in the cytoprotective pathway. However, it`s controversial role in ischemia and ischemia-reperfusion is a topic of current interest. In this review, we have opted to focus on GSK3β interactions with mitochondria in ischemic heart disease and expand on the therapeutic interventions.

  8. Enflurane and isoflurane, but not halothane, protect against myocardial reperfusion injury after cardioplegic arrest with HTK solution in the isolated rat heart

    NARCIS (Netherlands)

    Preckel, B.; Schlack, W.; Thämer, V.

    1998-01-01

    To investigate the effects of halothane, enflurane, and isoflurane on myocardial reperfusion injury after ischemic protection by cardioplegic arrest, isolated perfused rat hearts were arrested by infusion of cold HTK cardioplegic solution containing 0.015 mmol/L Ca2+ and underwent 30 min of ischemia

  9. [Effect of Electroacupuncture at "Neiguan"(PC 6) on Serum and Myocardial Metabolites in Rats with Myocardial Ischemia Reperfusion Injury Based on Nuclear Magnetic Resonance Spectroscopy].

    Science.gov (United States)

    Tang, Ya-Ni; Tan, Cheng-Fu; Liu, Wei-Wei; Yan, Jie; Wang, Chao; Liu, Mi; Lin, Dong-Hai; Huang, Cai-Hua; Du, Lin; Chen, Mei-Lin; Li, Jiao-Lan; Zhu, Ding-Ming

    2018-03-25

    We have repeatedly demonstrated that electroacupuncture (EA) of "Neiguan"(PC 6) can improve myocardial ischemia in rats. The present study was designed to investigate the metabolomic profile of peripheral blood se-rum and myocardium involving EA-induced improvement of myocardial ischemia-reperfusion injury (MIRI) in rats by using nuclear magnetic resonance spectroscopy. Thirty male SD rats were equally randomized into blank control, model and EA groups. Rats of the control group were only banded for 20 min, once a day for 7 days. The MIRI model was established by occlusion of the anterior descending branch of the left coronary artery for 40 min, followed by reperfusion for 60 min, and rats of the model group were banded as those in the control group. EA (10 Hz/50 Hz, 1 mA) was applied to bilateral PC 6 for 20 min, once daily for 7 days. The blood samples and left ventricular myocardial tissues were collected for assaying the profiles of differential metabolites using 1 H nuclear magnetic resonance ( 1 H NMR) spectroscopy and multivariate statistical analysis such as the principal components analysis (PCA), partial least squares-discriminant analysis (PLS-DA) and orthogonal PLS-DA (O-PLS-DA) with SIMCA-P software 12.0. A total of 19 differential metabolites (17 down-regulated, 2 up-regulated) in the serum and 14 differential metabolites (13 down-regulated and 1 up-regulated) in the ischemic left myocardium were identified after MIRI. Of the 19 serum differential metabolites, amino acids (leucine, isoleucine, valine,alanine, lysine, glycine, glutamine), 3-hydroxy butyric acid (3-HB), lactic acid, acetate, N-acetyl glycoprotein (NAc), acetone, acetoacetate, succinate, polyunsaturated fatty acids (PUFA), creatine, glycerophosphocholine (GPC) were down-regulated; while low density lipoprotein (LDL), LDL/very low density lipoprotein(LDL/VLDL)and glucose obviously up-regulated. Of the 14 myocardial differential metabolites, amino acids (alanine, lysine, glutamate

  10. Myocardial Ablation of G Protein-Coupled Receptor Kinase 2 (GRK2 Decreases Ischemia/Reperfusion Injury through an Anti-Intrinsic Apoptotic Pathway.

    Directory of Open Access Journals (Sweden)

    Qian Fan

    Full Text Available Studies from our lab have shown that decreasing myocardial G protein-coupled receptor kinase 2 (GRK2 activity and expression can prevent heart failure progression after myocardial infarction. Since GRK2 appears to also act as a pro-death kinase in myocytes, we investigated the effect of cardiomyocyte-specific GRK2 ablation on the acute response to cardiac ischemia/reperfusion (I/R injury. To do this we utilized two independent lines of GRK2 knockout (KO mice where the GRK2 gene was deleted in only cardiomyocytes either constitutively at birth or in an inducible manner that occurred in adult mice prior to I/R. These GRK2 KO mice and appropriate control mice were subjected to a sham procedure or 30 min of myocardial ischemia via coronary artery ligation followed by 24 hrs reperfusion. Echocardiography and hemodynamic measurements showed significantly improved post-I/R cardiac function in both GRK2 KO lines, which correlated with smaller infarct sizes in GRK2 KO mice compared to controls. Moreover, there was significantly less TUNEL positive myocytes, less caspase-3, and -9 but not caspase-8 activities in GRK2 KO mice compared to control mice after I/R injury. Of note, we found that lowering cardiac GRK2 expression was associated with significantly lower cytosolic cytochrome C levels in both lines of GRK2 KO mice after I/R compared to corresponding control animals. Mechanistically, the anti-apoptotic effects of lowering GRK2 expression were accompanied by increased levels of Bcl-2, Bcl-xl, and increased activation of Akt after I/R injury. These findings were reproduced in vitro in cultured cardiomyocytes and GRK2 mRNA silencing. Therefore, lowering GRK2 expression in cardiomyocytes limits I/R-induced injury and improves post-ischemia recovery by decreasing myocyte apoptosis at least partially via Akt/Bcl-2 mediated mitochondrial protection and implicates mitochondrial-dependent actions, solidifying GRK2 as a pro-death kinase in the heart.

  11. Acute myocarditis mimicking myocardial infarction can misdirect the diagnostic approach

    Directory of Open Access Journals (Sweden)

    Erkan Yildirim

    2016-03-01

    Full Text Available Acute myocarditis is a well-recognized but rare manifestation of mostly viral infections. It can present with various clinical manifestations and may mimic myocardial infarction (MI since patients usually present with chest pain, and the electrocardiographic changes similar to those observed in acute ST-elevation MI. We, herein, present such an extreme case of acute myocarditis characterized by dynamic ST segment elevation with reciprocal changes in the electrocardiogram.

  12. Semen cassiae attenuates myocardial ischemia and reperfusion injury in high-fat diet streptozotocin-induced type 2 diabetic rats.

    Science.gov (United States)

    Fu, Feng; Tian, Fei; Zhou, Heping; Lv, Weifeng; Tie, Ru; Ji, Lele; Li, Rong; Shi, Zhenwei; Yu, Liming; Liang, Xiangyan; Xing, Wenjuan; Xing, Jinliang; Yu, Jun; Sun, Lijun; Zhu, Hailong; Zhang, Haifeng

    2014-01-01

    Obese patients with type 2 diabetes mellitus (T2DM), which is characterized by hyperglycemia, are liable to more severe myocardial infarction. Semen Cassiae is proven to reduce serum lipid levels. This study investigated whether the Semen Cassiae extract (SCE) reduces myocardial ischemia and reperfusion (MI/R) injury with or without diabetes and the underlying mechanisms. The high-fat diet-fed streptozotocin (HFD-STZ) rat model was created as a T2DM model. Normal and DM rats received SCE treatment orally (10 mg/kg/day) for one week. Subsequently these animals were subjected to MI/R. Compared with the normal animals, DM rats showed increased plasma total cholesterol (TC) and triacylglycerol (TG), and more severe MI/R injury and cardiac functional impairment. SCE treatment significantly reduced the plasma TC and TG, improved the instantaneous first derivation of left ventricle pressure and reduced infarct size, decreased plasma creatine kinase and lactate dehydrogenase levels, and apoptosis index at the end of reperfusion in diabetic rats. Moreover, SCE treatment increased the antiapoptotic protein Akt and ERK1/2 phosphorylation levels. Pretreatment with a PI3K inhibitor wortmannin or an ERK1/2 inhibitor PD98059 not only blocked Akt and ERK1/2 phosphorylation respectively, but also inhibited the cardioprotective effects of SCE. However, SCE treatment did not show any effects on the MI/R injury in the normal rats. Our data suggest that SCE effectively improves myocardial function and reduces MI/R-induced injury in diabetic but not normal animals, which is possibly attributed to the reduced TC/TG levels and the triggered cell survival signaling Akt and ERK1/2.

  13. Buckberg's blood cardioplegia for protection of adult and senile myocardium in a rat in vitro model of acute myocardial infarction.

    Science.gov (United States)

    Boening, Andreas; Assling-Simon, Lena; Heep, Martina; Boengler, Kerstin; Niemann, Bernd; Grieshaber, Philippe

    2018-04-01

    In patients undergoing surgical myocardial revascularization for acute myocardial infarction, excellent myocardial protection can be achieved by blood cardioplegia. We investigated the influence of age on cardiac function, metabolism, and infarct size using Buckberg's blood cardioplegia (BCP). The hearts of male Wistar rats ("adult", age 3 months, n = 8; "senile", age 24 months, n = 8) were excised and mounted on a blood-perfused isolated heart apparatus. An acute myocardial infarction was induced by coronary artery ligation for 30 min before aortic clamping and infusion of Buckberg's BCP. Throughout the experiment, functional parameters were recorded: coronary blood flow (normalized by heart weight), left ventricular peak developed pressure (LVpdP), and positive and negative derived left ventricular pressure over time (dLVPdt max and dLVPdt min ). Oxygen consumption (MVO 2 ) and lactate production of the hearts were calculated. The infarct size after 90 min of reperfusion (in % of the area at risk) was measured with triphenyl tetrazolium chloride staining of the myocardium. The baseline coronary flow normalized by heart weight was significantly lower in the senile hearts (1.6 ± 0.4 ml/(min ∗ g)) compared with the adult hearts (2.0 ± 0.3 ml/(min ∗ g); p = 0.04). After 90 min of aortic clamping, hemodynamic function of senile hearts recovered better than that of adult hearts: LVpdP (adult 57% of baseline [BL]; senile 88% BL; p = 0.044) and dLVPdt max (adult 74% BL, senile 102% BL; p = 0.12). In contrast, myocardial infarct size was similar between the adult (26%) and senile (21%; p = 0.45) hearts, and coronary flow recovered to a similar extent (55% BL and 58% BL, respectively). During reperfusion, MVO 2 (80% BL and 81% BL) and lactate production (1.2 and 1.3 μmol/min) were similar in the two groups. After acute myocardial infarction in a rat model, hearts recovered function after reperfusion with

  14. SPECT imaging of myocardial infarction using {sup 99m}Tc-labeled C2A domain of synaptotagmin I in a porcine ischemia-reperfusion model

    Energy Technology Data Exchange (ETDEWEB)

    Fang Wei [Department of Nuclear Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing 100037 (China); Wang Feng [Nuclear Medicine Department, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing 210006 (China); Ji Shundong [Jiangsu Institute of Hematology, 1st Hospital of Suzhou University, Suzhou 215006 (China); Zhu Xiaoguang [Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin, WI 53226 (United States); Meier, Heidi T. [Clinical Veterinarian and Radiology Research, Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin, WI 53295 (United States); Hellman, Robert S. [Department of Radiology, Medical College of Wisconsin, Milwaukee, Wisconsin, WI 53226 (United States); Brindle, Kevin M. [MRC Laboratory of Molecular Biology, Cambridge CB2 2QH (United Kingdom); Davletov, Bazbek [Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA (United Kingdom); Zhao Ming [Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin, WI 53226 (United States)], E-mail: mzhao@mcw.edu

    2007-11-15

    Introduction: The C2A domain of synaptotagmin I recognizes necrotic and apoptotic cells by binding to exposed anionic phospholipids. The goal is to explore the potential imaging utility of {sup 99m}Tc-labeled C2A in the detection of acute cardiac cell death in a porcine model that resembles human cardiovascular physiology. Methods: Ischemia (20-25 min) was induced in pigs (M/F, 20-25 kg) using balloon angioplasty. {sup 99m}Tc-C2A-GST (n=7) or {sup 99m}Tc-BSA (n=2) was injected intravenously 1-2 h after reperfusion. Noninfarct animals were injected with {sup 99m}Tc-C2A-GST (n=4). SPECT images were acquired at 3 and 6 h postinjection. Cardiac tissues were analyzed to confirm the presence of cell death. Results: Focal uptake was detected in five out of seven subjects at 3 h and in all infarct subjects at 6 h postinjection but not in infarct animals injected with {sup 99m}Tc-BSA or in noninfarct animals with {sup 99m}Tc-C2A-GST. Gamma counting of infarct versus normal myocardium yielded a 10.2{+-}5.7-fold elevation in absolute radioactivity, with histologically confirmed infarction. Conclusions: We present data on imaging myocardial cell death in the acute phase of infarction in pigs. C2A holds promise and warrants further development as an infarct-avid molecular probe.

  15. Thrombus composition in sudden cardiac death from acute myocardial infarction.

    Science.gov (United States)

    Silvain, Johanne; Collet, Jean-Philippe; Guedeney, Paul; Varenne, Olivier; Nagaswami, Chandrasekaran; Maupain, Carole; Empana, Jean-Philippe; Boulanger, Chantal; Tafflet, Muriel; Manzo-Silberman, Stephane; Kerneis, Mathieu; Brugier, Delphine; Vignolles, Nicolas; Weisel, John W; Jouven, Xavier; Montalescot, Gilles; Spaulding, Christian

    2017-04-01

    It was hypothesized that the pattern of coronary occlusion (thrombus composition) might contribute to the onset of ventricular arrhythmia and sudden cardiac death (SCD) in myocardial infarction (MI). The TIDE (Thrombus and Inflammation in sudden DEath) study included patients with angiographically-proven acute coronary occlusion as the cause of a ST elevation MI (STEMI) complicated by Sudden Cardiac Death (SCD group) or not (STEMI group). Thrombi were obtained by thrombo-aspiration before primary percutaneous coronary stenting and analyzed with a quantitative method using scanning electron microscopy. We compared the composition of the thrombi responsible for the coronary occlusion between the two groups and evaluated factors influencing its composition. We included 121 patients and found that thrombus composition was not different between the SCD group (n=23) and the STEMI group (n=98) regarding content of fibrin fibers (60.3±18.4% vs. 62.4±18.4% respectively, p=0.68), platelets (16.3±19.2% vs. 15.616.7±%, p=0.76), erythrocytes (14.6±12.5% vs. 13±12.1%, p=0.73) and leukocytes (0.6±0.9% vs. 0.8±1.5%, p=0.93). Thrombus composition did not differ between patients receiving upstream-use of glycoprotein IIb/IIIa platelet receptor inhibitors (GPI) and patients free of GPI. The only factor found to influence thrombus composition was the ischemic time from symptom onset to primary PCI, with a decreased content in fibrin fibers (57.8±18.5% vs. 71.9±10.1%, p=0.0008) and a higher platelet content (19.2±19.1% vs. 7.9±5.7% p=0.014) in early presenters (6h of ischemic time). Composition of intracoronary thrombi in STEMI patients does not differ between those presenting with and without SCD. Time from symptom onset to coronary reperfusion seems to be the strongest factor influencing thrombus composition in MI. Copyright © 2017 Elsevier B.V. All rights reserved.

  16. A successfully thrombolysed acute inferior myocardial infarction due to type A aortic dissection with lethal consequences: the importance of early cardiac echocardiography

    Directory of Open Access Journals (Sweden)

    Bousoula Eleni

    2011-08-01

    Full Text Available Abstract Thrombolysis, a standard therapy for ST elevation myocardial infarction (STEMI in non-PCI-capable hospitals, may be catastrophic for patients with aortic dissection leading to further expansion, rupture and uncontrolled bleeding. Stanford type A aortic dissection, rarely may mimic myocardial infarction. We report a case of a patient with an inferior STEMI thrombolysed with tenecteplase and followed by clinical and electrocardiographic evidence of successful reperfusion, which was found later to be a lethal acute aortic dissection. Prognostic implications of early diagnosis applying transthoracic echocardiography (TTE are described.

  17. Computational modeling of acute myocardial infarction.

    Science.gov (United States)

    Sáez, P; Kuhl, E

    2016-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.

  18. Limited clinical diagnostic specificity of /sup 99m/Tc stannous pyrophosphate myocardial imaging in acute myocardial infarction

    International Nuclear Information System (INIS)

    Ahmad, M.; Dubiel, J.P.; Logan, K.W.; Verdon, T.A.; Martin, R.H.

    1977-01-01

    To test the sensitivity and specificity of technetium-99m stannous pyrophosphate myocardial imaging in the diagnosis of acute myocardial infarction, myocardial scintigrams were performed in 115 patients. Positive scintigrams were found in all 48 patients with acute myocardial infarction; uptake was localized in 29 patients with transmural infarction and diffuse in 2 patients with transmural infarction and in the remaining 17 patients with subendocardial myocardial infarction. Positive scintigrams were also found in 31 of 67 patients without clinical evidence of acute myocardial infarction. Our data confirm the previously reported sensitivity of /sup 99m/Tc-pyrophosphate imaging in detection of acute myocardial infarction but indicate that positive scintigrams are not specific for this entity

  19. Prognostic usefulness of repeated echocardiographic evaluation after acute myocardial infarction. TRACE Study Group. TRAndolapril Cardiac Evaluation

    DEFF Research Database (Denmark)

    Korup, E; Køber, L; Torp-Pedersen, C

    1999-01-01

    The prognostic value of repeated echocardiographic measurement of left ventricular function after acute myocardial infarction was evaluated. We found that repeated measurements of wall motion index in survivors of acute myocardial infarction, with no reinfarction, provide important prognostic...

  20. Luteolin Modulates SERCA2a Leading to Attenuation of Myocardial Ischemia/ Reperfusion Injury via Sumoylation at Lysine 585 in Mice.

    Science.gov (United States)

    Du, Yinping; Liu, Ping; Xu, Tongda; Pan, Defeng; Zhu, Hong; Zhai, Nana; Zhang, Yanbin; Li, Dongye

    2018-01-01

    The myocardial sarcoplasmic reticulum calcium ATPase (SERCA2a) is a pivotal pump responsible for calcium cycling in cardiomyocytes. The present study investigated the effect of luteolin (Lut) on restoring SERCA2a protein level and stability reduced by myocardial ischemia/reperfusion (I/R) injury. We verified a hypothesis that Lut protected against myocardial I/R injury by regulating SERCA2a SUMOylation. The hemodynamic data, myocardial infarct size of intact hearts, apoptotic analysis, mitochondrial membrane potential (ΔΨm), the level of SERCA2a SUMOylation, and the activity and expression of SERCA2a were examined in vivo and in vitro to clarify the cardioprotective effects of Lut after SUMO1 was knocked down or over-expressed. The putative SUMO conjugation sites in mouse SERCA2a were investigated as the possible regulatory mechanism of Lut. Initially, we found that Lut reversed the SUMOylation and stability of SERCA2a as well as the expression of SUMO1, which were reduced by I/R injury in vitro. Furthermore, Lut increased the expression and activity of SERCA2a partly through SUMO1, thus improving ΔΨm and reducing apoptotic cells in vitro and promoting the recovery of heart function and reducing infarct size in vivo. We also demonstrated that SUMO acceptor sites in mouse SERCA2a involving lysine 585, 480 and 571. Among the three acceptor sites, Lut enhanced SERCA2a stability via lysine 585. Our results suggest that Lut regulates SERCA2a through SUMOylation at lysine 585 to attenuate myocardial I/R injury. © 2018 The Author(s). Published by S. Karger AG, Basel.

  1. Luteolin Modulates SERCA2a Leading to Attenuation of Myocardial Ischemia/ Reperfusion Injury via Sumoylation at Lysine 585 in Mice

    Directory of Open Access Journals (Sweden)

    Yinping Du

    2018-02-01

    Full Text Available Background/Aims: The myocardial sarcoplasmic reticulum calcium ATPase (SERCA2a is a pivotal pump responsible for calcium cycling in cardiomyocytes. The present study investigated the effect of luteolin (Lut on restoring SERCA2a protein level and stability reduced by myocardial ischemia/reperfusion (I/R injury. We verified a hypothesis that Lut protected against myocardial I/R injury by regulating SERCA2a SUMOylation. Methods: The hemodynamic data, myocardial infarct size of intact hearts, apoptotic analysis, mitochondrial membrane potential (ΔΨm, the level of SERCA2a SUMOylation, and the activity and expression of SERCA2a were examined in vivo and in vitro to clarify the cardioprotective effects of Lut after SUMO1 was knocked down or over-expressed. The putative SUMO conjugation sites in mouse SERCA2a were investigated as the possible regulatory mechanism of Lut. Results: Initially, we found that Lut reversed the SUMOylation and stability of SERCA2a as well as the expression of SUMO1, which were reduced by I/R injury in vitro. Furthermore, Lut increased the expression and activity of SERCA2a partly through SUMO1, thus improving ΔΨm and reducing apoptotic cells in vitro and promoting the recovery of heart function and reducing infarct size in vivo. We also demonstrated that SUMO acceptor sites in mouse SERCA2a involving lysine 585, 480 and 571. Among the three acceptor sites, Lut enhanced SERCA2a stability via lysine 585. Conclusions: Our results suggest that Lut regulates SERCA2a through SUMOylation at lysine 585 to attenuate myocardial I/R injury.

  2. Usefulness of dual energy single photon emission computed tomography with 99mTc-pyrophosphate and 201TlCl in diagnosis of acute myocardial infarction

    International Nuclear Information System (INIS)

    Shohgase, Takashi; Okita, Kohichi; Sakai, Hiroto; Fukuda, Hiroyuki; Anzai, Teisuke; Yamaguchi, Masashi; Koseki, Yukio; Tsujita, Naoyuki; Itoh, Hideki

    1990-01-01

    The dual energy single photon emission computed tomography (D-SPECT) with 99m Tc-Pyrophosphate and 201 TlCl was evaluated, using Bull's Eye Map representation in 30 patients with acute myocardial infarction. D-SPECT imaging for infarct detection was 100% sensitive. The patients were divided into two groups. One group had an overlap of accumulation of 99m Tc and 201 TlCl in the infarct zone and the other had no overlap. Fifteen of 19 patients (78.9%) in whom reperfusion was successful showed an overlap. Ten of 11 patients in whom reperfusion was unsuccessful showed no overlap. In the patients with successful reperfusion, the group that showed an overlap had a shorter interval between the onset of acute myocardial infarction and the reperfusion of coronary artery than the group that showed no overlap. But one case showed that collateral circulation had an influence on the overlap. In conclusion, using Bull's Eye Map representation, D-SPECT was useful to detect infarct and the overlap of accumulation of 99m Tc and 201 TlCl might be used as an index of early recanalization. (author)

  3. Prospective evaluation of where reperfusion ventricular arrhythmia "bursts" fit into optimal reperfusion in STEMI

    NARCIS (Netherlands)

    van der Weg, Kirian; Kuijt, Wichert J.; Tijssen, Jan G. P.; Bekkers, Sebastiaan C. A. M.; Haeck, Joost D. E.; Green, Cynthia L.; Lemmert, Miguel E.; de Winter, Robbert J.; Gorgels, Anton P. M.; Krucoff, Mitchell W.

    2015-01-01

    Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT. The hypothesis was tested that this finding

  4. The value of exercise tests after acute myocardial infarction

    DEFF Research Database (Denmark)

    Nielsen, F E; Nielsen, S L; Knudsen, F

    1992-01-01

    The aim of the present study was to relate the clinical course in patients after a first acute myocardial infarction with the response to exercise-tests performed one month after discharge. 90 consecutive patients who suffered an acute myocardial infarction for the first time were followed-up after.......6% did not return to work because of the heart disease. 80 patients were in function groups I-II and 10 in function groups III-IV (New York Heart Association's Classification). Occurrence of ST-segment displacements was without prognostic value. Left ventricular function index (dRPP) and working capacity...

  5. Acute ethanol exposure increases the susceptibility of the donor hearts to ischemia/reperfusion injury after transplantation in rats.

    Directory of Open Access Journals (Sweden)

    Shiliang Li

    Full Text Available BACKGROUND: Many donor organs come from youths involved in alcohol-related accidental death. The use of cardiac allografts for transplantation from donors after acute poisoning is still under discussion while acute ethanol intoxication is associated with myocardial functional and morphological changes. The aims of this work were 1 to evaluate in rats the time-course cardiac effects of acute ethanol-exposure and 2 to explore how its abuse by donors might affect recipients in cardiac pump function after transplantation. METHODS: Rats received saline or ethanol (3.45 g/kg, ip. We evaluated both the mechanical and electrical aspects of cardiac function 1 h, 6 h or 24 h after injection. Plasma cardiac troponin-T and glucose-levels were measured and histological examination of the myocardium was performed. In addition, heart transplantation was performed, in which donors received ethanol 6 h or 24 h prior to explantation. Graft function was measured 1 h or 24 h after transplantation. Myocardial TBARS-concentration was measured; mRNA and protein expression was assessed by quantitative real-time PCR and Western blot, respectively. RESULTS: Ethanol administration resulted in decreased load-dependent (-34 ± 9% and load-independent (-33 ± 12% contractility parameters, LV end-diastolic pressure and elevated blood glucose levels at 1 h, which were reversed to the level of controls after 6 h and 24 h. In contrast to systolic dysfunction, active relaxation and passive stiffness are slowly recovered or sustained during 24 h. Moreover, troponin-T-levels were increased at 1 h, 6 h and 24 h after ethanol injection. ST-segment elevation (+47 ± 10%, elongated QT-interval (+38 ± 4%, enlarged cardiomyocyte, DNA-strand breaks, increased both mRNA and protein levels of superoxide dismutase-1, glutathione peroxydase-4, cytochrome-c-oxidase and metalloproteinase-9 were observed 24 h following ethanol-exposure. After heart transplantation, decreased myocardial

  6. Analysis of temporal dynamics in imagery during acute limb ischemia and reperfusion

    Science.gov (United States)

    Irvine, John M.; Regan, John; Spain, Tammy A.; Caruso, Joseph D.; Rodriquez, Maricela; Luthra, Rajiv; Forsberg, Jonathon; Crane, Nicole J.; Elster, Eric

    2014-03-01

    Ischemia and reperfusion injuries present major challenges for both military and civilian medicine. Improved methods for assessing the effects and predicting outcome could guide treatment decisions. Specific issues related to ischemia and reperfusion injury can include complications arising from tourniquet use, such as microvascular leakage in the limb, loss of muscle strength and systemic failures leading to hypotension and cardiac failure. Better methods for assessing the viability of limbs/tissues during ischemia and reducing complications arising from reperfusion are critical to improving clinical outcomes for at-risk patients. The purpose of this research is to develop and assess possible prediction models of outcome for acute limb ischemia using a pre-clinical model. Our model relies only on non-invasive imaging data acquired from an animal study. Outcome is measured by pathology and functional scores. We explore color, texture, and temporal features derived from both color and thermal motion imagery acquired during ischemia and reperfusion. The imagery features form the explanatory variables in a model for predicting outcome. Comparing model performance to outcome prediction based on direct observation of blood chemistry, blood gas, urinalysis, and physiological measurements provides a reference standard. Initial results show excellent performance for the imagery-base model, compared to predictions based direct measurements. This paper will present the models and supporting analysis, followed by recommendations for future investigations.

  7. Acute myocardial infarction in a young patient

    International Nuclear Information System (INIS)

    Hameed, A.; Ata-ur-Rehman Quraishi

    2004-01-01

    Myocardial infarction (MI) is considered to be the disease of the fifth and sixth decade as seen in the West but an earlier age incidence is not infrequently encountered in the South Asian population. However, occurrence of MI in the teen-age still remains a rare happening. We are reporting a case of a teenager, who suffered a myocardial infarction with cardiogenic shock and pulmonary edema on two separate occasions with ECG and biochemical evidence of myocardial infarction. An exercise stress test done in between the two episodes was negative at a workload of 13.5 METs. A coronary angiogram done after the second event revealed normal coronary arteries and a preserved left ventricular systolic and segmental function. Except for low HDL (high density lipoprotein) and mildly raised homocysteine levels, the patient did not have other conventional or novel risk factors for coronary artery disease. (author)

  8. Effect of intravenous streptokinase on the relation between initial ST-predicted size and final QRS-estimated size of acute myocardial infarcts

    DEFF Research Database (Denmark)

    Clemmensen, P; Grande, P; Saunamäki, K

    1990-01-01

    who did not receive streptokinase as a control group. Final myocardial infarct size, which was estimated from the QRS score, was predicted from the admission standard ECG by previously developed formulas based on ST segment elevation. In the 40 control patients there was no change from ST......-predicted to final QRS-estimated infarct size (median 17.7% versus 18.3%; p = NS). In the 33 patients in the streptokinase group, there was a highly significant decrease from predicted to final myocardial infarct size (median 21.9% versus 16.2%; p less than 0.0002). This decrease was found for both anterior (median......Thrombolytic therapy has been documented to reduce acute myocardial infarct size. The previously established relation between initial ST segment elevation and final electrocardiographic (ECG) myocardial infarct size in patients without coronary reperfusion might therefore be altered by thrombolytic...

  9. ST segment elevations: Always a marker of acute myocardial infarction?

    Directory of Open Access Journals (Sweden)

    G. Coppola

    2013-07-01

    Full Text Available Chest pain is one of the chief presenting complaints among patients attending Emergency department. The diagnosis of acute myocardial infarction may be a challenge. Various tools such as anamnesis, blood sample (with evaluation of markers of myocardial necrosis, ultrasound techniques and coronary computed tomography could be useful. However, the interpretation of electrocardiograms of these patients may be a real concern. The earliest manifestations of myocardial ischemia typically interest T waves and ST segment. Despite the high sensitivity, ST segment deviation has however poor specificity since it may be observed in many other cardiac and non-cardiac conditions. Therefore, when ST–T abnormalities are detected the physicians should take into account many other parameters (such as risk factors, symptoms and anamnesis and all the other differential diagnoses. The aim of our review is to overview of the main conditions that may mimic a ST segment Elevation Myocardial Infarction (STEMI.

  10. Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction.

    Science.gov (United States)

    Bobi, Joaquim; Solanes, Núria; Fernández-Jiménez, Rodrigo; Galán-Arriola, Carlos; Dantas, Ana Paula; Fernández-Friera, Leticia; Gálvez-Montón, Carolina; Rigol-Monzó, Elisabet; Agüero, Jaume; Ramírez, José; Roqué, Mercè; Bayés-Genís, Antoni; Sánchez-González, Javier; García-Álvarez, Ana; Sabaté, Manel; Roura, Santiago; Ibáñez, Borja; Rigol, Montserrat

    2017-05-03

    Autologous adipose tissue-derived mesenchymal stem cells (ATMSCs) therapy is a promising strategy to improve post-myocardial infarction outcomes. In a porcine model of acute myocardial infarction, we studied the long-term effects and the mechanisms involved in allogeneic ATMSCs administration on myocardial performance. Thirty-eight pigs underwent 50 minutes of coronary occlusion; the study was completed in 33 pigs. After reperfusion, allogeneic ATMSCs or culture medium (vehicle) were intracoronarily administered. Follow-ups were performed at short (2 days after acute myocardial infarction vehicle-treated, n=10; ATMSCs-treated, n=9) or long term (60 days after acute myocardial infarction vehicle-treated, n=7; ATMSCs-treated, n=7). At short term, infarcted myocardium analysis showed reduced apoptosis in the ATMSCs-treated animals (48.6±6% versus 55.9±5.7% in vehicle; P =0.017); enhancement of the reparative process with up-regulated vascular endothelial growth factor, granulocyte macrophage colony-stimulating factor, and stromal-derived factor-1α gene expression; and increased M2 macrophages (67.2±10% versus 54.7±10.2% in vehicle; P =0.016). In long-term groups, increase in myocardial perfusion at the anterior infarct border was observed both on day-7 and day-60 cardiac magnetic resonance studies in ATMSCs-treated animals, compared to vehicle (87.9±28.7 versus 57.4±17.7 mL/min per gram at 7 days; P =0.034 and 99±22.6 versus 43.3±14.7 22.6 mL/min per gram at 60 days; P =0.0001, respectively). At day 60, higher vascular density was detected at the border zone in the ATMSCs-treated animals (118±18 versus 92.4±24.3 vessels/mm 2 in vehicle; P =0.045). Cardiac magnetic resonance-measured left ventricular ejection fraction of left ventricular volumes was not different between groups at any time point. In this porcine acute myocardial infarction model, allogeneic ATMSCs-based therapy was associated with increased cardioprotective and reparative

  11. Acute aortic dissection mimics acute inferoposterior wall myocardial infarction in a Marfan syndrome patient

    OpenAIRE

    Phowthongkum, Prasit

    2010-01-01

    A 30-year old man with acute chest pain was diagnosed with acute inferoposterior wall myocardial infarction following electrocardiography. After a failed coronary angiography, an echocardiogram revealed an aortic intimal flap after which acute aortic dissection was diagnosed. The patient received a successful Bentall operation without immediate complication. Retrospective examination then confirmed the diagnosis of Marfan syndrome. This case demonstrates acute aortic dissection may mimic acut...

  12. Nitrate-enhanced gated SPECT in patients with primary angioplasty for acute myocardial infarction: evidence of a reversible and nitrate-sensitive impairment of myocardial perfusion

    Energy Technology Data Exchange (ETDEWEB)

    Djaballah, Wassila [CHU-Nancy, Department of Nuclear Medicine, Nancy (France); UHP-INSERM ERI13, Nancy (France); Hopital de Brabois, Service de Medecine Nucleaire, CHU-Nancy, Vandoeuvre Cedex (France); Muller, Marc A.; Karcher, Gilles [CHU-Nancy, Department of Nuclear Medicine, Nancy (France); Angioi, Michael [CHU-Nancy, Department of Cardiology, Nancy (France); UHP-INSERM U684, Nancy (France); Moulin, Frederic; Ethevenot, Gerard; Aliot, Etienne [CHU-Nancy, Department of Cardiology, Nancy (France); Codreanu, Andrei [UHP-INSERM ERI13, Nancy (France); CHU-Nancy, Department of Cardiology, Nancy (France); Mandry, Damien [UHP-INSERM ERI13, Nancy (France); CHU-Nancy, Department of Radiology, Nancy (France); Marie, Pierre Y. [CHU-Nancy, Department of Nuclear Medicine, Nancy (France); UHP-INSERM U684, Nancy (France)

    2007-12-15

    Reperfusion of myocardial infarction (MI) leads to a reversible dysfunction of coronary vessels. We hypothesised that vasodilating drugs such as nitrates might improve sestamibi uptake within viable areas of recently reperfused MI, thereby enhancing prediction of subsequent improvements in perfusion and contractility. This study was aimed at assessing nitrate-enhanced sestamibi gated SPECT after MI reperfusion. Twenty-nine patients underwent rest followed by nitrate sestamibi gated SPECT at 9 {+-} 3 days after primary angioplasty for acute MI and at follow-up, 4-10 months later. Four MBq/kg of {sup 99m}Tc-sestamibi was injected at rest, and 12 MBq/kg after nitroglycerin spray. Follow-up improvements were documented for both perfusion (P+) and contractility (C+) in 18% of the 180 initially abnormal segments, in neither perfusion (P-) nor contractility (C-) in 44%, in contractility only (C+P-) in 16% and in perfusion only (C-P+) in 22%. Perfusion improvement was related to lower sestamibi uptake on baseline rest SPECT (P+: 42 {+-} 15% vs P-: 50 {+-} 15%, p = 0.001) and, moreover, to a higher increase between rest and nitrate uptake (P+: +9.5 {+-} 6.5% vs P-: +2.0 {+-} 5.9%, p < 0.001). Contractility improvement was related to sestamibi uptake on baseline nitrate SPECT (C+: 58 {+-} 15% vs C-: 38 {+-} 16%, p < 0.001), a variable enhancing the prediction provided by sestamibi uptake at rest (p < 0.05). The improvement in perfusion which is documented in the months following MI reperfusion is predicted by initial nitrate enhancement of sestamibi uptake, suggesting a mechanism of reversible vascular injury. In this particular setting, sestamibi uptake is a better predictor of contractility recovery when determined after nitrate administration rather than under conventional resting conditions. (orig.)

  13. Hybrid approach of ventricular assist device and autologous bone marrow stem cells implantation in end-stage ischemic heart failure enhances myocardial reperfusion

    Directory of Open Access Journals (Sweden)

    Khayat Andre

    2011-01-01

    Full Text Available Abstract We challenge the hypothesis of enhanced myocardial reperfusion after implanting a left ventricular assist device together with bone marrow mononuclear stem cells in patients with end-stage ischemic cardiomyopathy. Irreversible myocardial loss observed in ischemic cardiomyopathy leads to progressive cardiac remodelling and dysfunction through a complex neurohormonal cascade. New generation assist devices promote myocardial recovery only in patients with dilated or peripartum cardiomyopathy. In the setting of diffuse myocardial ischemia not amenable to revascularization, native myocardial recovery has not been observed after implantation of an assist device as destination therapy. The hybrid approach of implanting autologous bone marrow stem cells during assist device implantation may eventually improve native cardiac function, which may be associated with a better prognosis eventually ameliorating the need for subsequent heart transplantation. The aforementioned hypothesis has to be tested with well-designed prospective multicentre studies.

  14. Left ventricular global longitudinal strain in acute myocardial infarction

    DEFF Research Database (Denmark)

    Ersbøll, Mads

    Systolic dysfunction, clinical heart failure and elevated levels of neurohormonal peptides are major predictors of adverse outcome after acute myocardial infarction (MI). In the present thesis we evaluated global longitudinal strain (GLS) in patients with acute MI in relation to neurohormonal act...... activation, in-hospital heart failure and prognosis with specific attention to the group of patients with preserved LVEF that currently do not meet the criteria for anti remodeling therapies.......Systolic dysfunction, clinical heart failure and elevated levels of neurohormonal peptides are major predictors of adverse outcome after acute myocardial infarction (MI). In the present thesis we evaluated global longitudinal strain (GLS) in patients with acute MI in relation to neurohormonal...

  15. HIF-1α signaling activation by post-ischemia treatment with astragaloside IV attenuates myocardial ischemia-reperfusion injury.

    Directory of Open Access Journals (Sweden)

    Jingwen Si

    Full Text Available In this study, we evaluated the effect of astragaloside IV (Ast IV post-ischemia treatment on myocardial ischemia-reperfusion (IR injury (IRI. We also examined whether hypoxia inducible factor-1α (HIF-1α and its downstream gene-inducible nitric oxide (NO synthase (iNOS play roles in the cardioprotective effect of Ast IV. Cultured cardiomyocytes and perfused isolated rat hearts were exposed to Ast IV during reperfusion in the presence or absence of the HIF-1α inhibitor 2-methoxyestradiol (2-MeOE2. The post-ischemia treatment with Ast IV protected cardiomyocytes from the apoptosis and death induced by simulated IRI (SIRI. Additionally, in cardiomyocytes, 2-MeOE2 and HIF-1α siRNA treatment each not only abolished the anti-apoptotic effect of post-ischemia treatment with Ast IV but also reversed the upregulation of HIF-1α and iNOS expression. Furthermore, after treatment with Ast IV, post-ischemic cardiac functional recovery and lactate dehydrogenase (LDH release in the coronary flow (CF were improved, and the myocardial infarct size was decreased. Moreover, the number of apoptotic cells was reduced, and the upregulation of the anti-apoptotic protein Bcl2 and downregulation of the pro-apoptotic protein Caspase3 were reversed. 2-MeOE2 reversed these effects of Ast IV on IR-injured hearts. These results suggest that post-ischemia treatment with Ast IV can attenuate IRI by upregulating HIF-1α expression, which transmits a survival signal to the myocardium.

  16. Evaluation of the relationship between hyperinsulinaemia and myocardial ischaemia/reperfusion injury in a rat model of depression.

    Science.gov (United States)

    Solskov, Lasse; Løfgren, Bo; Pold, Rasmus; Kristiansen, Steen B; Nielsen, Torsten T; Overstreet, David H; Schmitz, Ole; Bøtker, Hans Erik; Lund, Sten; Wegener, Gregers

    2009-11-09

    Major depression is associated with medical co-morbidity, such as ischaemic heart disease and diabetes, but the underlying pathophysiological mechanisms remain unclear. The FSL (Flinders Sensitive Line) rat is a genetic animal model of depression exhibiting features similar to those of depressed individuals. The aim of the present study was to compare the myocardial responsiveness to I/R (ischaemia/reperfusion) injury and the effects of IPC (ischaemic preconditioning) in hearts from FSL rats using SD (Sprague-Dawley) rats as controls and to characterize differences in glucose metabolism and insulin sensitivity between FSL and SD rats. Hearts were perfused in a Langendorff model and were subjected or not to IPC before 40 min of global ischaemia, followed by 120 min of reperfusion. Myocardial infarct size was found to be significantly larger in the FSL rats than in the SD rats following I/R injury (62.4+/-4.2 compared with 46.9+/-2.9%; P<0.05). IPC reduced the infarct size (P<0.01) and improved haemodynamic function (P<0.01) in both FSL and SD rats. No significant difference was found in blood glucose levels between the two groups measured after 12 h of fasting, but fasting plasma insulin (70.1+/-8.9 compared with 40.9+/-4.7 pmol/l; P<0.05) and the HOMA (homoeostatic model assessment) index (P<0.01) were significantly higher in FSL rats compared with SD rats. In conclusion, FSL rats had larger infarct sizes following I/R injury and were found to be hyperinsulinaemic compared with SD rats, but appeared to have a maintained cardioprotective mechanism against I/R injury, as IPC reduced infarct size in these rats. This animal model may be useful in future studies when examining the mechanisms that contribute to the cardiovascular complications associated with depression.

  17. Overexpression of TIMP3 Protects Against Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Apoptosis Through ROS/Mapks Pathway.

    Science.gov (United States)

    Liu, Hui; Jing, Xibo; Dong, Aiqiao; Bai, Baobao; Wang, Haiyan

    2017-01-01

    Myocardial ischemia/reperfusion (I/R) injury remains a great challenge in clinical therapy. Tissue inhibitor of metalloproteinases 3 (TIMP3) plays a crucial role in heart physiological and pathophysiological processes. However, the effects of TIMP3 on I/R injury remain unknown. C57BL/6 mice were infected with TIMP3 adenovirus by local delivery in myocardium followed by I/R operation or doxorubicin treatment. Neonatal rat cardiomyocytes were pretreated with TIMP3 adenovirus prior to anoxia/reoxygenation (A/R) treatment in vitro. Histology, echocardiography, in vivo phenotypical analysis, flow cytometry and western blotting were used to investigate the altered cardiac function and underlying mechanisms. The results showed that upregulation of TIMP3 in myocardium markedly inhibited myocardial infarct areas and the cardiac dysfunction induced by I/R or by doxorubicin treatment. TUNEL staining revealed that TIMP3 overexpression attenuated I/R-induced myocardial apoptosis, accompanied by decreased Bax/Bcl-2 ratio, Cleaved Caspase-3 and Cleaved Caspase-9 expression. In vitro, A/R-induced cardiomyocyte apoptosis was abrogated by pharmacological inhibition of reactive oxygen species (ROS) production or MAPKs signaling. Attenuation of ROS production reversed A/R-induced MAPKs activation, whereas MAPKs inhibitors showed on effect on ROS production. Furthermore, in vivo or in vitro overexpression of TIMP3 significantly inhibited I/R- or A/R-induced ROS production and MAPKs activation. Our findings demonstrate that TIMP3 upregulation protects against cardiac I/R injury through inhibiting myocardial apoptosis. The mechanism may be related to inhibition of ROS-initiated MAPKs pathway. This study suggests that TIMP3 may be a potential therapeutic target for the treatment of I/R injury. © 2017 The Author(s). Published by S. Karger AG, Basel.

  18. Gaseous hydrogen sulfide protects against myocardial ischemia-reperfusion injury in mice partially independent from hypometabolism

    NARCIS (Netherlands)

    Snijder, Pauline M.; de Boer, Rudolf A.; Bos, Eelke M.; van den Born, Joost C.; Ruifrok, Willem-Peter T.; Vreeswijk-Baudoin, Inge; van Dijk, Marcory C. R. F.; Hillebrands, Jan-Luuk; Leuvenink, Henri G. D.; van Goor, Harry

    2013-01-01

    Background: Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H2S) is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant

  19. Thrombolytic therapy of acute myocardial infarction alters collagen metabolism

    DEFF Research Database (Denmark)

    Høst, N B; Hansen, S S; Jensen, L T

    1994-01-01

    The objective of the study was to monitor collagen metabolism after thrombolytic therapy. Sequential measurements of serum aminoterminal type-III procollagen propeptide (S-PIIINP) and carboxyterminal type-I procollagen propeptide (S-PICP) were made in 62 patients suspected of acute myocardial...

  20. Clinical features of acute myocardial infarction: A report from Halibet ...

    African Journals Online (AJOL)

    Introduction. Acute myocardial infarction (AMI) still remains a major reason for ICU admission although mortality ... of patients admitted to the ICU with AMI during four years period from May 1997 to June 2001 were ... Characteristic findings on 12 lead electrocardiogram tracing of elevation of ST segment in contiguous leads ...

  1. Myocardial stress in patients with acute cerebrovascular events

    DEFF Research Database (Denmark)

    Jespersen, C.M.; Hansen, J.F.

    2008-01-01

    Signs of myocardial involvement are common in patients with acute cerebrovascular events. ST segment deviations, abnormal left ventricular function, increased N-terminal pro-brain natriuretic peptide (NT-proBNP), prolonged QT interval, and/or raised troponins are observed in up to one third...

  2. The inflammatory response in myocarditis and acute myocardial infarction

    NARCIS (Netherlands)

    Emmens, R.W.

    2016-01-01

    This thesis is about myocarditis and acute myocardial infarction (AMI). These are two cardiac diseases in which inflammation of the cardiac muscle occurs. In myocarditis, inflammation results in the elimination of a viral infection of the heart. During AMI, one of the coronary arteries is occluded,

  3. Thrombolysis in acute myocardial infarction : factors determining its efficacy

    NARCIS (Netherlands)

    Brügemann, Johannes

    1994-01-01

    Insight in the mechanisms leading to acute myocardial infarction (MI) has resulted in the administration of exogenous plasminogen activator, later called thrombolytic therapy. This treatment was associated with a significant reduction in mortality and morbidity. However, success has not always been

  4. Silent ischemia and severity of pain in acute myocardial infarction

    DEFF Research Database (Denmark)

    Nielsen, F E; Nielsen, S L; Knudsen, F

    1991-01-01

    An overall low tendency to complain of pain, due to a low perception of pain, has been suggested in the pathogenesis of silent ischemia, independent of the extent of the diseased coronaries and a history of previous acute myocardial infarction. This hypothesis has been tested indirectly...

  5. Depressed natural killer cell activity in acute myocardial infarction

    DEFF Research Database (Denmark)

    Klarlund, K; Pedersen, B K; Theander, T G

    1987-01-01

    Natural killer (NK) cell activity against K562 target cells was measured in patients within 24 h of acute myocardial infarction (AMI) and regularly thereafter for 6 weeks. NK cell activity was suppressed on days 1, 3, and 7 (P less than 0.01), day 14 (P less than 0.05) and at 6 weeks (P = 0.05) w...

  6. Frequency and Pattern of Acute Myocardial Infarction in the ...

    African Journals Online (AJOL)

    Acute myocardial infarction has been regarded as one of the rarest cardiovascular diseases in the African continent. Recent findings have shown that the incidence is on the increase. To provide more information on the burden of this deadly disease in Nigeria and in the West African sub –region. This study is a 10 - year ...

  7. COLIN trial: Value of colchicine in the treatment of patients with acute myocardial infarction and inflammatory response.

    Science.gov (United States)

    Akodad, Mariama; Lattuca, Benoît; Nagot, Nicolas; Georgescu, Vera; Buisson, Mathilde; Cristol, Jean-Paul; Leclercq, Florence; Macia, Jean-Christophe; Gervasoni, Richard; Cung, Thien-Tri; Cade, Stéphane; Cransac, Frédéric; Labour, Jessica; Dupuy, Anne-Marie; Roubille, François

    Inflammation is involved during acute myocardial infarction, and could be an interesting target to prevent ischaemia-reperfusion injuries. Colchicine, known for its pleiotropic anti-inflammatory effects, could decrease systemic inflammation in this context. To evaluate the impact of colchicine on inflammation in patients admitted for ST-segment elevation myocardial infarction (STEMI). All patients admitted for STEMI with one of the main coronary arteries occluded, and successfully treated with percutaneous coronary intervention, were included consecutively. Patients were randomized to receive either 1mg colchicine once daily for 1 month plus optimal medical treatment or optimal medical treatment only. C-reactive protein (CRP) was assessed at admission and daily until hospital discharge. The primary endpoint was CRP peak value during the index hospitalization. Forty-four patients were included: 23 were treated with colchicine; 21 received conventional treatment only. At baseline, both groups were well balanced regarding age, sex, risk factors, thrombolysis in myocardial infarction flow and reperfusion delay. The culprit artery was more often the left anterior descending artery in the colchicine group (P=0.07), reflecting a more severe group. There was no significant difference in mean CRP peak value between the colchicine and control groups (29.03mg/L vs 21.86mg/L, respectively; P=0.36), even after adjustment for type of culprit artery (26.99 vs 24.99mg/L, respectively; P=0.79). In our study, the effect of colchicine on inflammation in the context of STEMI could not be demonstrated. Further larger studies may clarify the impact of colchicine in acute myocardial infarction. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  8. Intrapulmonary shear stress enhancement: a new therapeutic approach in acute myocardial ischemia.

    Science.gov (United States)

    Nour, Sayed; Yang, Daya; Dai, Gong; Wang, Qinmei; Feng, Minze; Lila, Nermine; Chachques, Juan Carlos; Wu, Guifu

    2013-10-09

    Ischemic heart disease (IHD) is a leading cause of mortality with insufficient results of current therapies, most probably due to maintained endothelial dysfunction conditions. Alternatively, we propose a new treatment that promotes endothelial shear stress (ESS) enhancement using an intrapulmonary pulsatile catheter. Twelve piglets, divided in equal groups of 6: pulsatile (P) and non-pulsatile (NP), underwent permanent left anterior descending coronary artery ligation through sternotomy. After 1 h of ischemia and heparin injection (150 IU/kg): in P group, a pulsatile catheter was introduced into the pulmonary trunk and pulsated intermittently over 1 h, and irrespective of heart rate (110 bpm). In NP group, nitrates were given (7 ± 2 mg/kg/min) for 1 h. In P group all 6 animals survived ischemia for 120 min, but in NP group only 2 animals survived. The 4 animals that died during the experiment in NP group survived for 93 ± 14 min. Hemodynamics and cardiac output (CO) were significantly improved in P group compared with NP group: CO was 0.92 ± 0.15 vs. 0.52 ± 0.08 in NP group (L/min; p p P group versus NP group: pulmonary resistance was 119 ± 13 vs. 400 ± 42 and systemic resistance was 319 ± 43 vs. 1857 ± 326, respectively. Myocardial apoptosis was significantly (p P group (0.66 ± 0.07) vs. (4.18 ± 0.27) in NP group. Myocardial endothelial NO synthase mRNA expression was significantly (p P group (0.90 ± 0.09) vs. (0.25 ± 0.04) in NP group. Intrapulmonary pulsatile catheter could improve hemodynamics and myocardial contractility in acute myocardial ischemia. This represents a cost-effective method, suitable for emergency setting as a first priority, regardless of classical coronary reperfusion. © 2013.

  9. Acute myocardial infarction mortality in Cuba, 1999-2008.

    Science.gov (United States)

    Armas, Nurys B; Ortega, Yanela Y; de la Noval, Reinaldo; Suárez, Ramón; Llerena, Lorenzo; Dueñas, Alfredo F

    2012-10-01

    Acute myocardial infarction is one of the leading causes of death in the world. This is also true in Cuba, where no national-level epidemiologic studies of related mortality have been published in recent years. Describe acute myocardial infarction mortality in Cuba from 1999 through 2008. A descriptive study was conducted of persons aged ≥25 years with a diagnosis of acute myocardial infarction from 1999 through 2008. Data were obtained from the Ministry of Public Health's National Statistics Division database for variables: age; sex; site (out of hospital, in hospital or in hospital emergency room) and location (jurisdiction) of death. Proportions, age- and sex-specific rates and age-standardized overall rates per 100,000 population were calculated and compared over time, using the two five-year time frames within the study period. A total of 145,808 persons who had suffered acute myocardial infarction were recorded, 75,512 of whom died, for a case-fatality rate of 51.8% (55.1% in 1999-2003 and 49.7% in 2004-2008). In the first five-year period, mortality was 98.9 per 100,000 population, falling to 81.8 per 100,000 in the second; most affected were people aged ≥75 years and men. Of Cuba's 14 provinces and special municipality, Havana, Havana City and Camagüey provinces, and the Isle of Youth Special Municipality showed the highest mortality; Holguín, Ciego de Ávila and Granma provinces the lowest. Out-of-hospital deaths accounted for the greatest proportion of deaths in both five-year periods (54.8% and 59.2% in 1999-2003 and 2004-2008, respectively). Although risk of death from acute myocardial infarction decreased through the study period, it remains a major health problem in Cuba. A national acute myocardial infarction case registry is needed. Also required is further research to help elucidate possible causes of Cuba's high acute myocardial infarction mortality: cardiovascular risk studies, studies of out-of-hospital mortality and quality of care

  10. Suboptimal medical care of patients with ST-Elevation Myocardial Infarction and Renal Insufficiency: results from the Korea acute Myocardial Infarction Registry

    Directory of Open Access Journals (Sweden)

    Choi Joon

    2012-09-01

    Full Text Available Abstract Background The clinical outcomes of ST-segment elevation myocardial infarction (STEMI are poor in patients with renal insufficiency. This study investigated changes in the likelihood that patients received optimal medical care throughout the entire process of myocardial infarction management, on the basis of their glomerular filtration rate (GFR. Methods This study analyzed 7,679 patients (age, 63 ± 13 years; men 73.6% who had STEMI and were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR from November 2005 to August 2008. The study subjects were divided into 5 groups corresponding to strata used to define chronic kidney disease stages. Results Patients with lower GFR were less likely to present with typical chest pain. The average symptom-to-door time, door-to-balloon time, and symptom-to-balloon time were longer with lower GFR than higher GFR. Primary reperfusion therapy was performed less frequently and the results of reperfusion therapy were poorer in patients with renal insufficiency; these patients were less likely to receive adjunctive medical treatment, such as treatment with aspirin, clopidogrel, β-blocker, angiotensin-converting enzyme (ACE inhibitor/angiotensin-receptor blocker (ARB, or statin, during hospitalization and at discharge. Patients who received less intense medical therapy had worse clinical outcomes than those who received more intense medical therapy. Conclusions Patients with STEMI and renal insufficiency had less chance of receiving optimal medical care throughout the entire process of MI management, which may contribute to worse outcomes in these patients.

  11. [Variability in the management and prognosis at short- and medium-term of myocardial infarct in Spain: the PRIAMHO study. Registration Project of Hospital Acute Myocardial Infarct].

    Science.gov (United States)

    Cabadés, A; López-Bescós, L; Arós, F; Loma-Osorio, A; Bosch, X; Pabón, P; Marrugat, J

    1999-10-01

    The paucity of data on myocardial infarction management and results in Spain lead to the design of the PRIAMHO study (Proyecto de Registro de Infarto Agudo de Miocardio Hospitalario [Acute Myocardial Infarction Hospital Registration Project]) which developed standard methods to collect information on the management of patients with such a condition and their characteristics. The variability results among hospitals in myocardial infarction management and in one-year mortality are presented. A cohort study with a one-year follow-up was designed to register all patients diagnosed with acute myocardial infarction discharged from 24 Spanish hospitals that completed all the requisites to participate. The demographic and clinical characteristics of the patients, their management during the coronary care unit stage, and the outcome and complications were prospectively registered. Standard definitions for diagnosis were used. Confidentiality regarding patient identity and participating centers was guaranteed. 5,242 (77.6%) of the 6,756 patients with myocardial infarction admitted in the 24 participating hospitals were registered in the coronary care units. Half of the centers had an on-site hemodynamic laboratory and in seven coronary surgery. The delay between symptom-onset and emergency room admission was 2 hours. Acute pulmonary edema or cardiogenic shock was developed by 16.6% of patients and 41.8% received thrombolysis. Mean time delay between symptom-onset and thrombolysis was 3 hours. A large variability in the use of beta-blockers, thrombolysis, echocardiography, coronary catheterization angiography and invasive revascularization was observed among hospitals. Mortality in the coronary care unit was 10.9% and increased to 14.0% at 28 days and to 18.5% at one year with considerable variation among hospitals. Four hospitals showed higher mortality among their patients, independently from the proportion of diabetes, hypertension, women, anterior location of myocardial

  12. The Influence of findings of coronary artery on myocardial salvage in acute myocardial infarction

    International Nuclear Information System (INIS)

    Itano, Midoriko; Naruse, Hitoshi; Morita, Masato; Kawamoto, Hideo; Yamamoto, Juro; Fukutake, Naoshige; Ohyanagi, Mitsumasa; Iwasaki, Tadaaki; Fukuchi, Minoru

    1992-01-01

    201 Tl stress myocardial scintigraphy was performed in convalescent patients with acute myocardial infarction, to evaluate the influence of stenosis and collateral circulation of coronary artery in acute phase, on myocardial salvage in chronic phase. In 14 cases of unsuccessful coronary revascularization (complete occlusion), a complete defect of thallium imaging in chronic phase was seen in only one case of four cases with good collateral circulation, while eight of 10 cases with poor collateral circulation. In 16 cases with collateral circulation, six cases showed a complete defect, although the target vessel had improved to less than 75% of stenosis. However, in cases of good collateral circulation, no case showed a complete defect when the target vessel had improved to less than 75% of stenosis. The myocardial salvage is quite possible (p<0.05), when the coronary angiography in acute phase showed the forward flow (99% or 90% of stenosis) before coronary revascularization and/or good collateral circulation (Rentrop 2deg or 3deg). (author)

  13. Technetium-99m stannous pyrophosphate myocardial scintigraphy. Reliability and limitations in assessment of acute myocardial infraction

    International Nuclear Information System (INIS)

    Cowley, M.J.; Mantle, J.A.; Rogers, W.J.; Rossell, R.O. Jr.; Rackley, C.E.; Logic, J.R.

    1977-01-01

    Two hundred-three patients had technetium 99m (stannous) pyrophosphate myocardial scintigrams for the evaluation of chest pain and suspected acute myocardial infarction. In addition to routine imaging at 60 to 90 minutes after injection of the radiopharmaceutical, the blood pool was imaged immediately in each patient for comparison with routine anterior, left anterior oblique, and left lateral views. Further delayed studies were obtained when residual blood pool activity was identified. Seventy patients had acute myocardial infarction by clinical, electrocardiographic, and enzymatic (CK-MB) criteria. Sixty-five of these 70 patients with acute infarction had positive myocardial scintigrams, with one technically unsatisfactory study. Only four of the 70 patients had negative scintigrams when imaged 18 to 72 hours after infarction in this study. Technically satisfactory scintigrams were recorded in 125 patients without evidence of infarction. Ninety-six had negative scintigrams at 60 to 90 minutes, while 19 patients (15%) had precordial activity at 60 to 90 minutes which was identical in distribution to early blood pool images and cleared with further delay. With these included, the true negative incidence was 92%. Ten of 125 patients had false positive scintigrams; two had recent cardioversion with resultant chest wall damage. The other eight patients had previous infarction 1 1 / 2 to 72 months earlier and had akinetic segments shown angiographically in the areas of the persistently positive scintigrams

  14. Association between coronary flow reserve, left ventricular systolic function, and myocardial viability in acute myocardial infarction

    DEFF Research Database (Denmark)

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

    2010-01-01

    /s (8.5;12.5), P = 0.04] and end-systolic volume increased [49.5 mL (38;66) vs. 42 (31;61), P = 0.04] in patients with low compared with preserved CFR. Among 87 (58%) patients with resting wall motion abnormalities, 28 met the criteria for viability. One of 53 (2%) met the criteria for viability......AIMS: To investigate the relationships between coronary flow reserve (CFR), left ventricular (LV) systolic function, and myocardial viability in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: In 149 patients with a first AMI, we estimated CFR non-invasively and assessed LV...

  15. Correlation of ABO blood groups with spontaneous recanalization in acute myocardial infarction.

    Science.gov (United States)

    Lin, Xian-Liang; Zhou, Bing-Yang; Li, Sha; Li, Xiao-Lin; Luo, Zhu-Rong; Li, Jian-Jun

    2017-08-01

    Although previous studies have demonstrated the relationship between ABO blood groups and cardiovascular disease, the association of ABO blood type with spontaneous recanalization (SR) in patients with acute myocardial infarction (AMI) has not been previously investigated. We performed an initial exploratory study on the association of ABO blood groups with the presence of SR in 1209 patients with AMI. They were divided into two groups according to the thrombolysis in myocardial infarction (TIMI) grades: no-SR group (TIMI 0-1, n = 442) and SR group (TIMI 2-3, n = 767). To confirm our primary findings, data from a second AMI population (n = 200) was analyzed. In the initial data, SR group had a significantly higher percentage of blood type O and a lower percentage of blood type A compared to the no-SR group. Multivariate logistic regression analysis showed that blood type O was positively associated with SR (odds ratio: 1.40, 95% confidence interval: 1.05-1.87, p = .02), and this finding was confirmed in our second population. The present study demonstrates that blood type O was independently and positively associated with an open culprit artery in patients with AMI, suggesting that the ABO blood type is not only associated with the susceptibility to coronary artery disease but also to spontaneous reperfusion in AMI patients.

  16. Suspected acute myocardial infarction in a dystrophin-deficient dog.

    Science.gov (United States)

    Schneider, Sarah Morar; Coleman, Amanda Erickson; Guo, Lee-Jae; Tou, Sandra; Keene, Bruce W; Kornegay, Joe N

    2016-06-01

    Golden retriever muscular dystrophy (GRMD) is a model for the genetically homologous human disease, Duchenne muscular dystrophy (DMD). Unlike the mildly affected mdx mouse, GRMD recapitulates the severe DMD phenotype. In addition to skeletal muscle involvement, DMD boys develop cardiomyopathy. While the cardiomyopathy of DMD is typically slowly progressive, rare early episodes of acute cardiac decompensation, compatible with myocardial infarction, have been described. We report here a 7-month-old GRMD dog with an apparent analogous episode of myocardial infarction. The dog presented with acute signs of cardiac disease, including tachyarrhythmia, supraventricular premature complexes, and femoral pulse deficits. Serum cardiac biomarkers, cardiac-specific troponin I (cTnI) and N-terminal prohormone of B-type natriuretic peptide (NT-proBNP), were markedly increased. Echocardiography showed areas of hyperechoic myocardial enhancement, typical of GRMD cardiomyopathy. Left ventricular dyskinesis and elevated cTnI were suggestive of acute myocardial damage/infarction. Over a 3-year period, progression to a severe dilated phenotype was observed. Copyright © 2016 Elsevier B.V. All rights reserved.

  17. Gaseous hydrogen sulfide protects against myocardial ischemia-reperfusion injury in mice partially independent from hypometabolism

    OpenAIRE

    Snijder, Pauline M.; de Boer, Rudolf A.; Bos, Eelke M.; van den Born, Joost C.; Ruifrok, Willem-Peter T.; Vreeswijk-Baudoin, Inge; van Dijk, Marcory C. R. F.; Hillebrands, Jan-Luuk; Leuvenink, Henri G. D.; van Goor, Harry

    2013-01-01

    BACKGROUND: Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H2S) is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant properties. We investigated whether gaseous H2S administration is protective in cardiac IRI and whether non-hypometabolic concentrations of H2S have similar protective properties. METHODS: Male C57BL/6...

  18. Oxidative Stress-Related Biomarkers in Essential Hypertension and Ischemia-Reperfusion Myocardial Damage

    OpenAIRE

    Rodrigo, Ram?n; Libuy, Mat?as; Feli?, Felipe; Hasson, Daniel

    2013-01-01

    Cardiovascular diseases are a leading cause of mortality and morbidity worldwide, with hypertension being a major risk factor. Numerous studies support the contribution of reactive oxygen and nitrogen species in the pathogenesis of hypertension, as well as other pathologies associated with ischemia/reperfusion. However, the validation of oxidative stress-related biomarkers in these settings is still lacking and novel association of these biomarkers and other biomarkers such as endothelial pr...

  19. Protective effect of sauchinone against regional myocardial ischemia/reperfusion injury: inhibition of p38 MAPK and JNK death signaling pathways.

    Science.gov (United States)

    Kim, Seok Jai; Jeong, Cheol Won; Bae, Hong Beom; Kwak, Sang Hyun; Son, Jong-Keun; Seo, Chang-Seob; Lee, Hyun-Jung; Lee, JongUn; Yoo, Kyung Yeon

    2012-05-01

    Sauchinone has been known to have anti-inflammatory and antioxidant effects. We determined whether sauchinone is beneficial in regional myocardial ischemia/reperfusion (I/R) injury. Rats were subjected to 20 min occlusion of the left anterior descending coronary artery, followed by 2 hr reperfusion. Sauchinone (10 mg/kg) was administered intraperitoneally 30 min before the onset of ischemia. The infarct size was measured 2 hr after resuming the perfusion. The expression of cell death kinases (p38 and JNK) and reperfusion injury salvage kinases (phosphatidylinositol-3-OH kinases-Akt, extra-cellular signal-regulated kinases [ERK1/2])/glycogen synthase kinase (GSK)-3β was determined 5 min after resuming the perfusion. Sauchinone significantly reduced the infarct size (29.0% ± 5.3% in the sauchinone group vs 44.4% ± 6.1% in the control, P death signaling pathways.

  20. Rat Models of Ventricular Fibrillation Following Acute Myocardial Infarction

    DEFF Research Database (Denmark)

    Hundahl, Laura A.; Tfelt-Hansen, Jacob; Jespersen, Thomas

    2017-01-01

    A number of animal models have been designed in order to unravel the underlying mechanisms of acute ischemia-induced arrhythmias and to test compounds and interventions for antiarrhythmic therapy. This is important as acute myocardial infarction (AMI) continues to be the major cause of sudden car...... for ventricular arrhythmias occurring during the acute phase of AMI. It provides a description of models developed, advantages and disadvantages of rats, as well as an overview of the most important interventions investigated and the relevance for human pathophysiology....

  1. B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

    Science.gov (United States)

    Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

    2014-01-01

    Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6Chi monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell–selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction. PMID:24037091

  2. A CLINICAL CASE OF ACUTE ALLERGIC MYOCARDITIS SIMULATING MYOCARDIAL INFARCTION

    Directory of Open Access Journals (Sweden)

    N. A. Shostak

    2015-01-01

    Full Text Available Objective: to describe a clinical case of evolving acute eosinophilic myocarditis simulating coronary heart disease. Subjects and methods. Patient B. aged 62 years was admitted to Intensive Care Unit Fifteen, N.I. Pirogov First Moscow City Clinical Hospital, by being transferred from Thailand with a referral diagnosis of acute myocardial infarction made on November 1, 2012, with complaints of pressing and aching heart pains. At a Phuket hospital, his electrocardiogram recorded atrial fibrillation; indirect cardiac massage, electric pulse therapy, and mechanical ventilation were performed. After being admitted to the N.I. Pirogov First Moscow City Clinical Hospital, the patient underwent examination: estimation of laboratory indicators over time, electrocardiography (ECG, echocardiography, Holter ECG monitoring, and myocardial scintigraphy. Results. The patient had a history of an allergic reaction as urticaria to the ingestion of fish products. His examination showed practically all diagnostic criteria for allergic myocarditis: hypereosinophilia (the admission level of eosinophils was 9% with their further normalization; the characteristic clinical presentation of myocarditis (pressing retrosternal pain; elevated levels of cardiac specific enzymes (creatinine phosphokinase-MB, lactate dehydrogenase, troponin T; ECG changes – myocardial hypokinesis in the acute period, followed by its pattern normalization. of the pattern. Myocardial scintigraphy (by taking into account the fact that the patient had had a new allergic reaction episode, the investigators decided not to perform coronary angiography revealed decreased radiopharmaceutical accumulation in the lower left ventricular wall in the right coronary arterial bed; perfusion remained in the other myocardial walls. Conclusion. This clinical case reflects the specific features of the course of and difficulties in the diagnosis of acute allergic myocarditis that, in most cases, has no specific

  3. Development of novel {sup 99m} T C-labeled radiopharmaceutical for imaging acute myocardial infarction in patients

    Energy Technology Data Exchange (ETDEWEB)

    Mariani, Giuliano [Genoa Univ. (Italy). Nuclear Medicine Service; Strauss, H. Willian [Stanford University, CA (United States). School of Medicine. Dept. of Radiology

    1997-12-31

    Full text. Definitive diagnosis of acute myocardial infarction is often difficult in the emergency room. Although electrocardiograms, serum enzyme assays, and clinical history are helpful, the diagnosis remains elusive in a significant fraction of patients, in this lecture. We review the sequential steps that have led to the development of a novel {sup 99m} Tc-labeled radio pharmaceutical for imaging acute myocardial infarction in patients. In particular, we will focus on the results of a human study which was performed to determine if radionuclide imaging with {sup 99m} Tc labeled D-Glucaric acid ({sup 99m} Tc- G L A), an agent that locates in zones of necrosis within 30 min of vessel occlusion in the animal mode, could be used to identify acute myocardial infarction shortly after onset of chest pain. Twenty-eight presenting to the emergency with symptoms suggestive of acute infarction were evaluated with {sup 99m} Tc-G L A imaging. The agent was injected as early as possible in the course of the patients clinical care (average 11,5 hours {l_brace}range 1-41 {r_brace}) after onset of chest pain, and imaging was. Of 15 patients with acute infarction injected within 9 hours of onset of chest pain, all patients had positive scans. Negative scans were found in 13 patients including 10 patients with acute infarction injected later than 9 hours, and 3 patients who were subsequently found not to have myocardial infarction (unstable angina) even though they were injected within 9 hours of chest pain. In the 15 patients with positive scans, concentration of {sup 99m} Tc - G L A in the zone of necrosis was greater in patients who had successful reperfusion therapy than in those with occlusion at the time of injection. However, even in patients with occlusion, uptake was observed in the zone of necrosis. Six patients reinjected with {sup 99m} Tc- G L A 4-6 weeks after their initial study had negative scans. This study suggests that {sup 99m} Tc-glucaric acid locates in zones

  4. Hospital process intervals, not EMS time intervals, are the most important predictors of rapid reperfusion in EMS Patients with ST-segment elevation myocardial infarction.

    Science.gov (United States)

    Clark, Carol Lynn; Berman, Aaron D; McHugh, Ann; Roe, Edward Jedd; Boura, Judith; Swor, Robert A

    2012-01-01

    To assess the relationship of emergency medical services (EMS) intervals and internal hospital intervals to the rapid reperfusion of patients with ST-segment elevation myocardial infarction (STEMI). We performed a secondary analysis of a prospectively collected database of STEMI patients transported to a large academic community hospital between January 1, 2004, and December 31, 2009. EMS and hospital data intervals included EMS scene time, transport time, hospital arrival to myocardial infarction (MI) team activation (D2Page), page to catheterization laboratory arrival (P2Lab), and catheterization laboratory arrival to reperfusion (L2B). We used two outcomes: EMS scene arrival to reperfusion (S2B) ≤90 minutes and hospital arrival to reperfusion (D2B) ≤90 minutes. Means and proportions are reported. Pearson chi-square and multivariate regression were used for analysis. During the study period, we included 313 EMS-transported STEMI patients with 298 (95.2%) MI team activations. Of these STEMI patients, 295 (94.2%) were taken to the cardiac catheterization laboratory and 244 (78.0%) underwent percutaneous coronary intervention (PCI). For the patients who underwent PCI, 127 (52.5%) had prehospital EMS activation, 202 (82.8%) had D2B ≤90 minutes, and 72 (39%) had S2B ≤90 minutes. In a multivariate analysis, hospital processes EMS activation (OR 7.1, 95% CI 2.7, 18.4], Page to Lab [6.7, 95% CI 2.3, 19.2] and Lab arrival to Reperfusion [18.5, 95% CI 6.1, 55.6]) were the most important predictors of Scene to Balloon ≤ 90 minutes. EMS scene and transport intervals also had a modest association with rapid reperfusion (OR 0.85, 95% CI 0.78, 0.93 and OR 0.89, 95% CI 0.83, 0.95, respectively). In a secondary analysis, Hospital processes (Door to Page [OR 44.8, 95% CI 8.6, 234.4], Page 2 Lab [OR 5.4, 95% CI 1.9, 15.3], and Lab arrival to Reperfusion [OR 14.6 95% CI 2.5, 84.3]), but not EMS scene and transport intervals were the most important predictors D2B ≤90

  5. Myocardial infarction with acute valvular regurgitation.

    Science.gov (United States)

    Murthy, Sandhya; Greenberg, Mark; Wharton, Ronald

    2012-08-01

    Left-sided valvular lesions are commonly associated with acute and chronic coronary syndromes. Ischemic mitral regurgitation is well described in the literature. We report a case of acute ischemic right-sided valvular disease in which the presenting symptom of an infarction was severe tricuspid regurgitation. This rare entity is usually caused by distortion of the valve apparatus due to underlying wall motion abnormalities. In conclusion, tricuspid regurgitation is an important yet uncommon presentation of acute ischemia that requires a high degree of suspicion for diagnosis.

  6. Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction.

    Science.gov (United States)

    Cottin, Y; Doise, J M; Maupoil, V; Tannière-Zeller, M; Dalloz, F; Maynadié, M; Walker, M K; Louis, P; Carli, P M; Wolf, J E; Rochette, L

    1998-01-01

    Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in

  7. Ablation of C/EBP homologous protein increases the acute phase mortality and doesn't attenuate cardiac remodeling in mice with myocardial infarction.

    Science.gov (United States)

    Luo, Guangjin; Li, Qingman; Zhang, Xiajun; Shen, Liang; Xie, Jiahe; Zhang, Jingwen; Kitakaze, Masafumi; Huang, Xiaobo; Liao, Yulin

    2015-08-14

    Endoplasmic reticulum stress is a proapoptotic and profibrotic stimulus. Ablation of C/EBP homologous protein (CHOP) is reported to reverse cardiac dysfunction by attenuating cardiac endoplasmic reticulum stress in mice with pressure overload or ischemia/reperfusion, but it is unclear whether loss of CHOP also inhibits cardiac remodeling induced by permanent-infarction. In mice with permanent ligation of left coronary artery, we found that ablation of CHOP increased the acute phase mortality. For the mice survived to 4 weeks, left ventricular anterior (LV) wall thickness was larger in CHOP knockout mice than in the wildtype littermates, while no difference was noted on posterior wall thickness, LV dimensions, LV fractional shortening and ejection fraction. Similarly, invasive assessment of LV hemodynamics, morphological analysis of heart and lung weight indexes, myocardial fibrosis and TUNEL-assessed apoptosis showed no significant differences between CHOP knockout mice and their wildtype ones, while in mice with ischemia for 45 min and reperfusion for 1 week, myocardial fibrosis and apoptosis in the infarct area were significantly attenuated in CHOP knockout mice. These findings indicate that ablation of CHOP doesn't ameliorate cardiac remodeling induced by permanent-myocardial infarction, which implicates that early reperfusion is a prerequisite for ischemic myocardium to benefit from CHOP inhibition. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

  8. Relationship between availability of the collateral circulation and ischemic time for myocardial viability in patients with acute myocardial infarction. Assessment by technetium-99m tetrofosmin single photon emission computed tomography

    International Nuclear Information System (INIS)

    Kanamori, Norio; Kondo, Makoto; Fukuoka, Yoshitomo; Higuchi, Hirokazu; Kubota, Tomoyuki; Matsuoka, Ryota; Araki, Makoto; Tanio, Hitoshi; Doyama, Kiyoshi

    2007-01-01

    Myocardial accumulation before reperfusion therapy of a radioactive tracer in the completely occluded region, conceivably reflects the viability of myocytes and degree of collateral circulation. To confirm this, the present study examined the relationship in the title. Subjects were 33 patients (F 7, M 26; average age 65 y) of the first 1-branch acute myocardial infarction and of TIMI (thrombolysis in myocardial infarction trial) grade 0 who recovered to TIMI 3 within 12 hr after attack: 99m Tc-tetrofosmin, 740 MBq, was intravenously injected before reperfusion and just after which, SPECT imaging (TF-SPECT) was conducted with Toshiba E. CAM, and regional severity score index (RSSI) (0-3) was calculated. About 1 week later, to see the myocardial viability in the chronic phase, GITl (Glucose-Insulin- 201 Tl) (111 MBq) SPECT was performed 30 min after its injection to calculate RSSI as above, and the echocardiography with ALOKA Pro Sound SSD-4000 or SIEMENS Acuson SEQUOIA C256 was done to calculate the regional wall motion score index (RWMSI) (0-4). RWMSI was found significantly correlated with TF-RSSI, the group with the better collateral circulation (TF-RSSI, 1.9 or less) exhibited significantly lower GITl-RSSI and RWMSI, and correlation between the ischemic time and neither TF-RSSI, GITl-RSSI nor RWMSI was found. Thus under these conditions, the development of collateral vessels was found to have potential protective effects on myocardium independently on the ischemic time. (T.I.)

  9. Combined analysis of the safety of intra-coronary drug delivery during primary percutaneous coronary intervention for acute myocardial infarction: A study of three clinical trials

    Directory of Open Access Journals (Sweden)

    Krishnaraj S Rathod

    2017-08-01

    Full Text Available Background The local injection of novel cardioprotective study drugs prior to percutaneous coronary intervention could cause embolisation of thrombus, resulting in increased reperfusion injury and subsequent infarct size. The aim of this study was to assess the safety of the delivery of an intracoronary therapy delivered during primary percutaneous coronary intervention for acute myocardial infarction prior to the re-establishment of thrombolysis in myocardial infarction III flow. Methods One hundred sixty-seven patients with acute myocardial infarction successfully reperfused through primary percutaneous coronary intervention and undergoing Cardiac MRI within the first week after reperfusion were studied. Patients either underwent the delivery of an intracoronary agent (IMP or placebo prior to balloon dilatation ( n  = 80 or standard primary percutaneous coronary intervention procedure ( n  = 117. Results Baseline characteristics were similar between the two groups. There were a similar number of successful procedures (IC IMP 75 (93.8% vs. No IMP 114, (97.4%, p  = 0.374, rates of no-reflow (IC IMP 1 (1.3% vs. No IMP 2 (1.7%, p  = 0.99 and levels of ST segment resolution (88.5% IC IMP vs. No IC IMP 87.0%, p  = 0.669 between the two groups. Similar levels of microvascular obstruction were seen between the two groups with a trend to reduced infarct size, and improved ejection fractions in the IMP group. Lower MACE rates were seen in the IMP group. Conclusion The local intracoronary infusion of potential cardioprotective agents prior to the restoration of TIMI flow in patients undergoing primary percutaneous coronary intervention for acute myocardial infarction appears to be safe and does not increase microvascular damage. This route should be considered when testing novel cardioprotective agents.

  10. Microvascular Coronary Flow Comparison in Acute Myocardial Infarction Angioplasty treated with a mesh covered stent (MGUARD Stent) versus Bare Metal Stent

    Energy Technology Data Exchange (ETDEWEB)

    Lindefjeld, Dante S., E-mail: dslindef@puc.cl [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Hospital Dr. Sótero del Río, Santiago-Chile (Chile); Guarda, Eduardo [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Méndez, Manuel [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Hospital Dr. Sótero del Río, Santiago-Chile (Chile); Martínez, Alejandro [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Pérez, Osvaldo [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Hospital Dr. Sótero del Río, Santiago-Chile (Chile); Fajuri, Alejandro; Marchant, Eugenio [Hospital Clínico, Pontificia Universidad Católica de Chile (Chile); Aninat, Mauricio; Torres, Humberto [Hospital Dr. Gustavo Fricke, Viña del Mar-Chile (Chile); Dussaillant, Gastón [Hospital Clínico Universidad de Chile, Santiago-Chile (Chile)

    2013-01-15

    Background: Distal embolization of thrombus/platelet aggregates decreases myocardial reperfusion during primary percutaneous coronary intervention (PCI), and is associated with worse immediate and long-term prognosis of patients with ST-elevation myocardial infarction (STEMI). Objective: Assess the efficacy of a mesh covered stent (MGuard™ stent, MGS) in preventing distal embolization and microvascular reperfusion impairment during primary PCI, compared with a bare metal stent (BMS). Methods: Forty patients with STEMI referred for primary PCI were randomized for stenting the culprit lesion with the MGS (n = 20) or a BMS (n = 20). Blinded experts performed off-line measurements of angiographic epicardial and microvascular reperfusion criteria: TIMI flow grade, myocardial blush, corrected TIMI frame count (cTFC). Results: At baseline clinical, angiographic and procedural variables were not different between groups. Post PCI TIMI flow grade was similar in both groups. We observed better myocardial Blush grade in group MGS compared to BMS (median value 3.0 vs 2.5, 2p = 0.006) and cTFC (mean cTFC: MGS 19.65 ± 4.07 vs BMS 27.35 ± 7.15, 2p < 0.001, cTFC mean difference MGS-BMS: 7.7, CI 95%: 3.94 to 11.46). MGS stent group had a higher percentage of successful angioplasty (cTFC ≤ 23: MGS 85% vs BMS 30%, 2p < 0.001). We had two cases of acute stent thrombosis (one for each group) at 30 days follow up, but no clinical events at 6 months follow up. Conclusions: In this exploratory study, MGS significantly improved microvascular reperfusion criteria compared with a BMS in primary PCI. However its safety and impact on clinical outcomes should be verified in larger randomized clinical trials.

  11. PET imaging of angiogenesis after myocardial infarction/reperfusion using a one-step labeled integrin-targeted tracer {sup 18}F-AlF-NOTA-PRGD2

    Energy Technology Data Exchange (ETDEWEB)

    Gao, Haokao [The Fourth Military Medical University, Department of Cardiology, Xijing Hospital, Xi' an (China); National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Laboratory of Molecular Imaging and Nanomedicine (LOMIN), Bethesda, MD (United States); Lang, Lixin; Guo, Ning; Quan, Qimeng; Hu, Shuo; Kiesewetter, Dale O.; Niu, Gang; Chen, Xiaoyuan [National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Laboratory of Molecular Imaging and Nanomedicine (LOMIN), Bethesda, MD (United States); Cao, Feng [The Fourth Military Medical University, Department of Cardiology, Xijing Hospital, Xi' an (China)

    2012-04-15

    The {alpha}{sub v}{beta}{sub 3} integrin represents a potential target for noninvasive imaging of angiogenesis. The purpose of this study was to evaluate a novel one-step labeled integrin {alpha}{sub v}{beta}{sub 3}-targeting positron emission tomography (PET) probe, {sup 18}F-AlF-NOTA-PRGD2, for angiogenesis imaging in a myocardial infarction/reperfusion (MI/R) animal model. Male Sprague-Dawley rats underwent 45-min transient left coronary artery occlusion followed by reperfusion. The myocardial infarction was confirmed by ECG, {sup 18}F-fluorodeoxyglucose (FDG) imaging, and cardiac ultrasound. In vivo PET imaging was used to determine myocardial uptake of {sup 18}F-AlF-NOTA-PRGD2 at different time points following reperfusion. The control peptide RAD was labeled with a similar procedure and used to confirm the specificity. Ex vivo autoradiographic analysis and CD31/CD61 double immunofluorescence staining were performed to validate the PET results. Myocardial origin of the {sup 18}F-AlF-NOTA-PRGD2 accumulation was confirmed by {sup 18}F-FDG and autoradiography. PET imaging demonstrated increased focal accumulation of {sup 18}F-AlF-NOTA-PRGD2 in the infarcted area which started at day 3 (0.28 {+-} 0.03%ID/g, p < 0.05) and peaked between 1 and 3 weeks (0.59 {+-} 0.16 and 0.55 {+-} 0.13%ID/g, respectively). The focal accumulation decreased but still kept at a higher level than the sham group after 4 months of reperfusion (0.31 {+-} 0.01%ID/g, p < 0.05). Pretreatment with unlabeled arginine-glycine-aspartic acid (RGD) peptide significantly decreased tracer uptake, indicating integrin specificity of this tracer. At 1 week after MI/R, uptake of the control tracer {sup 18}F-AlF-NOTA-RAD that does not bind to integrin, in the infarcted area, was only 0.21 {+-} 0.01%ID/g. Autoradiographic imaging showed the same trend of uptake in the myocardial infarction area. The time course of focal tracer uptake was consistent with the pattern of vascular density and integrin {beta

  12. Feature-tracking myocardial strain analysis in acute myocarditis. Diagnostic value and association with myocardial oedema

    Energy Technology Data Exchange (ETDEWEB)

    Luetkens, Julian A.; Schlesinger-Irsch, Ulrike; Kuetting, Daniel L.; Dabir, Darius; Homsi, Rami; Schmeel, Frederic C.; Sprinkart, Alois M.; Naehle, Claas P.; Schild, Hans H.; Thomas, Daniel [University of Bonn, Department of Radiology, Bonn (Germany); Doerner, Jonas [University Hospital Cologne, Department of Radiology, Cologne (Germany); Fimmers, Rolf [University of Bonn, Department of Medical Biometry, Informatics, and Epidemiology, Bonn (Germany)

    2017-11-15

    To investigate the diagnostic value of cardiac magnetic resonance (CMR) feature-tracking (FT) myocardial strain analysis in patients with suspected acute myocarditis and its association with myocardial oedema. Forty-eight patients with suspected acute myocarditis and 35 control subjects underwent CMR. FT CMR analysis of systolic longitudinal (LS), circumferential (CS) and radial strain (RS) was performed. Additionally, the protocol allowed for the assessment of T1 and T2 relaxation times. When compared with healthy controls, myocarditis patients demonstrated reduced LS, CS and RS values (LS: -19.5 ± 4.4% vs. -23.6 ± 3.1%, CS: -23.0 ± 5.8% vs. -27.4 ± 3.4%, RS: 28.9 ± 8.5% vs. 32.4 ± 7.4%; P < 0.05, respectively). LS (T1: r = 0.462, P < 0.001; T2: r = 0.436, P < 0.001) and CS (T1: r = 0.429, P < 0.001; T2: r = 0.467, P < 0.001) showed the strongest correlations with T1 and T2 relaxations times. Area under the curve of LS (0.79) was higher compared with those of CS (0.75; P = 0.478) and RS (0.62; P = 0.008). FT CMR myocardial strain analysis might serve as a new tool for assessment of myocardial dysfunction in the diagnostic work-up of patients suspected of having acute myocarditis. Especially, LS and CS show a sufficient diagnostic performance and were most closely correlated with CMR parameters of myocardial oedema. (orig.)

  13. Reperfusion facilitates reversible disruption of the human blood-brain barrier following acute ischaemic stroke

    International Nuclear Information System (INIS)

    Liu, Chang; Zhang, Sheng; Yan, Shenqiang; Zhang, Ruiting; Shi, Feina; Lou, Min; Ding, Xinfa; Parsons, Mark

    2018-01-01

    We aimed to detect early changes of the blood-brain barrier permeability (BBBP) in acute ischaemic stroke (AIS), with or without reperfusion, and find out whether BBBP can predict clinical outcomes. Consecutive AIS patients imaged with computed tomographic perfusion (CTP) before and 24 h after treatment were included. The relative permeability-surface area product (rPS) was calculated within the hypoperfused region (rPS hypo-i ), non-hypoperfused region of ischaemic hemisphere (rPS nonhypo-i ) and their contralateral mirror regions (rPS hypo-c and rPS nonhypo-c ). The changes of rPS were analysed using analysis of variance (ANOVA) with repeated measures. Logistic regression was used to identify independent predictors of unfavourable outcome. Fifty-six patients were included in the analysis, median age was 76 (IQR 62-81) years and 28 (50%) were female. From baseline to 24 h after treatment, rPS hypo-i , rPS nonhypo-i and rPS hypo-c all decreased significantly. The decreases in rPS hypo-i and rPS hypo-c were larger in the reperfusion group than non-reperfusion group. The rPS hypo-i at follow-up was a predictor for unfavourable outcome (OR 1.131; 95% CI 1.018-1.256; P = 0.022). Early disruption of BBB in AIS is reversible, particularly when greater reperfusion is achieved. Elevated BBBP at 24 h after treatment, not the pretreatment BBBP, predicts unfavourable outcome. (orig.)

  14. Justification for intravenous magnesium therapy in acute myocardial infarction

    DEFF Research Database (Denmark)

    Rasmussen, H S

    1988-01-01

    Recent studies have shown that patients with acute myocardial infarction (AMI) are magnesium-deficient and develop an additional transient decrease in serum magnesium concentrations (S-Mg c) during the acute phase of the infarct. Animal experiments, as well as studies on humans, have indicated...... that the acute decrease in S-Mg c as well as a more chronic magnesium (Mg) deficiency state are harmful to the myocardium in the setting of acute ischaemia. This knowledge has led during the last couple of years to the performance of four double-blind placebo controlled studies in which the effect of i.......v. magnesium therapy on mortality and incidence of arrhythmias in patients with AMI has been evaluated. Magnesium treatment more than halved the acute mortality and incidence of arrhythmias requiring treatment in three of the four intervention studies. The mechanisms behind the beneficial effect of magnesium...

  15. Effect of hydroxy safflower yellow A on myocardial apoptosis after acute myocardial infarction in rats.

    Science.gov (United States)

    Zhou, M X; Fu, J H; Zhang, Q; Wang, J Q

    2015-04-10

    This study aimed to investigate the effect of hydroxy safflower yellow A (HSYA) on myocardial apoptosis after acute myocardial infarction (AMI) in rats. We randomly divided 170 male Wistar rats into 6 groups (N = 23): normal control, sham, control, SY (90 mg/kg), HSYA high-dose (HSYA-H, 40 mg/kg), and HSYA low-dose groups (HSYA-L, 20 mg/kg). Myocardial ischemic injury was induced by ligating the anterior descending coronary artery, and the degree of myocardial ischemia was evaluated using electrocardiography and nitroblue tetrazolium staining. Bax and Bcl-2 expressions in the ischemic myocardium were determined using immunohistochemical analysis. Peroxisome proliferator-activated receptor-γ (PPAR-γ) expression in the myocardium of rats with AMI was determined using reverse transcription-polymerase chain reaction. Compared to rats in the control group, those in the HYSA-H, HSYA-L, and SY groups showed a decrease in the elevated ST segments and an increase in the infarct size. The rats in the drug-treated groups showed a significantly lower percentage of Bax-positive cells and a significantly higher percentage of Bcl-2-positive cells than those in the control group (P myocardial ischemia in rats, possibly by increasing the level of Bcl-2/Bax, and PPAR-γ may be not a necessary link in this process.

  16. Effects of calcium antagonist and free radical scavengers on ischemic and reperfused myocardium due to acute occlusion of coronary arteries

    International Nuclear Information System (INIS)

    Ohsuzu, Fumitaka; Sakata, Nobuhiro; Yanagida, Shigeki

    1988-01-01

    The Langendorff perfused rat heart was used to investigate whether ischemic and reperfused injury could be protected by anti-free radical intervention alone or combined treatment with calcium antagonist. Hearts were subjected to 10 min. of aerobic perfusion with Krebs-Henseleit solution (K-H) and then randomized into three groups (GP): Control group received only K-H, FRS group K-H with superoxide dismutase (24 IU/ml) and catalase (22 IU/ml) and Combined group the same solution of FRS group with verapamil (10'-'7M) for 10 min; and three groups were subjected to 20 min. of global ischemia; and each group was reperfused by the prior perfusate for 20 min. LV developed pressure (DP) and heart rate (HR) were measured by an intraventricular baloon. Phosphorus-31 NMR spectroscopy allowed continuous monitoring of myocardial phosphocreatine (PCr), inorganic phosphate (Pi) and β-ATP content. Each group consisted of 5 experiments. PCr in Combined group was significantly higher than that of Control group with significantly higher values of DP and DPxHR compared to Combined group in the early phase of ischemia. By the middle phase of reperfusion, significant reduction in Pi was found only in Combined group with the reduction of HR. However, no significant difference of β-ATP was found between Control group and Combined group through ischemia and reperfusion. These results suggest that free radical scavengers alone could not protect ischemic and reperfused myocardium from injury, but that the reduction of oxygen consumption by verapamil might be predominantly effective in preventing myocardial damage partially from ischemia and reperfusion. (author)

  17. Huangzhi Oral Liquid Prevents Arrhythmias by Upregulating Caspase-3 and Apoptosis Network Proteins in Myocardial Ischemia-Reperfusion Injury in Rats

    Directory of Open Access Journals (Sweden)

    Xu Ran

    2015-01-01

    Full Text Available To study the effect of Huangzhi oral liquid (HZOL on I/R after 2 h and 4 h and determine its regulatory function on caspase-3 and protein networks. 70 SD male rats were randomly divided into seven groups and established myocardial I/R injury model by ligating the left anterior descending coronary artery. Myocardial infarction model was defined by TTC staining and color of the heart. The levels of CK-MB, CTnI, C-RPL, SOD, and MDA were tested at 2 h and 4 h after reperfusion. HE staining and ultramicrostructural were used to observe the pathological changes. The apoptotic index (AI of cardiomyocyte was marked by TUNEL. The expression levels of caspase-3, p53, fas, Bcl-2, and Bax were tested by immunohistochemistry and western blot. HZOL corrected arrhythmia, improved the pathologic abnormalities, decreased CK-MB, CTnI, C-RPL, MDA, AI, caspase-3, p53, fas, and Bax, and increased SOD ans Bcl-2 with different times of myocardial reperfusion; this result was similar to the ISMOC (P>0.05. HZOL could inhibit arrhythmia at 2 and 4 h after I/R and ameliorate cardiac function, which was more significant at 4 h after reperfusion. This result may be related to decreased expression of caspase-3, p53, and fas and increased Bcl-2/Bax ratio.

  18. [Social and occupational repercussions of acute myocardial infarction].

    Science.gov (United States)

    Ouldzein, Horma; Aounallah Skhiri, Hajer; Zouaoui, Walid; Nacef, Mzabi Hanane; Kafsi, Nacer; Ben Romdhane, Habiba; Ben Jemaa, Abdel Majid

    2005-05-01

    The aim of this work was to study the family, social and occupational repercussions of acute myocardial infarction. Our study concerns 70 patients less than 66 years old, working before their hospitalization and having been admitted for acute myocardial infarction between January 1st, 1999 and December 31, 2000 in the Department of Cardiac Resuscitation of hospital La Rabta of Tunis. Data were collected from retrospective review of folders and answers to a questionnaire. There were 70 patients almost exclusively men (n=69). The mean age was 49.0 +/- 6.8 years. The mean follow-up was 27.2 +/- 7.7 months. After the infarction, the majority of patients modified their activities (75.7%) notably their leisure activities (37.1%) and their travels (25.7%). Myocardial infarction had a bring about a bother in current life to 50.0% of the patients, had an influence on emotional life of 41.4% and on sexual activities of 50.0% of the population. The direct repercussions of myocardial infarction on the professional capacities was observed in the majority of the patients. The average delay of return to work has been 91 +/- 111 days. Fight against the isolation of the patient and its exclusion by an adequate and early psychological coverage is the best way to assure the return in a normal family and professional life.

  19. [Sexuality in acute myocardial infarction patients].

    Science.gov (United States)

    Casado Dones, Ma J; de Andrés Gimeno, B; Moreno González, C; Fernández Balcones, C; Cruz Martín, R Ma; Colmenar García, C

    2002-01-01

    We as nurses in the Coronary Unit we do not see the sexuality of the patients sufficiently addressed neither by us nor by the patients themselves. In this article we are trying to analize the reasons and to emphasize the need to include this subject in our Nursing Problem List. In it we explaine the fears and the wrong ideas that we have identified in our patients. The sexual function is not affected by a myocardial infarction but psychological factors, age, drugs and other associated diseases might be a reason. A quiet enviroment, a fit training plan and looking for personalise proper alternatives may help the patient to start a satisfactory sexual life again.

  20. Increased myocardial vulnerability to ischemia-reperfusion injury in the presence of left ventricular hypertrophy

    DEFF Research Database (Denmark)

    Mølgaard, Søren; Faricelli, Barbara; Salomonsson, Max

    2016-01-01

    with or without exendin-4 (Exe-4), a glucagon-like peptide-1 receptor agonist. Infarct size relative to area-at-risk was determined. Separately, mitochondria were isolated after global ischemia. Activities of complexes III and IV and amounts of selected complex subunits and cytochromes a, b, c, and c1 were.......  Conclusion: Hearts from hypertensive (SHR-SP) rats with left ventricle hypertrophy appeared more vulnerable to ischemia-reperfusion injury, as supported by a more profound infarct development and an earlier loss of postconditioning by Exe-4. Mitochondrial complexes III and IV were identified among possible...... loci of this increased, hypertrophy-associated vulnerability....

  1. Cancer risk of patients discharged with acute myocardial infarct

    DEFF Research Database (Denmark)

    Dreyer, L; Olsen, J H

    1998-01-01

    We studied whether common shared environmental or behavioral risk factors, other than tobacco smoking, underlie both atherosclerotic diseases and cancer. We identified a group of 96,891 one-year survivors of acute myocardial infarct through the Danish Hospital Discharge Register between 1977...... in acute myocardial infarct patients were similar to those of the general population, as were the rates for hormone-related cancers, including endometrial and postmenopausal breast cancers. We found a moderate increase in the risk for tobacco-related cancers, which was strongest for patients with early...... and 1989. We calculated the incidence of cancer in this group by linking it to the Danish Cancer Registry for the period 1978-1993. There was no consistent excess over the expected figures for any of the categories of cancer not related to tobacco smoking. Specifically, the rates of colorectal cancer...

  2. [Type of treatment and short-term outcome in elderly patients with acute myocardial infarction admitted to hospitals with a primary coronary angioplasty facility. The TRIANA (TRatamiento del Infarto Agudo de miocardio eN Ancianos) Registry].

    Science.gov (United States)

    Bardají, Alfredo; Bueno, Héctor; Fernández-Ortiz, Antonio; Cequier, Angel; Augé, Josep M; Heras, Magda

    2005-04-01

    The nature and outcome of treatment for acute myocardial infarction in elderly patients admitted to Spanish hospitals with primary angioplasty facilities are not well documented. Prospective analysis of registry data on patients > or =75 years old with ST-segment-elevation acute myocardial infarction admitted between April and July 2002 to Spanish hospitals with an active primary angioplasty program. We followed up 410 consecutive patients for 1 month. Their mean age was 80 (4.3) years and 46% were female. The median delay between symptom onset and arrival at hospital was 190 minutes. Around 42% of patients received no reperfusion therapy, 35% were treated by thrombolysis, and 22% by primary angioplasty. Patients who underwent reperfusion therapy were younger, were more frequently male, had a shorter delay from symptom onset to hospital arrival, and had a better initial hemodynamic status (Killip Class). However, they were more likely to have extensive anterior infarctions. Overall, 30-day mortality was 24.9%. Independent predictors of death were age, systolic blood pressure, and Killip class >1, but not use of thrombolysis or primary angioplasty. Over 42% of elderly patients with myocardial infarction admitted to Spanish hospitals with angioplasty facilities did not receive reperfusion therapy. Thrombolysis was the most frequently used reperfusion therapy. However, neither thrombolysis nor primary angioplasty improved 30-day mortality.

  3. Histochemical and immunohistochemical analyses of the myocardial scar fallowing acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Tatić Vujadin

    2012-01-01

    Full Text Available Background/Aim. The heart has traditionally been considered as a static organ without capacity of regeneration after trauma. Currently, the more and more often asked question is whether the heart has any intrinsic capacities to regenerate myocytes after myocardial infarction. The aim of this study was to present the existence of the preserved muscle fibers in the myocardial scar following myocardial infarction as well as the presence of numerous cells of various size and form that differently reacted to the used immunohistochemical antibodies. Methods. Histological, histochemical and immunohistochemical analyses of myocardial sections taken from 177 patients who had died of acute myocardial infarction and had the myocardial scar following myocardial infarction, were carried out. More sections taken both from the site of acute infarction and scar were examined by the following methods: hematoxylin-eosin (HE, periodic acid schiff (PAS, PAS-diastasis, Masson trichrom, Malory, van Gieson, vimentin, desmin, myosin, myoglobin, alpha actin, smoth muscle actin (SMA, p53, leukocyte common antigen (LCA, proliferating cell nuclear antigen (PCNA, Ki-67, actin HHF35, CD34, CD31, CD45, CD45Ro, CD8, CD20. Results. In all sections taken from the scar region, larger or smaller islets of the preserved muscle fibers with the signs of hypertrophy were found. In the scar, a large number of cells of various size and form: spindle, oval, elongated with abundant cytoplasm, small with one nucleus and cells with scanty cytoplasm, were found. The present cells differently reacted to histochemical and immunohistochemical methods. Large oval cells showed negative reaction to lymphocytic and leukocytic markers, and positive to alpha actin, actin HHF35, Ki-67, myosin, myoglobin and desmin. Elongated cells were also positive to those markers. Small mononuclear cells showed positive reaction to lymphocytic markers. Endothelial and smooth muscle cells in the blood vessel walls

  4. Acute Anterolateral Myocardial Infarction Due to Aluminum Phosphide Poisoning

    Directory of Open Access Journals (Sweden)

    2013-08-01

    Full Text Available Aluminum phosphide (AlP is a highly effective rodenticide which is used as a suicide poison. Herein, a 24 year-old man who’d intentionally ingested about 1liter of alcohol and one tablet of AlP is reported. Acute myocardial infarction due to AlP poisoning has been occurred secondary to AIP poisoning. Cardiovascular complications are poor prognostic factors in AlP poisoning

  5. Acute myocardial infarction in a teenager due to Adderall XR.

    Science.gov (United States)

    Sylvester, Angela L; Agarwala, Brojendra

    2012-01-01

    Adderall XR is commonly prescribed for children and adolescents with attention deficit/hyperactivity disorder. We present a case of a 15-year-old male who suffered a myocardial infarction after starting Adderall XR. Patient was otherwise in good health with no previous cardiac abnormalities. Cardiac catheterization was normal, and etiology was presumed to be secondary to acute vasospasm. The patient improved with cessation of medication. Physicians need to carefully screen patients for cardiac abnormalities prior to starting amphetamine-based medications.

  6. Oxidative Stress-Related Biomarkers in Essential Hypertension and Ischemia-Reperfusion Myocardial Damage

    Science.gov (United States)

    Rodrigo, Ramón; Feliú, Felipe; Hasson, Daniel

    2013-01-01

    Cardiovascular diseases are a leading cause of mortality and morbidity worldwide, with hypertension being a major risk factor. Numerous studies support the contribution of reactive oxygen and nitrogen species in the pathogenesis of hypertension, as well as other pathologies associated with ischemia/reperfusion. However, the validation of oxidative stress-related biomarkers in these settings is still lacking and novel association of these biomarkers and other biomarkers such as endothelial progenitor cells, endothelial microparticles, and ischemia modified albumin, is just emerging. Oxidative stress has been suggested as a pathogenic factor and therapeutic target in early stages of essential hypertension. Systolic and diastolic blood pressure correlated positively with plasma F2-isoprostane levels and negatively with total antioxidant capacity of plasma in hypertensive and normotensive patients. Cardiac surgery with extracorporeal circulation causes an ischemia/reperfusion event associated with increased lipid peroxidation and protein carbonylation, two biomarkers associated with oxidative damage of cardiac tissue. An enhancement of the antioxidant defense system should contribute to ameliorating functional and structural abnormalities derived from this metabolic impairment. However, data have to be validated with the analysis of the appropriate oxidative stress and/or nitrosative stress biomarkers. PMID:24347798

  7. Oxidative Stress-Related Biomarkers in Essential Hypertension and Ischemia-Reperfusion Myocardial Damage

    Directory of Open Access Journals (Sweden)

    Ramón Rodrigo

    2013-01-01

    Full Text Available Cardiovascular diseases are a leading cause of mortality and morbidity worldwide, with hypertension being a major risk factor. Numerous studies support the contribution of reactive oxygen and nitrogen species in the pathogenesis of hypertension, as well as other pathologies associated with ischemia/reperfusion. However, the validation of oxidative stress-related biomarkers in these settings is still lacking and novel association of these biomarkers and other biomarkers such as endothelial progenitor cells, endothelial microparticles, and ischemia modified albumin, is just emerging. Oxidative stress has been suggested as a pathogenic factor and therapeutic target in early stages of essential hypertension. Systolic and diastolic blood pressure correlated positively with plasma F2-isoprostane levels and negatively with total antioxidant capacity of plasma in hypertensive and normotensive patients. Cardiac surgery with extracorporeal circulation causes an ischemia/reperfusion event associated with increased lipid peroxidation and protein carbonylation, two biomarkers associated with oxidative damage of cardiac tissue. An enhancement of the antioxidant defense system should contribute to ameliorating functional and structural abnormalities derived from this metabolic impairment. However, data have to be validated with the analysis of the appropriate oxidative stress and/or nitrosative stress biomarkers.

  8. Acute myocardial infarction and stress cardiomyopathy following the Christchurch earthquakes.

    Science.gov (United States)

    Chan, Christina; Elliott, John; Troughton, Richard; Frampton, Christopher; Smyth, David; Crozier, Ian; Bridgman, Paul

    2013-01-01

    Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36 am on 4 September 2010, magnitude 7.1 and at 12:51 pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital was the region's only acute care hospital. It remained functional following both earthquakes. We were able to examine the effects of the 2 earthquakes on acute cardiac presentations. Patients admitted under Cardiology in Christchurch Hospital 3 week prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non cardiac chest pain, arrhythmia and others. There was a significant increase in overall admissions (pearthquake. This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6-6.4) in 4 days. There had been 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44-2.62). Statistical analysis showed this to be a significant difference between the earthquakes (pearthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake caused significantly more stress cardiomyopathy. Two major earthquakes occurring at different times of day differed in their effect on acute cardiac events.

  9. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Julio Perez-Downes

    2016-01-01

    Full Text Available Weight loss is one of the most researched and marketed topics in American society. Dietary regimens, medications that claim to boost the metabolism, and the constant pressure to fit into society all play a role in our patient’s choices regarding new dietary products. One of the products that are well known to suppress appetite and cause weight loss is amphetamines. While these medications suppress appetite, most people are not aware of the detrimental side effects of amphetamines, including hypertension, tachycardia, arrhythmias, and in certain instances acute myocardial infarction. Here we present the uncommon entity of an acute myocardial infarction due to chronic use of an amphetamine containing dietary supplement in conjunction with an exercise regimen. Our case brings to light further awareness regarding use of amphetamines. Clinicians should have a high index of suspicion of use of these substances when young patients with no risk factors for coronary artery disease present with acute arrhythmias, heart failure, and myocardial infarctions.

  10. Pancreatitis with Electrocardiographic Changes Mimicking Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Paul Khairy

    2001-01-01

    Full Text Available A 64-year-old woman with mild acute pancreatitis presented with epigastric pain, nausea and vomiting while undergoing hemodialysis for chronic renal insufficiency. Serial electrocardiograms revealed new onset ST segment elevations in leads V2 to V4 mimicking an anterior myocardial infarction, followed by diffusely inverted deep T waves. No cardiac pathology was demonstrated by echocardiography or coronary angiography. A review of the literature and possible pathophysiological mechanisms of electrocardiographic changes in acute pancreatitis, such as metabolic abnormalities, hemodynamic instability, vasopressors, pericarditis, myocarditis, a cardiobiliary reflex, exacerbation of underlying cardiac pathology, coagulopathy and coronary vasospasm, are discussed.

  11. Myocardial stress in patients with acute cerebrovascular events

    DEFF Research Database (Denmark)

    Jespersen, C.M.; Hansen, J.F.

    2008-01-01

    Signs of myocardial involvement are common in patients with acute cerebrovascular events. ST segment deviations, abnormal left ventricular function, increased N-terminal pro-brain natriuretic peptide (NT-proBNP), prolonged QT interval, and/or raised troponins are observed in up to one third of th...... and not coronary thrombosis. However, all patients with signs of cardiac involvement during acute cerebrovascular events should receive a cardiological follow-up in order to exclude concomitant ischemic heart disease. Copyright (C) 2007 S. Karger AG, Basel Udgivelsesdato: 2008...

  12. Myocardial capillary permeability for small hydrophilic indicators during normal physiological conditions and after ischemia and reperfusion

    DEFF Research Database (Denmark)

    Svendsen, J H

    1991-01-01

    Myocardial capillary permeability for small hydrophilic solutes (51Cr-EDTA or 99mTc-DTPA) has been measured using intracoronary indicator bolus injection and external radioactivity registration (the single injection, residue detection method). The method is based on kinetic separation...

  13. Antioxidant Vitamin Levels and Glutathione Peroxidase Activity During Ischemia/Reperfusion in Myocardial Infarction

    Czech Academy of Sciences Publication Activity Database

    Mužáková, V.; Kanďár, R.; Vojtíšek, P.; Skalický, J.; Vaňková, Radomíra; Čegan, A.; Červinková, Z.

    2001-01-01

    Roč. 50, č. 4 (2001), s. 389-396 ISSN 0862-8408 R&D Projects: GA ČR GA522/99/1130 Institutional research plan: CEZ:AV0Z5038910 Keywords : Myocardial infarction * Oxidative stress * Glutathione peroxidase Subject RIV: CE - Biochemistry Impact factor: 1.027, year: 2001

  14. Detection of viable myocardium in canine model with myocardial ischemia and ischemia-reperfusion by 125I-BMIPP: relation to regional blood flow

    International Nuclear Information System (INIS)

    Huang Gang; Zhao Huiyang; Shen Xuedong; Li Qing; Yuan Jimin; Zhu Cuiying

    1999-01-01

    Objective: The effects of BMIPP (β-methyl-iodophenyl pentadecanoic acid) on detecting viable myocardium and the relation between regional blood flow and the uptake of BMIPP were evaluated in canine model of myocardial ischemia and ischemia-reperfusion. Methods: 12 open-chest dogs under anesthesia were divided into two groups. Group I (ischemia group) had left circumflex coronary arterial occlusion for 2 h and group II (ischemia-reperfusion group) was occluded for 1 h and followed by 2 h reperfusion. Myocardial blood flow was measured with 99 Tc m -microspheres. 30 min after intravenous injection of 125 I-BMIPP and 99 Tc m -microspheres, the heart was excised rapidly and stained with Evans blue and NBT. Tissue samples (divided into approximately 1 g) of left ventricle were obtained, weighed and counted for 125 I and 99 Tc m . Regional blood flow and the uptake of BMIPP were expressed as percentages of average values in non-ischemic myocardium (two to three tissue samples) from the normal myocardium. Results: In ischemic myocardium (NBT positive samples), the uptake of BMIPP was relatively higher compared with regional blood flow [(67 +- 23)% vs (42 +- 19)%, P 0.05]. In ischemia-reperfusion group, regional blood flow was increased in ischemic and necrotic tissues, but the uptake of BMIPP was not enhanced with the increasing blood flow. Conclusions: BMIPP uptake seems to provide metabolic information independent of regional blood flow. The mismatching between regional blood flow and BMIPP uptake may indicate myocardial viability in the regions of hypoperfusion and the uptake of BMIPP in ischemic myocardium was related to existence of cellular metabolism

  15. Circadian variation of transient myocardial ischemia in the early out-of-hospital period after first acute myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H; Pless, P; Nielsen, J R

    1991-01-01

    Circadian rhythms have been demonstrated in acute myocardial infarction (AMI) and in other clinical cardiac dysfunctions. The purpose of this study was to elucidate whether a circadian pattern of transient myocardial ischemia exists after first AMI. Prospectively, 24-hour ambulatory ST-segment mo...

  16. New electrocardiographic criteria to differentiate acute pericarditis and myocardial infarction.

    Science.gov (United States)

    Rossello, Xavier; Wiegerinck, Rob F; Alguersuari, Joan; Bardají, Alfredo; Worner, Fernando; Sutil, Mario; Ferrero, Andreu; Cinca, Juan

    2014-03-01

    Transmural myocardial ischemia induces changes in QRS complex and QT interval duration but, theoretically, these changes might not occur in acute pericarditis provided that the injury is not transmural. This study aims to assess whether QRS and QT duration permit distinguishing acute pericarditis and acute transmural myocardial ischemia. Clinical records and 12-lead electrocardiogram (ECG) at ×2 magnification were analyzed in 79 patients with acute pericarditis and in 71 with acute ST-segment elevation myocardial infarction (STEMI). ECG leads with maximal ST-segment elevation showed longer QRS complex and shorter QT interval than leads with isoelectric ST segment in patients with STEMI (QRS: 85.9 ± 13.6 ms vs 81.3 ± 10.4 ms, P = .01; QT: 364.4 ± 38.6 vs 370.9 ± 37.0 ms, P = .04), but not in patients with pericarditis (QRS: 81.5 ± 12.5 ms vs 81.0 ± 7.9 ms, P = .69; QT: 347.9 ± 32.4 vs 347.3 ± 35.1 ms, P = .83). QT interval dispersion among the 12-ECG leads was greater in STEMI than in patients with pericarditis (69.8 ± 20.8 ms vs 50.6 ± 20.2 ms, P pericarditis, show prolongation of QRS complex and shortening of QT interval in ECG leads with ST-segment elevation. These new findings may improve the differential diagnostic yield of the classical ECG criteria. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

  17. Long-term prognostic value of ST-segment resolution in patients treated with fibrinolysis or primary percutaneous coronary intervention results from the DANAMI-2 (DANish trial in acute myocardial infarction-2)

    DEFF Research Database (Denmark)

    Sejersten, Maria; Valeur, Nana; Grande, Peer

    2009-01-01

    PCI, suggesting better epicardial and microvascular reperfusion, whereas no difference between treatment strategies was seen at 4 h. The ST-segment resolution at 4 h correlated with decreased mortality, but increased reinfarction rates among patients receiving fibrinolytic therapy, whereas no association was seen......OBJECTIVES: The purpose of this study was to determine the prognostic value of ST-segment resolution after primary percutaneous coronary intervention (pPCI) versus fibrinolysis. BACKGROUND: Resolution of the ST-segment has been used as a surrogate end point in trials evaluating reperfusion in acute...... myocardial infarction; however, its prognostic significance may be limited to patients treated with fibrinolysis. METHODS: In the DANAMI-2 (DANish trial in Acute Myocardial Infarction-2) substudy, including 1,421 patients, the ST-segment elevation at baseline, pre-intervention, 90 min, and 4 h was assessed...

  18. Clinical benefit of drugs targeting mitochondrial function as an adjunct to reperfusion in ST-segment elevation myocardial infarction

    DEFF Research Database (Denmark)

    Campo, Gianluca; Pavasini, Rita; Morciano, Giampaolo

    2017-01-01

    identified involving 5680 patients. When compared with placebo, drugs targeting mitochondrial component/pathway were not associated with significant reduction of cardiovascular and all-cause mortality (OR 0.9, 95% CI 0.7-1.17 and OR 0.92, 95% CI 0.69-1.23, respectively). However, these agents significantly......, those with indirect/unspecific action showed a significant effect on cardiovascular mortality (0.65, 95% CI 0.46-0.92), all-cause mortality (OR 0.69, 95% CI 0.52-0.92), hospital readmission for HF (OR 0.41, 95% CI 0.28-0.6) and LVEF (OR 1.49, 95% CI 1.09-2.05). CONCLUSIONS: Administration of drugs......AIMS: To perform a systematic review and meta-analysis of randomized clinical trials (RCT) comparing the effectiveness of drugs targeting mitochondrial function vs. placebo in patients with ST-segment elevation myocardial infarction (STEMI) undergoing mechanical coronary reperfusion. METHODS...

  19. Myocardial infarction, acute ischemic stroke, and hyperglycemia triggered by acute chlorine gas inhalation.

    Science.gov (United States)

    Kose, Ataman; Kose, Beril; Açikalin, Ayça; Gunay, Nurullah; Yildirim, Cuma

    2009-10-01

    Chlorine is one of the most common substances involved in toxic inhalation. Until now, several accidental exposures have been reported. The damage to the respiratory tract in the immediate phase after exposure to chlorine is well defined. Death occurs particularly due to pulmonary edema with respiratory failure and circulatory collapse. On the other hand, no association with myocardial infarction, acute stroke, severe hyperglycemia, and acute chlorine inhalation has been reported in literature. In the present study, an elderly (74-year-old) and diabetic case with myocardial infarction, acute stroke, hyperglycemia, and respiratory failure associated with acute chlorine intoxication after a diagnosis of acute chlorine poisoning and treatment in the emergency department is reported and the literature is revisited. Physicians should know that in elderly patients with a systemic disease who apply with chlorine gas inhalation, more serious complications along with damage in respiratory tract might be observed.

  20. Secular trends and seasonality in first-time hospitalization for acute myocardial infarction

    DEFF Research Database (Denmark)

    Fischer, Thomas; Lundbye-Christensen, Søren; Johnsen, Søren Paaske

    2004-01-01

    The incidence of acute myocardial infarction has declined in several Western countries during the last decades. The incidence and mortality of acute myocardial infarction follow a seasonal pattern. We examined if changes in the incidence of acute myocardial infarction were associated with any...... was estimated using a Poisson regression model. Results: The incidence rate decreased by 3.2 % (95% confidence interval: 2.7-3.3%) annually. Hospitalizations followed different seasonal patterns depending on age, but not on gender. In the

  1. [Acute inflammation phase reactants and interleukin-8 in myocardial infarction].

    Science.gov (United States)

    Zorin, N A; Podkhomutnikov, V M; Iankin, M Iu; Zorina, V N; Arkhipova, S V; Riabicheva, T G

    2009-04-01

    The study was undertaken to search for additional diagnostic criteria allowing the depth of myocardial damage to be estimated in males aged 57.2 +/- 9.6 years. Few interrelated acute phase reaction indices, including the levels of interleukin-8 (IL-8), lactoferrin (LF), alpha2-macroglobulin (alpha2-MG), plasmin (PL) and alpha2-MG-PL circulating complexes, were studied in serum on days 1, 7, and 17 of the onset of the disease. In small-focal myocardial infarction, the levels of alpha2-MG and PL were decreased on day 1 and those of LF and IL-8 were increased on day 14. On the contrary, in large-focal myocardial infarction, the concentrations of IL-8 and LF rose just on day 1 while those of alpha2-MG and PL remained unchanged. The detected differences may be used as additional criteria in differential diagnosis, particularly when ECG was of no informative value. Further, the concurrent elevation of alpha2-MG, PL, and PL-alpha2MG concentrations in large-focal myocardial infarction is indicative of poor prognosis.

  2. 3D cardiac wall thickening assessment for acute myocardial infarction

    Science.gov (United States)

    Khalid, A.; Chan, B. T.; Lim, E.; Liew, Y. M.

    2017-06-01

    Acute myocardial infarction (AMI) is the most severe form of coronary artery disease leading to localized myocardial injury and therefore irregularities in the cardiac wall contractility. Studies have found very limited differences in global indices (such as ejection fraction, myocardial mass and volume) between healthy subjects and AMI patients, and therefore suggested regional assessment. Regional index, specifically cardiac wall thickness (WT) and thickening is closely related to cardiac function and could reveal regional abnormality due to AMI. In this study, we developed a 3D wall thickening assessment method to identify regional wall contractility dysfunction due to localized myocardial injury from infarction. Wall thickness and thickening were assessed from 3D personalized cardiac models reconstructed from cine MRI images by fitting inscribed sphere between endocardial and epicardial wall. The thickening analysis was performed in 5 patients and 3 healthy subjects and the results were compared against the gold standard 2D late-gadolinium-enhanced (LGE) images for infarct localization. The notable finding of this study is the highly accurate estimation and visual representation of the infarct size and location in 3D. This study provides clinicians with an intuitive way to visually and qualitatively assess regional cardiac wall dysfunction due to infarction in AMI patients.

  3. Bronchogenic Carcinoma with Cardiac Invasion Simulating Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Anirban Das

    2016-01-01

    Full Text Available Cardiac metastases in bronchogenic carcinoma may occur due to retrograde lymphatic spread or by hematogenous dissemination of tumour cells, but direct invasion of heart by adjacent malignant lung mass is very uncommon. Pericardium is frequently involved in direct cardiac invasion by adjacent lung cancer. Pericardial effusion, pericarditis, and tamponade are common and life threatening presentation in such cases. But direct invasion of myocardium and endocardium is very uncommon. Left atrial endocardium is most commonly involved in such cases due to anatomical contiguity with pulmonary hilum through pulmonary veins, and in most cases left atrial involvement is asymptomatic. But myocardial compression and invasion by adjacent lung mass may result in myocardial ischemia and may present with retrosternal, oppressive chest pain which clinically may simulate with the acute myocardial infarction (AMI. As a result, it leads to misdiagnosis and delayed diagnosis of lung cancer. Here we report a case of non-small-cell carcinoma of right lung which was presented with asymptomatic invasion in left atrium and retrosternal chest pain simulating AMI due to myocardial compression by adjacent lung mass, in a seventy-four-year-old male smoker.

  4. Ischemic mitral regurgitation in patients with acute myocardial infarction.

    Science.gov (United States)

    Petris, A O; Iliescu, D; Alexandrescu, D M; Costache, Irina-Iuliana

    2014-01-01

    Echocardiographic evaluation of mitral regurgitation (MR) during the evolution of patients with acute myocardial infarction (MI). The study included 104 patients (73 males and 31 females), aged between 38-85, diagnosed with acute myocardial infarction (based on clinical, ECG and enzymatic evidences), in order to assess the MR (clinically--a new systolic murmur, and by echocardiography--the severity of MR). Echocardiography was performed upon admission and at 10-30 and 180 days after the onset of acute MI. The evaluation of MR was based on the following parameters: jet area, jet area indexed to left atrium, regurgitated volume, left atrial and left ventricular size, the evaluation of mitral valve apparatus in order to eliminate other possible causes of MR. MR was found in 35 patients from 104 diagnosed with acute MI, as follows: severe in 20 patients (jet area > 8 square cm, jet area indexed to left atrium > 40%, regurgitated volume > 30 mL) and mild in 15 patients (jet area diagnosis of MR, estimating its severity, the mechanisms and also the prognosis.

  5. PSYCHOLOGICAL REACTIONS AND HEALTH BEHAVIOR FOLLOWING ACUTE MYOCARDIAL INFARCTION

    Directory of Open Access Journals (Sweden)

    Tatjana Milenković

    2011-06-01

    Full Text Available Psychological reactions, risk health behavior and cardiac parameters can influence rehospitalization after acute myocardial infarction.The aim of the paper was to determine the presence of psychological reactions and risk health behavior in patients with acute myocardial infarction on admission as well as the differences after six months.The research included thirty-trhee patients of both sexes, who were consecutively hospitalized due to acute myocardial infarction. A prospective clinical investigation involved the following: semi-structured interview, Mini International Neuropsychiatric Interview (M.I.N.I for pcychiatric disorders, Beck Anxiety Inventory (BAI for measuring the severity of anxiety, Beck Depression Inventory (BDI for measuring the severity of depression, KON-6 sigma test for aggression, Holms-Rahe Scale (H-R for exposure to stressful events, and Health Behavior Questionnaire: alcohol consumption, cigarette smoking, lack of physical activity. Measurement of the same parameters was done on admission and after six months. The differences were assessed using the t-test and chi-square test for p<0.05.On admission, anxiety (BAI=8.15±4.37 and depression (BDI=8.67±3.94 were mild without significant difference after six months in the group of examinees. Aggression was elevated and significantly lowered after six monts (KON-6 sigma =53,26±9, 58:41,42±7.67, t=2,13 for p<0.05. Exposure to stressful events in this period decreased (H-R=113.19±67.37:91,65±63,81, t=3,14 for p<0.05; distribution of physical activity was significantly higher compared to admission values (54.83%: 84.84%. χ2=5.07 for p<0.01.In the group of examinees with acute myocardial infarction in the period of six months, anxiety and depression remained mildly icreased, while the levels of aggression and exposure to stressful events were lowered. Risk health behavior was maintained, except for the improvement in physical activity. In the integrative therapy and

  6. Intracoronary and systemic melatonin to patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L; Busch, Sarah Ekeløf; Jensen, Svend Eggert

    2014-01-01

    . The endogenous hormone, melatonin, works as an antioxidant and could potentially minimise the ischaemia-reperfusion injury. Given intracoronarily, it enables melatonin to work directly at the site of reperfusion. We wish to test if melatonin, as an antioxidant, can minimise the reperfusion injury following p...

  7. Dexamethasone Protects Against Tourniquet-Induced Acute Ischemia-Reperfusion Injury in Mouse Hindlimb

    Directory of Open Access Journals (Sweden)

    Ryan M. Corrick

    2018-03-01

    Full Text Available Extremity injuries with hemorrhage have been a significant cause of death in civilian medicine and on the battlefield. The use of a tourniquet as an intervention is necessary for treatment to an injured limb; however, the tourniquet and subsequent release results in serious acute ischemia-reperfusion (IR injury in the skeletal muscle and neuromuscular junction (NMJ. Much evidence demonstrates that inflammation is an important factor to cause acute IR injury. To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of dexamethasone, an anti-inflammatory drug, on tourniquet-induced acute IR injury in mouse hindlimb. In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left hindlimb at the hip joint for 3 h, and then released for 24 h to induce IR. Three hours of tourniquet and 24 h of release (24-h IR caused gastrocnemius muscle injuries including rupture of the muscle sarcolemma and necrosis (42.8 ± 2.3% for infarct size of the gastrocnemius muscle. In the NMJ, motor nerve terminals disappeared, and endplate potentials were undetectable in 24-h IR mice. There was no gastrocnemius muscle contraction in 24-h IR mice. Western blot data showed that inflammatory cytokines (TNFα and IL-1β were increased in the gastrocnemius muscle after 24-h IR. Treatment with dexamethasone at the beginning of reperfusion (1 mg/kg, i.p. significantly inhibited expression of TNFα and IL-1β, reduced rupture of the muscle sarcolemma and infarct size (24.8 ± 2.0%, and improved direct muscle stimulation-induced gastrocnemius muscle contraction in 24-h IR mice. However, this anti-inflammatory drug did not improve NMJ morphology and function, and sciatic nerve-stimulated skeletal muscle contraction in 24-h IR mice. The data suggest that one-time treatment with dexamethasone at the beginning of reperfusion only reduced structural and functional impairments of the skeletal muscle but not the

  8. Recovery of BMIPP uptake and regional wall motion in insulin resistant patients following angioplasty for acute myocardial infarction

    International Nuclear Information System (INIS)

    Fujino, Takayuki; Ishii, Yoshinao; Hirasawa, Kunihiko; Tateda, Kunihiko; Takeuchi, Toshiharu; Kikuchi, Kenjiro; Hasebe, Naoyuki

    2003-01-01

    The effect of insulin resistance (IR) on the fatty acid metabolism of myocardium, and therefore on the recovery of left ventricular (LV) wall motion, has not been established in patients with acute myocardial infarction (AMI). A total of consecutive 58 non-diabetic AMI patients who had successfully undergone emergency coronary angioplasty were analyzed retrospectively. They were categorized into 2 groups, normal glucose tolerance (NGT) and impaired glucose tolerance (IGT), based on a 75-g oral glucose tolerance test (OGTT). The parameters of OGTT, myocardial scintigraphy (n=58) (thallium-201 (Tl) and iodine-123-β-methyl-iodophenylpentadecanoic acid (BMIPP)) and left ventriculography (n=24) were compared in the 2 groups after reperfusion (acute phase) and 3-4 weeks after the AMI (chronic phase). The IR, estimated by the serum concentration of insulin at 120 min (IRI 120') of the OGTT and by the HOMA (the homeostasis model assessment) index, was higher in the IGT group than in NGT group. An inverse correlation was found between the recovery of regional LV wall motion in the ischemic lesion and the IRI 120' and HOMA index. Although the recovery of BMIPP uptake from the acute to the chronic phase was higher in the IGT group, it was only correlated with the degree of IRI 120', not with the HOMA. IR accompanied by IGT can negatively influence the recovery of regional LV wall motion. (author)

  9. Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p.

    Directory of Open Access Journals (Sweden)

    Chen Bian

    Full Text Available Luteolin (LUT, a kind of flavonoid which is extracted from a variety of diets, has been reported to convey protective effects of various diseases. Recent researches have suggested that LUT can carry out cardioprotective effects during ischemia/reperfusion (I/R. However, there have no reports on whether LUT can exert protective effects against myocardial I/R injury through the actions of specific microRNAs (miRs. The purpose of this study was to determine which miRs and target genes LUT exerted such function through.Expression of various miRs in perfused rat hearts was detected using a gene chip. Target genes were predicted with TargetScan, MiRDB and MiRanda. Anoxia/reoxygenation was used to simulate I/R. Cells were transfected by miR-208b-3p mimic, inhibitor and small interfering RNA of Ets1 (avian erythroblastosis virus E26 (v ets oncogene homolog 1. MiR-208b-3p and Ets1 mRNA were quantified by real-time quantitative polymerase chain reaction. The percentage of apoptotic cells was detected by annexin V-fluorescein isothiocyanate/propidium iodide dyeing and flow cytometry. The protein expression levels of cleaved caspase-3, Bcl-2, Bax, and Ets1 were examined by western blot analysis. A luciferase reporter assay was used to verify the combination between miR-208b-3p and the 3'-untranslated region of Ets1.LUT pretreatment reduced miR-208b-3p expression in myocardial tissue, as compared to the I/R group. And LUT decreased miR-208b-3p expression and apoptosis caused by I/R. However, overexpression of miR-208b-3p further aggravated the changes caused by I/R and blocked all the effects of LUT. Knockdown of miR-208b-3p expression also attenuated apoptosis, while knockdown of Ets1 promoted apoptosis. Further, the luciferase reporter assay showed that miR-208b-3p could inhibit Ets1 expression.LUT pretreatment conveys anti-apoptotic effects after myocardial I/R injury by decreasing miR-208b-3p and increasing Ets1 expression levels.

  10. Luteolin Inhibits Ischemia/Reperfusion-Induced Myocardial Injury in Rats via Downregulation of microRNA-208b-3p.

    Science.gov (United States)

    Bian, Chen; Xu, Tongda; Zhu, Hong; Pan, Defeng; Liu, Yang; Luo, Yuanyuan; Wu, Pei; Li, Dongye

    2015-01-01

    Luteolin (LUT), a kind of flavonoid which is extracted from a variety of diets, has been reported to convey protective effects of various diseases. Recent researches have suggested that LUT can carry out cardioprotective effects during ischemia/reperfusion (I/R). However, there have no reports on whether LUT can exert protective effects against myocardial I/R injury through the actions of specific microRNAs (miRs). The purpose of this study was to determine which miRs and target genes LUT exerted such function through. Expression of various miRs in perfused rat hearts was detected using a gene chip. Target genes were predicted with TargetScan, MiRDB and MiRanda. Anoxia/reoxygenation was used to simulate I/R. Cells were transfected by miR-208b-3p mimic, inhibitor and small interfering RNA of Ets1 (avian erythroblastosis virus E26 (v ets) oncogene homolog 1). MiR-208b-3p and Ets1 mRNA were quantified by real-time quantitative polymerase chain reaction. The percentage of apoptotic cells was detected by annexin V-fluorescein isothiocyanate/propidium iodide dyeing and flow cytometry. The protein expression levels of cleaved caspase-3, Bcl-2, Bax, and Ets1 were examined by western blot analysis. A luciferase reporter assay was used to verify the combination between miR-208b-3p and the 3'-untranslated region of Ets1. LUT pretreatment reduced miR-208b-3p expression in myocardial tissue, as compared to the I/R group. And LUT decreased miR-208b-3p expression and apoptosis caused by I/R. However, overexpression of miR-208b-3p further aggravated the changes caused by I/R and blocked all the effects of LUT. Knockdown of miR-208b-3p expression also attenuated apoptosis, while knockdown of Ets1 promoted apoptosis. Further, the luciferase reporter assay showed that miR-208b-3p could inhibit Ets1 expression. LUT pretreatment conveys anti-apoptotic effects after myocardial I/R injury by decreasing miR-208b-3p and increasing Ets1 expression levels.

  11. Cardio-protective effects of combined l-arginine and insulin: Mechanism and therapeutic actions in myocardial ischemia-reperfusion injury.

    Science.gov (United States)

    Venardos, Kylie M; Rajapakse, Niwanthi W; Williams, David; Hoe, Louise S; Peart, Jason N; Kaye, David M

    2015-12-15

    Reduced nitric oxide (NO) bioavailability plays a central role in the pathogenesis of myocardial ischemia-reperfusion injury (I-R), and reduced l-arginine transport via cationic amino acid transporter-1 is a key contributor to the reduced NO levels. Insulin can increase NO levels by increasing the transport of its substrate l-arginine but insulin alone exerts minimal cardiac protection in I-R. We hypothesized that combined insulin and l-arginine may provide cardioprotective effects in the setting of myocardial I-R. The effect of supplemental insulin, l-arginine and the combination was examined in cardiomyocytes exposed to hypoxia/reoxygenation and in isolated perfused mouse hearts undergoing ischemia/reperfusion. When compared to controls, cardiomyocytes treated upon reoxygenation with 1nM insulin+1mM l-arginine exhibited significant (all Pl-arginine uptake following hypoxia-reoxygenation (Pl-arginine-insulin treatment upon reperfusion significantly (all Pl-arginine or insulin treatment alone. In isolated cardiomyocytes (n=3-5), 1nM insulin caused cationic amino acid transporter-1 to redistribute to the cellular membrane from the cytosol and the effects of insulin on l-arginine uptake were partially dependent on the PI3K/Akt pathway. l-arginine-insulin treatment may be a novel strategy to ameliorate I-R injury. Copyright © 2015 Elsevier B.V. All rights reserved.

  12. Secondary prevention with calcium antagonists after acute myocardial infarction

    DEFF Research Database (Denmark)

    Hansen, J F

    1992-01-01

    and preventing reinfarction, nevertheless demonstrated pronounced differences between the 3 drugs. Nifedipine had no effect on reinfarction or death. Diltiazem had no overall effect but prevented first reinfarction or cardiac death (cardiac events) in patients without heart failure, and increased cardiac events......Experimental studies have demonstrated that the 3 calcium antagonists nifedipine, diltiazem, and verapamil have a comparable effect in the prevention of myocardial damage during ischaemia. Secondary prevention trials after acute myocardial infarction, which aimed at improving survival...... in patients with heart failure before randomisation. Verapamil prevented first reinfarction or death (major events); the most pronounced effect was found in patients without heart failure before randomisation. Verapamil did not have detrimental effects in patients treated for heart failure before...

  13. Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction

    DEFF Research Database (Denmark)

    Glinge, Charlotte; Sattler, Stefan; Jabbari, Reza

    2016-01-01

    of a family member is a risk factor for SCD and VF during acute myocardial infarction (MI), independent of traditional risk factors including family history of MI, suggesting a genetic component in the susceptibility to VF. To prevent SCD and VF due to MI, we need a better understanding of the genetic...... and molecular mechanisms causing VF in this apparently healthy population. Even though new insights and technologies have become available, the genetic predisposition to VF during MI remains poorly understood. Findings from a variety of different genetic studies have failed to reach reproducibility, although...... several genetic variants, both common and rare variants, have been associated to either VF or SCD. For this review, we searched PubMed for potentially relevant articles, using the following MeSH-terms: "sudden cardiac death", "ventricular fibrillation", "out-of-hospital cardiac arrest", "myocardial...

  14. Protein C deficiency in a patient of acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Tamzeed Ahmed

    2009-01-01

    Full Text Available A 42-year old male presented with acute myocardial infarction with no discernable risk factors; he never smoked; did not suffer from diabetes and had a well controlled blood pressure with single medication; plasma concentration of total cholesterol was on the upper normal limit, high and low density lipoprotein, cholesterol and triglyceride being normal. In addition to a single antihypertensive he received Allupurinol(Xanthine Oxidase inhibitorfor hyperuricaemia. Coronary angiogram revealed ectatic epicardial coronary arteries. The patient developed deep vein thrombosis of right leg after four days of the coronary angiogram. Coagulation analysis revealed protein C deficiency. The recognition of protein C deficiency as a risk factor for myocardial infarction is important as anticoagulators prevent further thrombotic events whereas inhibitors of platelet aggregation are ineffective. Ibrahim Med. Coll. J. 2009; 3(1: 34-35

  15. Hemorrhagic stroke the first 30 days after an acute myocardial infarction: incidence, time trends and predictors of risk.

    Science.gov (United States)

    Binsell-Gerdin, Emil; Graipe, Anna; Ögren, Joachim; Jernberg, Tomas; Mooe, Thomas

    2014-09-01

    Hemorrhagic stroke is a rare but serious complication after an acute myocardial infarction (AMI). The aims of our study were to establish the incidence, time trends and predictors of risk for hemorrhagic stroke within 30 days after an AMI in 1998-2008. We collected data from the Register of Information and Knowledge about Swedish Heart Intensive Care Admissions (RIKS-HIA). All patients with a myocardial infarction 1998-2008 were included, n=173,233. The data was merged with the National Patient Register in order to identify patients suffering a hemorrhagic stroke. To identify predictors of risk we used Cox models. Overall the incidence decreased from 0.2% (n=94) in 1998-2000 to 0.1% (n=41) in 2007-2008. In patients with ST-elevation myocardial infarction the corresponding incidences were 0.4% (n=76) in 1998-2000 and 0.2% (n=21) in 2007-2008, and after fibrin specific thrombolytic treatment 0.6% and 1.1%, respectively, with a peak of 1.4% during 2003-2004. In total 375 patients (0.22%) suffered a hemorrhagic stroke within 30 days of the AMI. The preferred method of reperfusion changed from thrombolysis to percutaneous coronary intervention (PCI). Older age (hazard ratio (HR) >65-≤ 75 vs ≤ 65 years 1.84, 95% confidence interval (CI) 1.38-2.45), thrombolysis (HR 6.84, 95% CI 5.51-8.48), history of hemorrhagic stroke (HR 12.52, CI 8.36-18.78) and prior hypertension (HR 1.52, CI 1.23-1.86) independently predicted hemorrhagic stroke within 30 days. The rate of hemorrhagic stroke within 30 days of an AMI has decreased by 50% between 1998 and 2008. The main reason is the shift in reperfusion method from thrombolysis to PCI. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  16. [Antagonistic effect and mechanism of Rosuvastatin on myocardial apoptosis in rats with acute myocardial infarction].

    Science.gov (United States)

    Song, Zhanchun; Bai, Jinghui; Wang, Qi; Chen, Liang; Guo, Qunping; Zhang, Di

    2015-12-01

    To investigate the protective effect of Rosuvastatin on myocardial cells in rats with acute myocardial infarction and its possible mechanism. Rats were randomly assigned to four groups: Control group, Sham group, AMI and Rosuvastatin group. The levels of lactate dehydrogenase (LDH) and creatine jubase (CK), the vitality of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by assay kits and the levels of C-reactive protein (CRP), tumor necrosis factor (TNF) alpha and interleukin (IL)-6 expression were detected by enzyme linked immunosorbent assay (ELISA). TTC/Evans blue staining was used to determine the relative myocardial infarction area, HE staining was used to detect pathologic changes and myocardial apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). What's more, Western blot was used to detect the protein expression of B-cell lymphoma-2 (Bcl-2), Bax, cleaved-Caspase-3, Rock1, Rock2, I-κB and NF-κBp65. The model of acute myocardial infarction rats was established. Compared with Sham group, the myocardial pathological changes were more severe, and the apoptosis number, the production of inflammatory factors and oxidative damage were significantly increased in AMI group. Compared with AMI group, the relative area of infarction myocardium (43% ± 4% vs 31% ± 8%, P=0.004 3) was dramatically reduced, the levels of LDH (2 545.45 ± 613.67 U/L vs 1 573.43 ± 373.72 U/L, P=0.02) and CK (7.49 ± 1.75 U/ml vs 4.42 ± 1.28 U/ml, P=0.04) in serum were significantly lower (Pmyocardial pathological damage degree was relieved, the apoptosis number (41% ± 8% vs 23% ± 6%, P=0.014 7) was significantly decreased, the expression of Bax (1.17 ± 0.10 vs 0.57 ± 0.08, P=0.003) and cleaved-Caspase-3 (1.31 ± 0.07 vs 0.70 ± 0.01, P=0.004) were dramatically reduced, and the expression of Bcl-2 (0.19 ± 0.01 vs 0.32 ± 0.01, P=0.003) was enhanced in Rosuvastatin group. Furthermore, the production of

  17. Cells involved in extracellular matrix remodeling after acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Garcia, Larissa Ferraz [Faculdade de Medicina do ABC, Santo André, SP (Brazil); Mataveli, Fábio D’Aguiar [Universidade Federal de São Paulo, São Paulo, SP (Brazil); Mader, Ana Maria Amaral Antônio; Theodoro, Thérèse Rachell [Faculdade de Medicina do ABC, Santo André, SP (Brazil); Justo, Giselle Zenker; Pinhal, Maria Aparecida da Silva [Universidade Federal de São Paulo, São Paulo, SP (Brazil)

    2015-07-01

    Evaluate the effects of VEGF{sub 165} gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF{sub 165} treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF{sub 165}. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF{sub 165}, suggesting greater tissue differentiation. The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF{sub 165} seems to provide a protective effect in the treatment of acute myocardial infarct.

  18. Cells involved in extracellular matrix remodeling after acute myocardial infarction.

    Science.gov (United States)

    Garcia, Larissa Ferraz; Mataveli, Fábio D'Aguiar; Mader, Ana Maria Amaral Antônio; Theodoro, Thérèse Rachell; Justo, Giselle Zenker; Pinhal, Maria Aparecida da Silva

    2015-01-01

    Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation. The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct.

  19. Reperfusion Strategies for Acute Ischaemic Stroke From Past to Present: An Overview Towards Future Perspectives

    Directory of Open Access Journals (Sweden)

    Isabella Canavero

    2015-07-01

    Full Text Available Timely reperfusion of brain ischaemic tissue is the main therapeutic target for acute stroke. In the last few decades many recanalisation strategies have been studied by randomised controlled trials (RCTs, including intravenous (IV, intra-arterial (IA, and combined approaches. Clinical research is addressed to identify the drug associated with the better reperfusion properties and the lower rate of side-effects. To date, according to current evidence-based guidelines, IV tissue plasminogen activator (tPA is the only approved treatment for acute ischaemic stroke (AIS within 4.5 hours from onset. Other IV thrombolytics, such as tenecteplase and desmoteplase, have shown promising results in preliminary RCTs and are currently being investigated to produce further evidence. Endovascular catheter-based treatments (including IA administration of thrombolytics or mechanical thrombectomy have quite inferior feasibility, being performed only by stroke-trained interventional neuroradiologists. Until a few months ago, many trials had investigated the safety and efficacy of endovascular techniques compared with IV tPA without consistent results, limiting their application to patients with contraindications or poor response to IV tPA. More recently, the Multicenter Randomized Clinical trial of Endovascular treatment for Acute ischemic stroke in the Netherlands (MR CLEAN, Endovascular treatment for Small Core and Anterior circulation Proximal occlusion with Emphasis on minimizing CT to recanalization times (ESCAPE, and Extending the Time for Thrombolysis in Emergency Neurological Deficits–Intra-arterial (EXTEND-IA trial results have demonstrated the superiority of endovascular procedures associated with standard care in AIS due to proximal arterial occlusion in the anterior cerebral circulation. These data are going to change the current decision-making process and the care pathway in AIS patients.

  20. Acute Myocardial Infarction: Changes in Patient Characteristics, Management, and 6-Month Outcomes Over a Period of 20 Years in the FAST-MI Program (French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction) 1995 to 2015.

    Science.gov (United States)

    Puymirat, Etienne; Simon, Tabassome; Cayla, Guillaume; Cottin, Yves; Elbaz, Meyer; Coste, Pierre; Lemesle, Gilles; Motreff, Pascal; Popovic, Batric; Khalife, Khalife; Labèque, Jean-Noel; Perret, Thibaut; Le Ray, Christophe; Orion, Laurent; Jouve, Bernard; Blanchard, Didier; Peycher, Patrick; Silvain, Johanne; Steg, Philippe Gabriel; Goldstein, Patrick; Guéret, Pascal; Belle, Loic; Aissaoui, Nadia; Ferrières, Jean; Schiele, François; Danchin, Nicolas

    2017-11-14

    ST-segment-elevation myocardial infarction (STEMI) and non-ST-segment-elevation myocardial infarction (NSTEMI) management has evolved considerably over the past 2 decades. Little information on mortality trends in the most recent years is available. We assessed trends in characteristics, treatments, and outcomes for acute myocardial infarction in France between 1995 and 2015. We used data from 5 one-month registries, conducted 5 years apart, from 1995 to 2015, including 14 423 patients with acute myocardial infarction (59% STEMI) admitted to cardiac intensive care units in metropolitan France. From 1995 to 2015, mean age decreased from 66±14 to 63±14 years in patients with STEMI; it remained stable (68±14 years) in patients with NSTEMI, whereas diabetes mellitus, obesity, and hypertension increased. At the acute stage, intended primary percutaneous coronary intervention increased from 12% (1995) to 76% (2015) in patients with STEMI. In patients with NSTEMI, percutaneous coronary intervention ≤72 hours from admission increased from 9% (1995) to 60% (2015). Six-month mortality consistently decreased in patients with STEMI from 17.2% in 1995 to 6.9% in 2010 and 5.3% in 2015; it decreased from 17.2% to 6.9% in 2010 and 6.3% in 2015 in patients with NSTEMI. Mortality still decreased after 2010 in patients with STEMI without reperfusion therapy, whereas no further mortality gain was found in patients with STEMI with reperfusion therapy or in patients with NSTEMI, whether or not they were treated with percutaneous coronary intervention. Over the past 20 years, 6-month mortality after acute myocardial infarction has decreased considerably for patients with STEMI and NSTEMI. Mortality figures continued to decline in patients with STEMI until 2015, whereas mortality in patients with NSTEMI appears stable since 2010. © 2017 American Heart Association, Inc.

  1. Low-Density Lipoprotein Receptor–Related Protein-1 Is a Therapeutic Target in Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Stefano Toldo, PhD

    2017-10-01

    Full Text Available Low-density lipoprotein receptor–related protein-1 (LRP1 is a ubiquitous membrane receptor functioning as a scavenger and regulatory receptor, inducing anti-inflammatory and prosurvival signals. Based on the known structure–activity of the LRP1 receptor binding site, the authors synthesized a small peptide (SP16. SP16 induced a >50% reduction in infarct size (p < 0.001 and preservation of left ventricular systolic function (p < 0.001, and treatment with an LRP1 blocking antibody eliminated the protective effects of SP16. In conclusion, LRP1 activation with SP16 given within 30 min of reperfusion during experimental acute myocardial infarction leads to a cardioprotective signal reducing infarct size and preservation of cardiac systolic function.

  2. Effect of additional treatment with EXenatide in patients with an Acute Myocardial Infarction (EXAMI: study protocol for a randomized controlled trial

    Directory of Open Access Journals (Sweden)

    Scholte Martijn

    2011-11-01

    Full Text Available Abstract Background Myocardial infarction causes irreversible loss of cardiomyocytes and may lead to loss of ventricular function, morbidity and mortality. Infarct size is a major prognostic factor and reduction of infarct size has therefore been an important objective of strategies to improve outcomes. In experimental studies, glucagon-like peptide 1 and exenatide, a long acting glucagon-like peptide 1 receptor agonist, a novel drug introduced for the treatment of type 2 diabetes, reduced infarct size after myocardial infarction by activating pro-survival pathways and by increasing metabolic efficiency. Methods The EXAMI trial is a multi-center, prospective, randomized, placebo controlled trial, designed to evaluate clinical outcome of exenatide infusion on top of standard treatment, in patients with an acute myocardial infarction, successfully treated with primary percutaneous coronary intervention. A total of 108 patients will be randomized to exenatide (5 μg bolus in 30 minutes followed by continuous infusion of 20 μg/24 h for 72 h or placebo treatment. The primary end point of the study is myocardial infarct size (measured using magnetic resonance imaging with delayed enhancement at 4 months as a percentage of the area at risk (measured using T2 weighted images at 3-7 days. Discussion If the current study demonstrates cardioprotective effects, exenatide may constitute a novel therapeutic option to reduce infarct size and preserve cardiac function in adjunction to reperfusion therapy in patients with acute myocardial infarction. Trial registration ClinicalTrials.gov: NCT01254123

  3. Serum aminoterminal type III procollagen peptide reflects repair after acute myocardial infarction

    DEFF Research Database (Denmark)

    Jensen, L T; Hørslev-Petersen, K; Toft, P

    1990-01-01

    similar to changes observed during wound healing in humans. PIIINP is cleaved off procollagen type III during the biosynthesis of type III collagen, which characterizes the early stages of repair and inflammation. Our findings suggest that serum PIIINP reflects the repair processes and scar formation...... following acute myocardial infarction. The serum PIIINP alterations in acute myocardial infarction differ essentially from the changes in myocardial enzymes reflecting myocardial injury. Serum PIIINP may therefore provide new and clinically relevant information on the healing of myocardial infarction....

  4. Data on administration of cyclosporine, nicorandil, metoprolol on reperfusion related outcomes in ST-segment Elevation Myocardial Infarction treated with percutaneous coronary intervention

    Directory of Open Access Journals (Sweden)

    Gianluca Campo

    2017-10-01

    Full Text Available Mortality and morbidity in patients with ST elevation myocardial infarction (STEMI treated with primary percutaneous coronary intervention (PCI are still high [1]. A huge amount of the myocardial damage is related to the mitochondrial events happening during reperfusion [2]. Several drugs directly and indirectly targeting mitochondria have been administered at the time of the PCI and their effect on fatal (all-cause mortality, cardiovascular (CV death and non fatal (hospital readmission for heart failure (HF outcomes have been tested showing conflicting results [3–16]. Data from 15 trials have been pooled with the aim to analyze the effect of drug administration versus placebo on outcome [17]. Subgroup analysis are here analyzed: considering only randomized clinical trial (RCT on cyclosporine or nicorandil [3–5,9–11], excluding a trial on metoprolol [12] and comparing trial with follow-up length <12 months versus those with longer follow-up [3–16]. This article describes data related article titled “Clinical Benefit of Drugs Targeting Mitochondrial Function as an Adjunct to Reperfusion in ST-segment Elevation Myocardial Infarction: a Meta-Analysis of Randomized Clinical Trials” [17].

  5. Effect of Intracoronary and Intravenous Melatonin on Myocardial Salvage Index in Patients with ST-Elevation Myocardial Infarction

    DEFF Research Database (Denmark)

    Ekeloef, Sarah; Halladin, Natalie; Fonnes, Siv

    2017-01-01

    Melatonin has attenuated myocardial ischemia reperfusion injury in experimental studies. We hypothesized that the administration of melatonin during acute myocardial reperfusion improves myocardial salvage index in patients with ST-elevation myocardial infarction. Patients (n = 48) were randomized...... in a 1:1 ratio to intracoronary and intravenous melatonin (total 50 mg) or placebo. The myocardial salvage index assessed by cardiac magnetic resonance imaging at day 4 (± 1 day) after primary percutaneous coronary intervention was similar in the melatonin group (n = 22) at 55.3% (95% CI 47...... did not differ between the groups. In conclusion, melatonin did not improve the myocardial salvage index after primary percutaneous coronary intervention in patients with ST elevation myocardial infarction compared with placebo....

  6. Extra-cellular expansion in the normal, non-infarcted myocardium is associated with worsening of regional myocardial function after acute myocardial infarction.

    Science.gov (United States)

    Garg, Pankaj; Broadbent, David A; Swoboda, Peter P; Foley, James R J; Fent, Graham J; Musa, Tarique A; Ripley, David P; Erhayiem, Bara; Dobson, Laura E; McDiarmid, Adam K; Haaf, Philip; Kidambi, Ananth; Crandon, Saul; Chew, Pei G; van der Geest, R J; Greenwood, John P; Plein, Sven

    2017-09-25

    Expansion of the myocardial extracellular volume (ECV) is a surrogate measure of focal/diffuse fibrosis and is an independent marker of prognosis in chronic heart disease. Changes in ECV may also occur after myocardial infarction, acutely because of oedema and in convalescence as part of ventricular remodelling. The objective of this study was to investigate changes in the pattern of distribution of regional (normal, infarcted and oedematous segments) and global left ventricular (LV) ECV using semi-automated methods early and late after reperfused ST-elevation myocardial infarction (STEMI). Fifty patients underwent cardiovascular magnetic resonance (CMR) imaging acutely (24 h-72 h) and at convalescence (3 months). The CMR protocol included: cines, T2-weighted (T2 W) imaging, pre-/post-contrast T1-maps and LGE-imaging. Using T2 W and LGE imaging on acute scans, 16-segments of the LV were categorised as normal, oedema and infarct. 800 segments (16 per-patient) were analysed for changes in ECV and wall thickening (WT). From the acute studies, 325 (40.6%) segments were classified as normal, 246 (30.8%) segments as oedema and 229 (28.6%) segments as infarct. Segmental change in ECV between acute and follow-up studies (Δ ECV) was significantly different for normal, oedema and infarct segments (0.8 ± 6.5%, -1.78 ± 9%, -2.9 ± 10.9%, respectively; P Normal segments which demonstrated deterioration in wall thickening at follow-up showed significantly increased Δ ECV compared with normal segments with preserved wall thickening at follow up (1.82 ± 6.05% versus -0.10 ± 6.88%, P normal myocardium demonstrates subtle expansion of the extracellular volume at 3-month follow up. Segmental ECV expansion of normal myocardium is associated with worsening of contractile function.

  7. Celastrol pretreatment attenuates rat myocardial ischemia/ reperfusion injury by inhibiting high mobility group box 1 protein expression via the PI3K/Akt pathway.

    Science.gov (United States)

    Tong, Suiyang; Zhang, Liangliang; Joseph, Jacob; Jiang, Xuejun

    2018-03-11

    Celastrol pretreatment has been shown to protect against myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism is poorly understood. This study aimed to investigate the cardioprotective effects of celastrol pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the phosphoinositide 3-kinase (PI3K)/Akt pathway. In a fixed-dose study, hematoxylin and eosin staining and myocardial enzyme measurements were used to determine the optimal dose of celastrol that elicited the best cardioprotective effects against I/R injury. Furthermore, rats were pretreated with 4 mg/kg celastrol, and infarct size and the levels of myocardial enzymes, apoptosis, inflammatory and oxidative indices, and HMGB1 and p-Akt expression were measured. Our results indicated that celastrol dose-dependently attenuated histopathological changes and the elevation in myocardial enzymes induced by I/R. Moreover, the celastrol pretreatment (4 mg/kg) not only significantly decreased infarct size as well as myocardial enzyme levels but also inhibited myocardial apoptosis, inflammatory response and oxidative stress. Additionally, celastrol downregulated HMGB1 expression and upregulated p-Akt expression in the myocardium. LY294002, a specific pI3k inhibitor, partially reversed the decreased HMGB1 expression, increased p-Akt expression induced by celastrol, and abolished the anti-apoptotic, anti-inflammatory and anti-oxidative effects of celastrol. These findings suggest that short-term pretreatment with celastrol protects against myocardial I/R injury by suppressing myocardial apoptosis, inflammatory response and oxidative stress via pI3k/Akt pathway activation and HMGB1 inhibition. Copyright © 2018. Published by Elsevier Inc.

  8. New echocardiographic technologies in the study of acute myocardial infarction.

    Science.gov (United States)

    Colonna, Paolo; D'Agostino, Carlo; Del Salvatore, Bibiana; Sorino, Margherita

    2004-06-01

    Echocardiography has a key role in the diagnostic and prognostic evaluation of patients in the different phases of acute myocardial infarction. Despite this important role of the conventional echocardiographic technologies, novel echocardiographic applications are under development or already used in the clinical practice. It is very difficult to distinguish which of these techniques will play a consistent role and will cover important diagnostic, prognostic and therapeutic use. The wise cardiologist will be the one who will choose the appropriate technology for the right subset of patients. In this review paper we try to assign to each novel echocardiographic technique its actual clinical weight in every pathophysiological condition: myocardial contrast echocardiography, contrast opacification of the left ventricle, coronary flow reserve study, integrated backscatter, tissue Doppler and strain rate imaging. For the best treatment choice, each patient has to be perfectly diagnosed and characterized in order to have a tailored therapy. A correct diagnosis of the extension of myocardial necrosis cannot ignore the transmural wavefront development, the amount of viable myocardium or the presence of microvascular damage. Also the simple echocardiographic wall motion akinesia can be caused by a variable extension of non-contracting, scarred myocardium. The different anatomic and functional intramyocardial patterns represent the basis for different functional outcome of regional and hence global left ventricular function. The greatest understanding of the pathology always leads to the best treatment.

  9. Increased risk of acute myocardial infarction in systemic sclerosis: a nationwide population-based study.

    Science.gov (United States)

    Chu, Szu-Ying; Chen, Yi-Ju; Liu, Chia-Jen; Tseng, Wei-Cheng; Lin, Ming-Wei; Hwang, Chian-Yaw; Chen, Chih-Chiang; Lee, Ding-Dar; Chen, Tzeng-Ji; Chang, Yun-Ting; Wang, Wen-Jen; Liu, Han-Nan

    2013-11-01

    Systemic sclerosis is a life-threatening autoimmune disease characterized by vasculopathy, which results in myocardial involvement in an extremely high percentage of patients. Nevertheless, there have been no large-scale epidemiological studies about the risk of acute myocardial infarction in patients with systemic sclerosis. The aims of this study were to evaluate the hazard ratio (HR) and risk factors of acute myocardial infarction in patients with systemic sclerosis, as well as to compare the risks of acute myocardial infarction among systemic sclerosis patients taking different immunosuppressors. The study cohort included 1344 patients with systemic sclerosis and 13,440 (1:10) age-, sex-, and comorbidity-matched controls during the period between 1997 and 2006, from the National Health Insurance Research Database. We compared the risk of acute myocardial infarction between patients with systemic sclerosis and controls and calculated the adjusted HRs for acute myocardial infarction in systemic sclerosis patients taking immunosuppressors and not taking immunosuppressors. The incidence rates of acute myocardial infarction were 535 and 313 cases per 100,000 person-years for systemic sclerosis cohort and reference cohort, respectively (P systemic sclerosis was found to be an independent risk factor for acute myocardial infarction (HR 2.45). Other risk factors included hypertension (HR 2.08) and diabetes (HR 2.14). The multivariate adjusted HR for acute myocardial infarction did not decrease among the systemic sclerosis patients taking systemic steroids, penicillamine, cyclophosphamide, azathioprine, methotrexate, or cyclosporine. Systemic sclerosis is independently associated with an increased risk of acute myocardial infarction. Immunosuppressors do not lower the risk of acute myocardial infarction in our study. Copyright © 2013 Elsevier Inc. All rights reserved.

  10. Nuclear myocardial perfusion imaging with a cadmium-telluride semiconductor detector gamma camera in patients with acute myocardial infarction

    International Nuclear Information System (INIS)

    Fukushima, Yoshimitsu; Kumita, Shin-ichiro; Kawaguchi, Tsuneaki; Maruyama, Takatoshi; Kawasaki, Yoshiyuki; Shinkai, Yasuhiro

    2014-01-01

    Since myocardial perfusion imaging (MPI) with conventional sodium iodine (NaI) device has low spatial resolution, there have been some cases in which small structures such as non-transmural myocardial infarction could not be properly detected. The purpose of this study was to evaluate potential usefulness of cadmium-telluride (CdTe) semiconductor detector-based high spatial resolution gamma cameras in detecting myocardial infarction sites, especially non-transmural infarction. A total of 38 patients (mean age ± SD: 64 ± 21 year) who were clinically diagnosed with acute myocardial infarction were included. Twenty-eight cases of them were with ST segment elevation myocardial infarction (STEMI) and 10 cases with non-ST segment elevation myocardial infarction (NSTEMI). In all patients, myocardial perfusion single photon emission computed tomography images were acquired with Infinia (NaI device) and R1-M (CdTe device), and the images were compared concerning the detectability of acute myocardial infarction sites. The detection rates of the myocardial infarction site in cases with STEMI were 100% both by NaI and CdTe images. In cases with NSTEMI, detection rate by NaI images was 50%, while that of CdTe images was 100% (p=0.033). The summed rest score (SRS) value derived from CdTe images was significantly higher than that from NaI images in cases with STEMI [NaI images: 12 (7-18) versus CdTe images: 14 (9-20)] (p < 0.001). SRS derived from CdTe images was significantly higher than that derived from NaI images in cases with NSTEMI [NaI images: 2 (0-5) versus CdTe images: 6 (6-8)] (p=0.006). These results indicate that MPI using CdTe-semiconductor device will provide a much more accurate assessment of acute myocardial infarction in comparison to current methods. (author)

  11. The opposite effects of nitric oxide donor, S-nitrosoglutathione, on myocardial ischaemia/reperfusion injury in diabetic and non-diabetic mice.

    Science.gov (United States)

    Liu, Yi; Xia, Chenhai; Wang, Rutao; Zhang, Jinglong; Yin, Tao; Ma, Yanzuo; Tao, Ling

    2017-08-01

    Nitric oxide is a potent anti-apoptotic and cardioprotective molecule in healthy animals. However, recent study demonstrates that overexpression of eNOS exacerbates the liver injury in diabetic animals. whether diabetes may also alter NO's biologic activity in ischaemic/reperfused heart remains unknown. The present experiment was designed to determine whether the nitric oxide donor, S-nitrosoglutathione, may exert different effects on diabetic and non-diabetic myocardial ischaemia/reperfusion (MI/R) injury. Diabetic state was induced in mice by multiple intraperitoneal injections of low-dose streptozotocin (STZ). The control or diabetic mice were subjected to 30 minutes ischaemia and 3 or 24 hours reperfusion. At 10 minutes before reperfusion, diabetic and non-diabetic mice were received an intraperitoneal injection of S-nitrosoglutathione (GSNO, a nitric oxide donor, 1 μmol/kg). GSNO attenuated MI/R injury in non-diabetic mice, as measured by improved cardiac function, reduced infarct size and decreased cardiomyocyte apoptosis. In contrast, GSNO failed to attenuate but, rather, aggravated the MI/R injury in diabetic mice. Mechanically, the diabetic heart exhibited an increased nitrative/oxidative stress level, as measured by peroxynitrite formation, compared with non-diabetic mice. Co-administration of GSNO with EUK134 (a peroxynitrite scavenger) or MnTE-2-PyP5 (a superoxide dismutase mimetic) or Apocynin (a NADPH oxidase inhibitor) 10 minutes before reperfusion significantly decreased the MI/R-induced peroxynitrite formation and the MI/R injury. Collectively, the present study for the first time demonstrated that diabetes may cause superoxide overproduction, increase NO inactivation and peroxynitrite formation, and thus convert GSNO from a cardioprotective molecule to a cardiotoxic molecule. © 2017 John Wiley & Sons Australia, Ltd.

  12. Protective effects of Tribulus terrestris L extract against acute kidney injury induced by reperfusion injury in rats.

    Science.gov (United States)

    Najafi, Houshang; Firouzifar, Mohammad Reza; Shafaat, Omid; Changizi Ashtiyani, Saeed; Hosseini, Nasser

    2014-07-01

    This study aimed to investigate the protective effect of aerial parts of the Tribulus terrestris L extract on acute kidney injury (AKI) induced by ischemia for 30 minutes and reperfusion for 24 hours in rats. Ten male Sprague-Dawley rats in the AKI and 10 in the Tribulus terrestris groups received the extract solvent and extract of the plant (11 mg/kg), respectively, for 13 days (oral administration). On day 14, ischemia for 30 minutes and reperfusion for 24 hours were induced on the rats. In the last 6 hours of the reperfusion period (24 hours), urine samples were collected in metabolic cages. At the end of this period, blood samples were also taken to determine plasma urea nitrogen, creatinine, and electrolyte concentrations. The kidney tissues were collected for measuring the level of oxidative stress and histological studies. They were compared with the sham operation group and a control group with normal diet and no operation. In the Tribulus terrestris group, the increase in plasma creatinine and urea nitrogen concentrations was significantly less following reperfusion, and their values reached the same level as that in the sham group. Creatinine clearance and urine osmolarity in the Tribulus terrestris group was higher in comparison with the AKI group, whereas sodium absolute excretion, fractional excretion of potassium, oxidative stress, and cellular damages were less. Oral administration of Tribulus terrestris extract for 2 weeks can decrease kidney functional disturbance, oxidative stress, and cellular damages following reperfusion injury in rats.

  13. THE SPEKL-TREKING PREDICTIVE VALUE OF THE ECHOCARDIOGRAPHY AT THE ACUTE MYOCARDIAL INFARCTION

    Directory of Open Access Journals (Sweden)

    N. A. Kosheleva

    2016-01-01

    Full Text Available Speckle-tracking echocardiography is a non-invasive method  for assessment of myocardial deformation, which is closely associated with its regional and global function. Although it is not yet introduced into clinical practice, deformation parameters are actively studied in different clinical conditions, particularly in acute myocardial infarction. Numerous studies show deformation  impairment may have important prognostic value at patients with a acute myocardial infarction.

  14. Berberine inhibits the ischemia-reperfusion injury induced inflammatory response and apoptosis of myocardial cells through the phosphoinositide 3-kinase/RAC-α serine/threonine-protein kinase and nuclear factor-κB signaling pathways.

    Science.gov (United States)

    Wang, Lixin; Ma, Hao; Xue, Yan; Shi, Haiyan; Ma, Teng; Cui, Xiaozheng

    2018-02-01

    Myocardial ischemia-reperfusion injury is one of the most common cardiovascular diseases, and can lead to serious damage and dysfunction of the myocardial tissue. Previous studies have demonstrated that berberine exhibits ameliorative effects on cardiovascular disease. The present study further investigated the efficacy and potential mechanism underlying the effects of berberine on ischemia-reperfusion injury in a mouse model. Inflammatory markers were measured in the serum and levels of inflammatory proteins in myocardial cells were investigated after treatment with berberine. In addition, the apoptosis of myocardial cells was investigated after berberine treatment. Apoptosis-associated gene expression levels and apoptotic signaling pathways were analyzed in myocardial cells after treatment with berberine. The phosphoinositide 3-kinase (PI3K)/RAC-α serine/threonine-protein kinase (AKT) and nuclear factor (NF)-κB signaling pathways were also analyzed in myocardial cells after treatment with berberine. Histological analysis was used to analyze the potential benefits of berberine in ischemia-reperfusion injury. The present study identified that inflammatory responses and inflammatory factors were decreased in the myocardial cells of the mouse model of ischemia-reperfusion injury. Mechanism analysis demonstrated that berberine inhibited apoptotic protease-activating factor 1, caspase-3 and caspase-9 expression in myocardial cells. The expression of Bcl2-associated agonist of cell death, Bcl-2-like protein 1 and cellular tumor antigen p53 was upregulated. Expression of NF-κB p65, inhibitor of NF-κB kinase subunit β (IKK-β), NF-κB inhibitor α (IκBα), and NF-κB activity, were inhibited in myocardial cells in the mouse model of ischemia-reperfusion injury. In conclusion, the results of the present study indicate that berberine inhibits inflammatory responses through the NF-κB signaling pathway and suppresses the apoptosis of myocardial cells via the PI3K

  15. Detection of acute myocardial infarction with digital image processing of two-dimensional echocardiograms

    NARCIS (Netherlands)

    Tak, T.; Visser, C.; Rahimtoola, S. H.; Chandraratna, P. A.

    1992-01-01

    We have previously described the ability of a computer-based image digitizing system to assess early textural changes in acute canine myocardial infarction. To determine whether this technique could be applied to human beings, we studied 12 patients with a first acute transmural myocardial

  16. Abnormal glucose metabolism in acute myocardial infarction: influence on left ventricular function and prognosis

    DEFF Research Database (Denmark)

    Høfsten, Dan E; Løgstrup, Brian B; Møller, Jacob E

    2009-01-01

    OBJECTIVES: We studied the influence of abnormal glucose metabolism on left ventricular (LV) function and prognosis in 203 patients with acute myocardial infarction. BACKGROUND: Abnormal glucose metabolism is associated with increased mortality after acute myocardial infarction. This appears to b...... alone did not explain the excess mortality in patients with newly detected or known diabetes....

  17. Significance of the invasive strategy after acute myocardial infarction on prognosis and secondary preventive medication

    DEFF Research Database (Denmark)

    Hvelplund, Anders; Galatius, Søren; Madsen, Mette

    2012-01-01

    To describe gender-specific long-term outcome and initiation of secondary preventive medication among patients with acute myocardial infarction (AMI).......To describe gender-specific long-term outcome and initiation of secondary preventive medication among patients with acute myocardial infarction (AMI)....

  18. Data on administration of cyclosporine, nicorandil, metoprolol on reperfusion related outcomes in ST-segment Elevation Myocardial Infarction treated with percutaneous coronary intervention

    DEFF Research Database (Denmark)

    Campo, Gianluca; Pavasini, Rita; Morciano, Giampaolo

    2017-01-01

    directly and indirectly targeting mitochondria have been administered at the time of the PCI and their effect on fatal (all-cause mortality, cardiovascular (CV) death) and non fatal (hospital readmission for heart failure (HF)) outcomes have been tested showing conflicting results [3], [4], [5], [6], [7......], [4], [5], [9], [10], [11], excluding a trial on metoprolol [12] and comparing trial with follow-up length 7], [8], [9], [10], [11], [12], [13], [14], [15], [16]. This article describes data related article titled "Clinical Benefit...... of Drugs Targeting Mitochondrial Function as an Adjunct to Reperfusion in ST-segment Elevation Myocardial Infarction: a Meta-Analysis of Randomized Clinical Trials" [17]....

  19. The protective effect of Luteolin on myocardial ischemia/reperfusion (I/R) injury through TLR4/NF-κB/NLRP3 inflammasome pathway.

    Science.gov (United States)

    Zhang, Xu; Du, Qianming; Yang, Yan; Wang, Jianing; Dou, Shuai; Liu, Chao; Duan, Junguo

    2017-07-01

    The purpose of the present study was to investigate the effect of Luteolin(Lut) on myocardial ischemia reperfusion injury and explore the underlying mechanism. Myocardial ischemia reperfusion injury (I/R) model was induced with 30min of left anterior descending (LAD) occlusion followed by 24h of reperfusion. In vivo, the rats were randomly divided into 5 groups: (1)Sham, (2)I/R, (3)I/R+Lut(40mg/kg), (4)I/R+Lut(80mg/kg) and (5)I/R+Lut(160mg/kg). In vitro, the H9c2 cells were assigned to five groups: (1)control, (2)hypoxia-reoxygenation(H/R), (3)H/R+Lut(5μM), (4)H/R+Lut(10μM) and (5)H/R+Lut(20μM). The H9c2 cells were stimulated with H/R protocol in the presence or absence of TAK-242, a TLR4 inhibitor. As a result, Lut ameliorated myocardial ischemia reperfusion injury and hypoxia-reoxygenation as evidenced by triphenyl tetrazolium chloride (TTC) staining and MTT assay, respectively. Lut was founded to decrease the levels of aspartate transaminase(AST), creatine phosphokinase-isoenzyme (CK-MB) and lactate dehydrogenase (LDH) in serum. Moreover, Lut could reduce the contents of interleukin-1β(IL-1β), interleukin-18 (IL-18) and tumor necrosis factor-α (TNF-α) in serum of rats and supernant of H9c2 cells. In addition, Lut remarkably downregulated the expressions of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor kappa B (NF-κB). Lut also inhibited the upregulations of inflammasome components, such as NOD-like receptor 3(NLRP3), apoptosis-associated speck-like protein containing CARD(ASC) in I/R-induced rats and H/R-induced H9c2 cells. In conclusion, Lut exhibited strong favorable cardioprotective effect on myocardial I/R injury which might be related to the down-regulation of the TLR4-meidated NF-κB/NLRP3 inflammasome in vivo and in vitro. Copyright © 2017. Published by Elsevier Masson SAS.

  20. Therapeutic Effect of Low Doses of Acenocoumarol in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

    Science.gov (United States)

    Warzecha, Zygmunt; Sendur, Paweł; Ceranowicz, Piotr; Cieszkowski, Jakub; Dembiński, Marcin; Sendur, Ryszard; Bonior, Joanna; Jaworek, Jolanta; Ambroży, Tadeusz; Olszanecki, Rafał; Kuśnierz-Cabala, Beata; Tomasz, Kaczmarzyk; Tomaszewska, Romana; Dembiński, Artur

    2017-04-21

    Intravascular activation of coagulation is observed in acute pancreatitis and is related to the severity of this inflammation. The aim of our study was to evaluate the impact of acenocoumarol therapy on the course of acute pancreatitis induced in male rats by pancreatic ischemia followed by reperfusion. Acenocoumarol at a dose of 50, 100, or 150 µg/kg/dose was administered intragastrically once a day, starting the first dose 24 h after the initiation of pancreatic reperfusion. Histological examination showed that treatment with acenocoumarol reduces pancreatic edema, necrosis, and hemorrhages in rats with pancreatitis. Moreover, the administration of acenocoumarol decreased pancreatic inflammatory infiltration and vacuolization of pancreatic acinar cells. These findings were accompanied with a reduction in the serum activity of lipase and amylase, concentration of interleukin-1β, and plasma d-Dimer concentration. Moreover, the administration of acenocoumarol improved pancreatic blood flow and pancreatic DNA synthesis. Acenocoumarol given at a dose of 150 µg/kg/dose was the most effective in the treatment of early phase acute pancreatitis. However later, acenocoumarol given at the highest dose failed to exhibit any therapeutic effect; whereas lower doses of acenocoumarol were still effective in the treatment of acute pancreatitis. Treatment with acenocoumarol accelerates the recovery of ischemia/reperfusion-induced acute pancreatitis in rats.

  1. Delayed percutaneous coronary intervention in patients with acute myocardial infarction

    International Nuclear Information System (INIS)

    Zhu Weiming; Tian Fang; Shi Li; Lan Xi

    2004-01-01

    Objective: To observe the clinical effects, safeness and prognosis of delayed percutaneous coronary intervention (PCI) for infarct related artery (IRA) in post-infarct patients. Methods: In total 53 patients with acute myocardial infarction (AMI) underwent delayed PCI within 5-15 days after the acute event. Conventional treatment (including thrombolytic therapy) was given in all patients as they were admitted. Results: Intervention was performed in 68 branches of IRA were, including 64 cases of PTCA followed by stent implantation and 4 cases of direct stent implantation. In total 68 stents were implanted. The TIMI classification was improved from the pre-PCI 0-2 to post-PCI 3. No patient died during the treatment. No repeated AMI, post-infarct angina and repeated recanalization happened in the hospitalization. A 5-48 month follow up showed there was 1 death (1.9%), 1 case of repeated myocardial infarction (1.9%), 3 cases of unstable angina (5.7%), 2 cases of repeated PCI and 1 case of CABG. The rate of repeated recanalization was 5.7%. Seven patients (13.2%) were admitted for the second time, who survived 6-48 months after the intervention. Conclusion: Delayed PCT can obviously improve the short and long term prognosis as well as the life quality of patients with AMI, which is a safe interventional procedure

  2. Serum magnesium status among acute myocardial infarction patients in Bangladesh.

    Science.gov (United States)

    Chakraborty, P K; Hoque, M R; Islam, M R; Paul, U K; Husain, F

    2014-01-01

    This case control cross sectional study was carried out in the Department of Biochemistry, Mymensingh Medical College in collaboration with Cardiology Department of Mymensingh Medical College Hospital, Mymensingh during the period of July 2004 to June 2005. The aim of the study was to explore the status of serum magnesium among acute myocardial infarction (AMI) patients as a means to monitor the possibility of management of these patients. A total of 100 subjects were selected and were grouped as Group I (50 healthy control subjects) and Group II (50 subjects of AMI Cases). Serum magnesium was estimated by colorimetric method from each sample. Statistical analysis was done by using SPSS windows package. Among the groups, mean±SD (Standard Deviation) of Group I and Group II serum magnesium were 2.16±0.25 and 1.71±0.17mg/dl respectively. By comparing Group I with Group II highly significant difference were found in case of serum magnesium (p<0.001). It is evident from the study that serum magnesium level significantly decreases among acute myocardial infarction patients in Bangladesh.

  3. Clinical evaluation of myocardial involvement in acute myopericarditis in young adults.

    Science.gov (United States)

    Saricam, Ersin; Saglam, Yasemin; Hazirolan, Tuncay

    2017-05-22

    Myocardial involvement in young adults has various causes. Acute myopericarditis is one of the myocardial involvements in young adults. It is easy to confuse with acute ST-elevation myocardial infarction because of the electrocardiographic features. This study aims to investigate a number of imaging techniques and clinical features for acute myopericarditis in young adults (defined as myocardial brightness in the left ventricle regions, especially in posterior and lateral wall. Focal echobright was observed in the 75 of 77 cases of acute myopericarditis in transthoracic echocardiogram. This sign was confirmed by cardiac magnetic resonance imaging. Focal echobright sensitivity was 95%; its specificity was 93%; its predictive was 95.2%. Pericardial effusion (83%) was observed in group I behind posterior wall. Its specificity was 81%; its sensitivity was 65%; predictivity was 73%. Pericardial effusion and myocardial focal echobright in echocardiography can be quite sensitive indicators for acute myopericarditis in young adults.

  4. Involvement of Proteasome and Macrophages M2 in the Protection Afforded by Telmisartan against the Acute Myocardial Infarction in Zucker Diabetic Fatty Rats with Metabolic Syndrome

    Directory of Open Access Journals (Sweden)

    C. Di Filippo

    2014-01-01

    Full Text Available This study investigated the involvement of proteasome and macrophages M2 in the protection afforded by telmisartan against the acute myocardial infarction in Zucker diabetic fatty (ZDF rats with metabolic syndrome. ZDF rats were treated for three weeks with telmisartan at doses of 7 and 12 mg/kg/day. After treatment, rats were subjected to a 25 min occlusion of the left descending coronary artery followed by 2 h reperfusion (I/R. At the end of the I/R period, biochemical, immunohistochemical, and echocardiographic evaluations were done. Telmisartan treatment (7 mg/kg and 12 mg/kg reduced the myocardial infarct size, the expression of proteasome subunits 20S and 26S, and the protein ubiquitin within the heart. The compound has led to an increased M2 macrophage phenotype within the cardiac specimens and a modification of the cardiac cytokine and chemokine profile. This was functionally translated in improved cardiac performance as evidenced by echography after 2 h reperfusion. 7 mg/kg/day telmisartan was sufficient to improve the left ventricular ejection fraction LVEF of the rat heart recorded after I/R (e.g., vehicle 38 ± 2.2%; telmisartan 54 ± 2.7% and was sufficient to improve the diastolic function and the myocardial performance index up to values of 0.6 ± 0.01 measured after I/R.

  5. [Non-invasive coronary flow reserve is an independent predictor of exercise capacity after acute anterior myocardial infarction].

    Science.gov (United States)

    Meimoun, P; Clerc, J; Ghannem, M; Neykova, A; Tzvetkov, B; Germain, A-L; Elmkies, F; Zemir, H; Luycx-Bore, A

    2012-11-01

    After acute myocardial infarction (MI) coronary microvascular impairment and reduced exercise capacity are both determinant of prognosis. We tested whether non-invasive coronary flow reserve (CFR) performed after MI predicts post-MI exercise capacity (EC). Fifty consecutive patients (pts) (mean age 56.5±11years, 30% women) with a first reperfused ST-elevation anterior MI, and sustained TIMI 3 flow after mechanical reperfusion, underwent prospectively non-invasive CFR in the distal part of the left anterior descending artery (LAD), using intravenous adenosine infusion (0.14mg/kg per minute, within 2min), within 24h after successful primary coronary angioplasty (CFR 1), and 4±1.6months later after a period of convalescence and a cardiac rehabilitation program (CFR 2). CFR was defined as peak hyperaemic LAD flow velocity divided by baseline flow velocity. All pts also underwent semi-supine exercise stress echocardiography (ESE) the same day of CFR 2. ESE was performed at an initial workload of 25-30watts with a 20watts increase at 2-minute intervals. Beta-blockers were withheld 24h before ESE. The mean CFR 2 increased significantly when compared to CFR 1 (2.9±0.65 versus 1.9±0.4, Paptitude after MI. Copyright © 2012. Published by Elsevier SAS.

  6. Influence of oxygen content immediately after graft reperfusion on occurrence of postoperative acute kidney injury in living donor liver transplantation.

    Science.gov (United States)

    Chae, Min Suk; Lee, Nuri; Park, Da Hye; Lee, Jisoo; Jung, Hyun Sik; Park, Chul Soo; Lee, Jaemin; Choi, Jong Ho; Hong, Sang Hyun

    2017-08-01

    Acute kidney injury (AKI) is a common complication after living donor liver transplantation (LDLT). In this study, we investigated perioperative factors, including oxygen content, related to the postoperative development of AKI after LDLT. The perioperative data of 334 patients were reviewed retrospectively. We identified the postoperative development of AKI based on the Acute Kidney Injury Network criteria. Perioperative variables, including oxygen content, were compared between patients with and without AKI. Potentially significant variables in a univariate analysis were evaluated by multivariate analysis. Postoperative AKI developed in 76 patients (22.7%). Univariate analysis revealed that preoperative factors (body mass index [BMI], diabetes mellitus, C-reactive protein) and intraoperative factors (severe postreperfusion syndrome, packed red blood cell transfusion, furosemide, and oxygen content at the anhepatic phase, 5 minutes and 1 hour after graft reperfusion, and at peritoneal closure) of recipients were significant. The multivariate analysis showed that oxygen content 5 minutes after graft reperfusion, BMI, and furosemide administration were independently associated with postoperative AKI. In conclusion, postoperative AKI was independently associated with oxygen content 5 minutes after graft reperfusion, BMI, and furosemide administration. Meticulous ventilator care and transfusion should be required to maintain sufficient oxygen content immediately after graft reperfusion in patients who undergo LDLT.

  7. Effect of Glucocorticoids on Ultrastructure of Myocardial Muscle in the Course of Experimentally Induced Acute Myocardial Ischemia

    Directory of Open Access Journals (Sweden)

    Piotr Kuropka

    2017-01-01

    Full Text Available The search for effective methods of myocardial cytoprotection against ischemia is the most significant issue in modern cardiology and cardiac surgery. Glucocorticoids are deemed very strong modulators of inflammatory response and thus can potentially protect heart muscle from postreperfusion injury and myocardial ischemia during cardiac surgery. Ultrastructural examination of the left ventricle heart samples revealed that the intravenous application of dexamethasone and hydrocortisone proved to exert cytoprotective effect on cardiomyocytes during experimentally induced acute ischemia in rats.

  8. Early Assistance With Left Ventricular Assist Device Limits Left Ventricular Remodeling After Acute Myocardial Infarction in a Swine Model.

    Science.gov (United States)

    Sun, Xiaotian; Li, Jun; Zhao, Weipeng; Lu, Shuyang; Guo, Changfa; Lai, Hao; Wang, Chunsheng

    2016-03-01

    Although left ventricular assist devices (LVADs) have been commonly used for patients with cardiogenic shock after acute myocardial infarction (AMI), their effects on post-AMI prognosis remain to be elucidated. In this study, we aimed to explore the effects of an LVAD on left ventricular (LV) remodeling and function at the postinfarction stage in a swine model. AMI was induced by ligation of the circumflex artery or its branches for 120 min, followed by 120 min of reperfusion. In the assist group (n = 6), LVAD was initiated at 90 min after ischemia and was maintained for support until 120 min after reperfusion, whereas the control group (n = 6) received no support. LV pressure, volume, wall stress, and stroke work were all decreased by LVAD assistance at the ischemia and reperfusion stages, and blood pressure and cardiac output were maintained. All swine were studied 1 month after the procedure, and those in the assist group showed less increased end-diastolic volumes (assist vs. 57.9 ± 6.6 vs. 79.0 ± 6.7 mL, P = 0.032) and sphericity (assist vs. 1.33 ± 0.16 vs. 1.51 ± 0.12, P = 0.01), as well as improved ejection fractions (assist vs. 59.0 ± 7.8 vs. 42.3 ± 6.0%, P = 0.002). Furthermore, despite a presence of a similar initial ischemic area, the percent of infarcted myocardium was reduced by 49.9% in the assist group (assist vs. 18.1 ± 4.8 vs. 35.3 ± 6.2%, P assistance with an LVAD in AMI limited LV remodeling, preserved postinfarction systolic function, and improved the prognosis. Copyright © 2015 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.

  9. Effect of intravenous TRO40303 as an adjunct to primary percutaneous coronary intervention for acute ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Atar, Dan; Arheden, Håkan; Berdeaux, Alain

    2015-01-01

    AIM: The MITOCARE study evaluated the efficacy and safety of TRO40303 for the reduction of reperfusion injury in patients undergoing revascularization for ST-elevation myocardial infarction (STEMI). METHODS: Patients presenting with STEMI within 6 h of the onset of pain randomly received TRO40303...... with contemporary mechanical revascularization principles did not show any effect of TRO40303 in limiting reperfusion injury of the ischaemic myocardium....

  10. Chymase mediates injury and mitochondrial damage in cardiomyocytes during acute ischemia/reperfusion in the dog.

    Science.gov (United States)

    Zheng, Junying; Wei, Chih-Chang; Hase, Naoki; Shi, Ke; Killingsworth, Cheryl R; Litovsky, Silvio H; Powell, Pamela C; Kobayashi, Tsunefumi; Ferrario, Carlos M; Rab, Andras; Aban, Inmaculada; Collawn, James F; Dell'Italia, Louis J

    2014-01-01

    Cardiac ischemia and reperfusion (I/R) injury occurs because the acute increase in oxidative/inflammatory stress during reperfusion culminates in the death of cardiomyocytes. Currently, there is no drug utilized clinically that attenuates I/R injury in patients. Previous studies have demonstrated degranulation of mast cell contents into the interstitium after I/R. Using a dog model of I/R, we tested the role of chymase, a mast cell protease, in cardiomyocyte injury using a specific oral chymase inhibitor (CI). 15 adult mongrel dogs had left anterior descending artery occlusion for 60 min and reperfusion for 100 minutes. 9 dogs received vehicle and 6 were pretreated with a specific CI. In vivo cardiac microdialysis demonstrated a 3-fold increase in interstitial fluid chymase activity in I/R region that was significantly decreased by CI. CI pretreatment significantly attenuated loss of laminin, focal adhesion complex disruption, and release of troponin I into the circulation. Microarray analysis identified an I/R induced 17-fold increase in nuclear receptor subfamily 4A1 (NR4A1) and significantly decreased by CI. NR4A1 normally resides in the nucleus but can induce cell death on migration to the cytoplasm. I/R caused significant increase in NR4A1 protein expression and cytoplasmic translocation, and mitochondrial degradation, which were decreased by CI. Immunohistochemistry also revealed a high concentration of chymase within cardiomyocytes after I/R. In vitro, chymase added to culture HL-1 cardiomyocytes entered the cytoplasm and nucleus in a dynamin-dependent fashion, and promoted cytoplasmic translocation of NR4A1 protein. shRNA knockdown of NR4A1 on pre-treatment of HL-1 cells with CI significantly decreased chymase-induced cell death and mitochondrial damage. These results suggest that the beneficial effects of an orally active CI during I/R are mediated in the cardiac interstitium as well as within the cardiomyocyte due to a heretofore-unrecognized chymase

  11. Role of TRPV1 channels in ischemia/reperfusion-induced acute kidney injury.

    Directory of Open Access Journals (Sweden)

    Lan Chen

    Full Text Available OBJECTIVES: Transient receptor potential vanilloid 1 (TRPV1 -positive sensory nerves are widely distributed in the kidney, suggesting that TRPV1-mediated action may participate in the regulation of renal function under pathophysiological conditions. Stimulation of TRPV1 channels protects against ischemia/reperfusion (I/R-induced acute kidney injury (AKI. However, it is unknown whether inhibition of these channels is detrimental in AKI or not. We tested the role of TRPV1 channels in I/R-induced AKI by modulating these channels with capsaicin (TRPV1 agonist, capsazepine (TRPV1 antagonist and using Trpv1-/- mice. METHODS AND RESULTS: Anesthetized C57BL/6 mice were subjected to 25 min of renal ischemia and 24 hrs of reperfusion. Mice were pretreated with capsaicin (0.3 mg/kg body weight or capsazepine (50 mg/kg body weight. Capsaicin ameliorated the outcome of AKI, as measured by serum creatinine levels, tubular damage,neutrophil gelatinase-associated lipocalin (NGAL abundance and Ly-6B.2 positive polymorphonuclear inflammatory cells in injured kidneys. Neither capsazepine nor deficiency of TRPV1 did deteriorate renal function or histology after AKI. Measurements of endovanilloids in kidney tissue indicate that 20-hydroxyeicosatetraeonic acid (20-HETE or epoxyeicosatrienoic acids (EETs are unlikely involved in the beneficial effects of capsaicin on I/R-induced AKI. CONCLUSIONS: Activation of TRPV1 channels ameliorates I/R-induced AKI, but inhibition of these channels does not affect the outcome of AKI. Our results may have clinical implications for long-term safety of renal denervation to treat resistant hypertension in man, with respect to the function of primary sensory nerves in the response of the kidney to ischemic stimuli.

  12. Carbonic anhydrase inhibitor attenuates ischemia-reperfusion induced acute lung injury.

    Directory of Open Access Journals (Sweden)

    Chou-Chin Lan

    Full Text Available Ischemia-reperfusion (IR-induced acute lung injury (ALI is implicated in several clinical conditions including lung transplantation, cardiopulmonary bypass surgery, re-expansion of collapsed lung from pneumothorax or pleural effusion and etc. IR-induced ALI remains a challenge in the current treatment. Carbonic anhydrase has important physiological function and influences on transport of CO2. Some investigators suggest that CO2 influences lung injury. Therefore, carbonic anhydrase should have the role in ALI. This study was undertaken to define the effect of a carbonic anhydrase inhibitor, acetazolamide (AZA, in IR-induced ALI, that was conducted in a rat model of isolated-perfused lung with 30 minutes of ischemia and 90 minutes of reperfusion. The animals were divided into six groups (n = 6 per group: sham, sham + AZA 200 mg/kg body weight (BW, IR, IR + AZA 100 mg/kg BW, IR + AZA 200 mg/kg BW and IR+ AZA 400 mg/kg BW. IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, pulmonary hypertension, neutrophilic sequestration, and an increase in the expression of pro-inflammatory cytokines. Increases in carbonic anhydrase expression and perfusate pCO2 levels were noted, while decreased Na-K-ATPase expression was noted after IR. Administration of 200mg/kg BW and 400mg/kg BW AZA significantly suppressed the expression of pro-inflammatory cytokines (TNF-α, IL-1, IL-6 and IL-17 and attenuated IR-induced lung injury, represented by decreases in pulmonary hyper-permeability, pulmonary edema, pulmonary hypertension and neutrophilic sequestration. AZA attenuated IR-induced lung injury, associated with decreases in carbonic anhydrase expression and pCO2 levels, as well as restoration of Na-K-ATPase expression.

  13. Dual antiplatelet and anticoagulant APAC prevents experimental ischemia-reperfusion-induced acute kidney injury.

    Science.gov (United States)

    Tuuminen, Raimo; Jouppila, Annukka; Salvail, Dan; Laurent, Charles-E; Benoit, Marie-Claude; Syrjälä, Simo; Helin, Heikki; Lemström, Karl; Lassila, Riitta

    2017-06-01

    Renal ischemia-reperfusion predisposes to acute kidney injury (AKI) and mortality. APAC, mast cell heparin proteoglycan mimetic is a potent dual antiplatelet and anticoagulant inhibiting thrombosis in several vascular models. Clinically relevant (0.06 and 0.13 mg/kg) and high (0.32 and 7.3 mg/kg) heparin doses of APAC and unfractionated heparin (UFH) were administered i.v. in pharmacological studies. Antithrombotic action of APAC and UFH was assessed with platelet aggregation to collagen, activated partial thromboplastin (APTT) and prothrombin (PT) times. Pharmacodynamics of [ 64 Cu]-APAC or -UFH were monitored by PET/CT. Next, APAC and UFH doses (0.06 and 0.13 mg/kg) were i.v. administered 10 min prior to renal ischemia-reperfusion injury (IRI) in rats. APAC in contrast to UFH inhibited platelet aggregation. During 0.06 and 0.13 mg/kg dose regimens APTT and PT remained at baseline, but at the high APTT prolonged fourfold to sixfold. Overall bio-distribution and clearance of APAC and UFH were similar. After bilateral 30-min renal artery clamping, creatinine, urea nitrogen and neutrophil gelatinase-associated lipocalin concentrations and histopathology indicated faster renal recovery by APAC (0.13 mg/kg). APAC, unlike UFH, prevented expression of innate immune ligand hyaluronan and tubulointerstitial injury marker Kim-1. Moreover, in severe bilateral 1-h renal artery clamping, APAC (0.13 mg/kg) prevented AKI, as demonstrated both by biomarkers and survival. Compatible with kidney protection APAC reduced the circulating levels of vascular destabilizing and pro-inflammatory angiopoietin-2 and syndecan-1. No tissue bleeding ensued. APAC and UFH were similarly eliminated via kidneys and liver. In contrast to UFH, APAC (0.13 mg/kg) was reno-protective in moderate and even severe IRI by attenuating vascular injury and innate immune activation.

  14. Elevated levels of adipokines predict outcome after acute myocardial infarction: A long-term follow-up of the Glucose Tolerance in Patients with Acute Myocardial Infarction cohort.

    Science.gov (United States)

    Ritsinger, Viveca; Brismar, Kerstin; Malmberg, Klas; Mellbin, Linda; Näsman, Per; Rydén, Lars; Söderberg, Stefan; Tenerz, Åke; Norhammar, Anna

    2017-03-01

    Adiponectin and leptin are associated with insulin resistance and cardiovascular disease. Information on the prognostic value after an acute myocardial infarction is still conflicting. Patients (n = 180) without known diabetes and with admission glucose of acute myocardial infarction in 1998-2000 were followed for mortality and cardiovascular events (first of cardiovascular mortality/acute myocardial infarction/stroke/heart failure) until the end of 2011 (median: 11.6 years). Plasma adiponectin and leptin were related to outcome in Cox proportional-hazard regression analyses. Median age was 64 years and 69% were male. Total mortality was 34% (n = 61) and 44% (n = 80) experienced a cardiovascular event. Adiponectin at discharge predicted cardiovascular events (hazard ratio; 95% confidence interval; 1.45; 1.02-2.07, p = 0.038), total mortality (2.53; 1.64-3.91, p myocardial infarction and heart failure, adiponectin predicted total mortality (1.79; 1.07-3.00, p = 0.027) but not cardiovascular events. High levels of leptin were associated with cardiovascular events during the first 7 years, after which the association was attenuated. Leptin did not predict total mortality. In patients with acute myocardial infarction but without previously known diabetes, high levels of adiponectin at discharge predicted total mortality. The present results support the hypothesis that high rather than low levels of adiponectin predict mortality after acute myocardial infarction.

  15. [Life Threatening Complications in Patients With ST-Elevation Acute Coronary Syndrome-Dependence on Reperfusion Interventions (Data of Federal Register of Patients With Acute Coronary Syndrome)].

    Science.gov (United States)

    Oshchepkova, E V; Dmitriev, V V

    2016-04-01

    to study rate and type of life-threatening complications (LC) in patients with ST-Elevation (STE) Acute Coronary Syndrome (ACS) and their relation to implementation of reperfusion measures. Database of the Federal Register of patients with ACS (FRACS) which functioned from 01/01/2009 to 01/01/2014 contains information on 212304 patients with verified diagnosis of ACS. From this pool using random number generator we selected a cohort comprising 10348 patients with STEACS (60% men, mean age 63.5+/-0.1 clinical systolic and diastolic arterial pressure [AP] 135.2+/-0.3 and 81.9+/-0.2 mm Hg, respectively). Killip class was used for determination of degree of acute heart failure. Most frequent forms of LC were heart rhythm disturbances (6.2%) and cardiogenic shock (5.4%). Patients subjected to percutaneous coronary intervention (PCI) including those in whom pharmacoinvasive approach was used had less LC and lower hospital mortality than patients who received only thrombolytic therapy (TLT). Reperfusion measures were administered mostly to patients with class I-II acute heart failure. Hospital mortality was highest (9.47%) among patients not subjected to reperfusion measures and lowest (1.09%) among patients treated with PCI+TLT. FRACS assesses LC in patients with STEACS in the context of implemented reperfusion measures. Data of FRACS can be used by the health service authorities for improvement of medical aid to patients with STEACS.

  16. Effects of Intracoronary Infusion of Escalating Doses of Cardiac Stem Cells in Rats With Acute Myocardial Infarction.

    Science.gov (United States)

    Tang, Xian-Liang; Rokosh, Gregg; Sanganalmath, Santosh K; Tokita, Yukichi; Keith, Matthew C L; Shirk, Gregg; Stowers, Heather; Hunt, Gregory N; Wu, Wenjian; Dawn, Buddhadeb; Bolli, Roberto

    2015-07-01

    Although c-kit(pos) cardiac stem cells (CSCs) preserve left ventricular (LV) function and structure after myocardial infarction, CSC doses have been chosen arbitrarily, and the dose-effect relationship is unknown. Rats underwent a 90-minute coronary occlusion followed by 35 days of reperfusion. Vehicle or CSCs at 5 escalating doses (0.3×10(6), 0.75×10(6), 1.5×10(6), 3.0×10(6), and 6.0×10(6) cells/heart) were given intracoronarily 4 h after reperfusion. The lowest dose (0.3×10(6)) had no effect on LV function and morphology, whereas 0.75, 1.5, and 3.0×10(6) significantly improved regional and global LV function (echocardiography and hemodynamic studies). These 3 doses had similar effects on echocardiographic parameters (infarct wall thickening fraction, LV end-systolic and end-diastolic volumes, LV ejection fraction) and hemodynamic variables (LV end-diastolic pressure, LV dP/dtmax, preload adjusted maximal power, end-systolic elastance, preload recruitable stroke work) and produced similar reductions in apoptosis, scar size, infarct wall thinning, and LV expansion index and similar increases in viable myocardium in the risk region (morphometry). Infusion of 6.0×10(6) CSCs markedly increased postprocedural mortality. Green fluorescent protein and 5-bromo-2'-deoxyuridine staining indicated that persistence of donor cells and formation of new myocytes were negligible with all doses. Surprisingly, in this rat model of acute myocardial infarction, the dose-response relationship for intracoronary CSCs is flat. A minimal dose between 0.3 and 0.75×10(6) is necessary for efficacy; above this threshold, a 4-fold increase in cell number does not produce greater improvement in LV function or structure. Further increases in cell dose are harmful. © 2015 American Heart Association, Inc.

  17. Comparison of Immediate With Delayed Stenting Using the Minimalist Immediate Mechanical Intervention Approach in Acute ST-Segment-Elevation Myocardial Infarction: The MIMI Study.

    Science.gov (United States)

    Belle, Loic; Motreff, Pascal; Mangin, Lionel; Rangé, Grégoire; Marcaggi, Xavier; Marie, Antoine; Ferrier, Nadine; Dubreuil, Olivier; Zemour, Gilles; Souteyrand, Géraud; Caussin, Christophe; Amabile, Nicolas; Isaaz, Karl; Dauphin, Raphael; Koning, René; Robin, Christophe; Faurie, Benjamin; Bonello, Laurent; Champin, Stanislas; Delhaye, Cédric; Cuilleret, François; Mewton, Nathan; Genty, Céline; Viallon, Magalie; Bosson, Jean Luc; Croisille, Pierre

    2016-03-01

    Delayed stent implantation after restoration of normal epicardial flow by a minimalist immediate mechanical intervention aims to decrease the rate of distal embolization and impaired myocardial reperfusion after percutaneous coronary intervention. We sought to confirm whether a delayed stenting (DS) approach (24-48 hours) improves myocardial reperfusion, versus immediate stenting, in patients with acute ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention. In the prospective, randomized, open-label minimalist immediate mechanical intervention (MIMI) trial, patients (n=140) with ST-segment-elevation myocardial infarction ≤12 hours were randomized to immediate stenting (n=73) or DS (n=67) after Thrombolysis In Myocardial Infarction 3 flow restoration by thrombus aspiration. Patients in the DS group underwent a second coronary arteriography for stent implantation a median of 36 hours (interquartile range 29-46) after randomization. The primary end point was microvascular obstruction (% left ventricular mass) on cardiac magnetic resonance imaging performed 5 days (interquartile range 4-6) after the first procedure. There was a nonsignificant trend toward lower microvascular obstruction in the immediate stenting group compared with DS group (1.88% versus 3.96%; P=0.051), which became significant after adjustment for the area at risk (P=0.049). Median infarct weight, left ventricular ejection fraction, and infarct size did not differ between groups. No difference in 6-month outcomes was apparent for the rate of major cardiovascular and cerebral events. The present findings do not support a strategy of DS versus immediate stenting in patients with ST-segment-elevation infarction undergoing primary percutaneous coronary intervention and even suggested a deleterious effect of DS on microvascular obstruction size. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01360242. © 2016 American Heart Association, Inc.

  18. Hyperintense acute reperfusion marker on FLAIR is not associated with early haemorrhagic transformation in the elderly

    International Nuclear Information System (INIS)

    Rozanski, Michal; Ebinger, Martin; Schmidt, Wolf U.; Hotter, Benjamin; Pittl, Sandra; Heuschmann, Peter U.; Jungehuelsing, Jan G.; Fiebach, Jochen B.

    2010-01-01

    The hyperintense acute reperfusion marker (HARM) has been described as a predictor for haemorrhagic transformation (HT) in acute ischaemic stroke. We hypothesised that this phenomenon is not present in the elderly. It was possible to assess 47/84 consecutive patients aged 80 and over with diagnosed ischaemic stroke or transient ischaemic attack (TIA). MRI was performed within 24 h of onset of symptoms with follow-up MRI within a further 48 h. Of 47 included patients, 19 showed HARM; it was only seen on follow-up examination. Ten of the 47 patients underwent thrombolysis with recombinant tissue plasminogen activator (rt-PA); 4 of them showed HARM, and 1 of those showed HT. HARM was found in three out of eight patients with haemorrhagic transformation on baseline and/or follow-up MRI. We did not observe an association between HARM and early HT either in the whole group or in the patients who received thrombolysis. HARM was not associated with HT in the elderly after ischaemic stroke, independent of treatment. While it may indicate dysfunction of the blood-brain barrier (BBB), it does not necessarily amount to HT. (orig.)

  19. Translation of Methdology used in Human Myocardial Imaging to a Sheep Model of Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Elizabeth A Bailey

    2013-10-01

    Full Text Available Introduction: Pre-clinical investigation of stem cells for repairing damaged myocardium predominantly used rodents, however large animals have cardiac circulation closely resembling the human heart. The aim of this study was to evaluate whether SPECT/CT myocardial perfusion imaging (MPI could be used for assessing sheep myocardium following an acute myocardial infarction (MI and response to intervention. Method: 18 sheep enrolled in a pilot study to evaluate [99mTc]-sestamibi MPI at baseline, post-MI and after therapy. Modifications to the standard MPI protocols were developed. All data was reconstructed with OSEM using CT-derived attenuation and scatter correction. Standard analyses were performed and inter-observer agreement were measured using Kappa (. Power determined the sample sizes needed to show statistically significant changes due to intervention. Results: Ten sheep completed the full protocol. Data processed were performed using pre-existing hardware and software used in human MPI scanning. No improvement in perfusion was seen in the control group, however improvements of 15% - 35% were seen after intra-myocardial stem cell administration. Inter-observer agreement was excellent (К=0.89. Using a target power of 0.9, 28 sheep were required to detect a 10-12% change in perfusion. Conclusions: Study demonstrates the suitability of large animal models for imaging with standard MPI protocols and it’s feasibility with a manageable number of animals. These protocols could be translated into humans to study the efficacy of stem cell therapy in heart regeneration and repair.

  20. Cost-effectiveness of optimal use of acute myocardial infarction treatments and impact on coronary heart disease mortality in China.

    Science.gov (United States)

    Wang, Miao; Moran, Andrew E; Liu, Jing; Coxson, Pamela G; Heidenreich, Paul A; Gu, Dongfeng; He, Jiang; Goldman, Lee; Zhao, Dong

    2014-01-01

    The cost-effectiveness of the optimal use of hospital-based acute myocardial infarction (AMI) treatments and their potential impact on coronary heart disease (CHD) mortality in China is not well known. The effectiveness and costs of optimal use of hospital-based AMI treatments were estimated by the CHD Policy Model-China, a Markov-style computer simulation model. Changes in simulated AMI, CHD mortality, quality-adjusted life years, and total healthcare costs were the outcomes. The incremental cost-effectiveness ratio was used to assess projected cost-effectiveness. Optimal use of 4 oral drugs (aspirin, β-blockers, statins, and angiotensin-converting enzyme inhibitors) in all eligible patients with AMI or unfractionated heparin in non-ST-segment-elevation myocardial infarction was a highly cost-effective strategy (incremental cost-effectiveness ratios approximately US $3100 or less). Optimal use of reperfusion therapies in eligible patients with ST-segment-elevation myocardial infarction was moderately cost effective (incremental cost-effectiveness ratio ≤$10,700). Optimal use of clopidogrel for all eligible patients with AMI or primary percutaneous coronary intervention among high-risk patients with non-ST-segment-elevation myocardial infarction in tertiary hospitals alone was less cost effective. Use of all the selected hospital-based AMI treatment strategies together would be cost-effective and reduce the total CHD mortality rate in China by ≈9.6%. Optimal use of most standard hospital-based AMI treatment strategies, especially combined strategies, would be cost effective in China. However, because so many AMI deaths occur outside of the hospital in China, the overall impact on preventing CHD deaths was projected to be modest.

  1. Development of solid lipid nanoparticles containing total flavonoid extract from Dracocephalum moldavica L. and their therapeutic effect against myocardial ischemia-reperfusion injury in rats.

    Science.gov (United States)

    Tan, Mei-E; He, Cheng-Hui; Jiang, Wen; Zeng, Cheng; Yu, Ning; Huang, Wei; Gao, Zhong-Gao; Xing, Jian-Guo

    2017-01-01

    Total flavonoid extract from Dracocephalum moldavica L. (TFDM) contains effective components of D. moldavica L. that have myocardial protective function. However, the cardioprotection function of TFDM is undesirable due to its poor solubility. In order to improve the solubility and efficacy of TFDM, we developed TFDM-loaded solid lipid nanoparticles (TFDM-SLNs) and optimized the formulation of TFDM-SLNs using central composite design and response surface methodology. The physicochemical properties of TFDM-SLNs were characterized, and the pharmacodynamics was investigated using the myocardial ischemia-reperfusion injury model in rats. The nanoparticles of optimal formulation for TFDM-SLNs were spherical in shape with the average particle size of 104.83 nm and had a uniform size distribution with the polydispersity index value of 0.201. TFDM-SLNs also had a negative zeta potential of -28.7 mV to ensure the stability of the TFDM-SLNs emulsion system. The results of pharmacodynamics demonstrated that both TFDM and TFDM-SLN groups afforded myocardial protection, and the protective effect of TFDM-SLNs was significantly superior to that of TFDM alone, based on the infarct area, histopathological examination, cardiac enzyme levels and inflammatory factors in serum. Due to the optimal quality and the better myocardial protective effect, TFDM-SLNs are expected to become a safe and effective nanocarrier for the oral delivery of TFDM.

  2. Acute myocardial infarction in young adults with Antiphospholipid syndrome: report of two cases and literature review

    OpenAIRE

    Abid, Leila; Frikha, Faten; Bahloul, Zouhir; Kammoun, Samir

    2011-01-01

    Abstract Acute myocardial infarction (AMI) is rarely associated with antiphospholipid syndrome. The treatment of these patients is a clinical challenge. We report the observations of 2 young adults (1 woman and 1 man), admitted in our acute care unit for acute myocardial infarction (AMI). A coagulopathy work-up concludes the existence of antiphospholipid syndrome (APS) in the 2 cases. APS syndrome was considered primary in 2 cases. All patients presented an intense inflammatory syndrome (high...

  3. Acute ST Elevation Myocardial Infarction in Patients With Immune Thrombocytopenia Purpura: A Case Report.

    Science.gov (United States)

    Dhillon, Sandeep K; Lee, Edwin; Fox, John; Rachko, Maurice

    2011-02-01

    Acute myocardial infarction (AMI) in patients with immune thrombocytopenic purpura (ITP) is rare. We describe a case of AMI in patient with ITP. An 81-year-old woman presented with acute inferoposterior MI with low platelet count on admission (34,000/µl). Coronary angiography revealed significant mid right coronary artery (RCA) stenosis with thrombus, subsequently underwent successful percutaneous coronary intervention (PCI). In some patients with immune thrombocytopenia purpura and acute myocardial infarction, percutaneous coronary intervention is a therapeutic option.

  4. The Frequency of Cerebral Microembolism in Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Masoud Mehrpour

    2010-11-01

    Full Text Available ABSTRACT Introduction: Stroke is more common in patients with cerebral microembolisms. Frequency of cerebral microembolisms (high intensity transient signals, HITS in acute myocardial infarction has been reported about 17%. The factors that influence on microembolism after myocardial infarction (MI are not definitive. Type of MI, Ejection fraction, Hx of Streptokinase is the factors that were studied. Methods: During three years we studied the frequency of cerebral microembolisms in AMI patients, we studied forty patients with microembolism as a case group and ninety patients without microembolism as a control group. We detected microembolism in patients by transcranial doppler study within 72 houre after myocardial infarction. Two-dimensional echocardiogram was performed for all patients during hospitalization. Excluding criteria were prosthetic heart valves, carotid stenosis >50% and poor window for TCD monitoring. Results: number of patients who had history of receiving SK were significantly more common in case group in comparison to control group. OR 2.4 CI(1.1-5.2 The frequency was more prevalent in anterolateral MI in comparison to inferior MI.OR=3.3 CI(1.4-7.4. Ejection fraction has no significant effect on frequency of microembolism. OR 0.5 CI(0.2-1.3.Hypokinesia is also a risk factor for increasing risk of microembolism. OR 4.5 CI(1.4.13.8 Discussion: frequency of microembolism has been increased in patients with history of streptokinase or in the type of Anterolateral MI or wall motion abnormality, so we should be careful for risk of microembolism in this groups.

  5. The effect of creatine supplementation on myocardial function, mitochondrial respiration and susceptibility to ischaemia/reperfusion injury in sedentary and exercised rats.

    Science.gov (United States)

    Webster, I; Du Toit, E F; Huisamen, B; Lochner, A

    2012-09-01

    To investigate the effects of dietary creatine supplementation alone and in combination with exercise on basal cardiac function, susceptibility to ischaemia/reperfusion injury and mitochondrial oxidative function. There has been an increase in the use of creatine supplementation among sports enthusiasts, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but not in the myocardium. Male Wistar rats were swim-trained for 8 weeks, 5 days per week. Hearts were excised and either freeze-clamped for biochemical analysis or perfused on the isolated heart perfusion system to assess function and ischaemia/reperfusion tolerance. Mechanical function was documented in working heart and retrograde mode. The left coronary artery was ligated and infarct size determined. Mitochondrial oxidative capacity was quantified. Aortic output recovery of hearts from the sedentary controls (CSed) was significantly higher than those from creatine-supplemented sedentary (CrSed), creatine-supplemented exercised (CrEx) as well as control exercised (CEx) groups. Ischaemic contracture of hearts from CrEx was significantly higher than that of CSed. There were no differences in infarct size and mitochondrial oxygen consumption. This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise-trained animals, by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.

  6. Chronic Co-Administration of Sepiapterin and L-Citrulline Ameliorates Diabetic Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury in Obese Type 2 Diabetic Mice.

    Science.gov (United States)

    Baumgardt, Shelley L; Paterson, Mark; Leucker, Thorsten M; Fang, Juan; Zhang, David X; Bosnjak, Zeljko J; Warltier, David C; Kersten, Judy R; Ge, Zhi-Dong

    2016-01-01

    Diabetic heart disease is associated with tetrahydrobiopterin oxidation and high arginase activity, leading to endothelial nitric oxide synthase dysfunction. Sepiapterin (SEP) is a tetrahydrobiopterin precursor, and L-citrulline (L-Cit) is converted to endothelial nitric oxide synthase substrate, L-arginine. Whether SEP and L-Cit are effective at reducing diabetic heart disease is not known. The present study examined the effects of SEP and L-Cit on diabetic cardiomyopathy and ischemia/reperfusion injury in obese type 2 diabetic mice. Db/db and C57BLKS/J mice at 6 to 8 weeks of age received vehicle, SEP, or L-Cit orally alone or in combination for 8 weeks. Cardiac function was evaluated with echocardiography. Db/db mice displayed hyperglycemia, obesity, and normal blood pressure and cardiac function compared with C57BLKS/J mice at 6 to 8 weeks of age. After vehicle treatment for 8 weeks, db/db mice had reduced ejection fraction, mitral E/A ratio, endothelium-dependent relaxation of coronary arteries, tetrahydrobiopterin concentrations, ratio of endothelial nitric oxide synthase dimers/monomers, and nitric oxide levels compared with vehicle-treated C57BLKS/J mice. These detrimental effects of diabetes mellitus were abrogated by co-administration of SEP and L-Cit. Myocardial infarct size was increased, and coronary flow rate and ± dP/dt were decreased during reperfusion in vehicle-treated db/db mice subjected to ischemia/reperfusion injury compared with control mice. Co-administration of SEP and L-Cit decreased infarct size and improved coronary flow rate and cardiac function in both C57BLKS/J and db/db mice. Co-administration of SEP and L-Cit limits diabetic cardiomyopathy and ischemia/reperfusion injury in db/db mice through a tetrahydrobiopterin/endothelial nitric oxide synthase/nitric oxide pathway. © 2016 American Heart Association, Inc.

  7. CPU0213, a novel endothelin type A and type B receptor antagonist, protects against myocardial ischemia/reperfusion injury in rats

    Directory of Open Access Journals (Sweden)

    Z.Y. Wang

    2011-11-01

    Full Text Available The efficacy of endothelin receptor antagonists in protecting against myocardial ischemia/reperfusion (I/R injury is controversial, and the mechanisms remain unclear. The aim of this study was to investigate the effects of CPU0123, a novel endothelin type A and type B receptor antagonist, on myocardial I/R injury and to explore the mechanisms involved. Male Sprague-Dawley rats weighing 200-250 g were randomized to three groups (6-7 per group: group 1, Sham; group 2, I/R + vehicle. Rats were subjected to in vivo myocardial I/R injury by ligation of the left anterior descending coronary artery and 0.5% sodium carboxymethyl cellulose (1 mL/kg was injected intraperitoneally immediately prior to coronary occlusion. Group 3, I/R + CPU0213. Rats were subjected to identical surgical procedures and CPU0213 (30 mg/kg was injected intraperitoneally immediately prior to coronary occlusion. Infarct size, cardiac function and biochemical changes were measured. CPU0213 pretreatment reduced infarct size as a percentage of the ischemic area by 44.5% (I/R + vehicle: 61.3 ± 3.2 vs I/R + CPU0213: 34.0 ± 5.5%, P < 0.05 and improved ejection fraction by 17.2% (I/R + vehicle: 58.4 ± 2.8 vs I/R + CPU0213: 68.5 ± 2.2%, P < 0.05 compared to vehicle-treated animals. This protection was associated with inhibition of myocardial inflammation and oxidative stress. Moreover, reduction in Akt (protein kinase B and endothelial nitric oxide synthase (eNOS phosphorylation induced by myocardial I/R injury was limited by CPU0213 (P < 0.05. These data suggest that CPU0123, a non-selective antagonist, has protective effects against myocardial I/R injury in rats, which may be related to the Akt/eNOS pathway.

  8. Acute Myocardial Infarction: The First Manifestation of Ischemic Heart Disease and Relation to Risk Factors

    Directory of Open Access Journals (Sweden)

    Manfroi Waldomiro Carlos

    2002-01-01

    Full Text Available OBJECTIVE: To assess the association between cardiovascular risk factors and acute myocardial infarction as the first manifestation of ischemic heart disease, correlating them with coronary angiographic findings. METHODS: We carried out a cross-sectional study of 104 patients with previous acute myocardial infarction, who were divided into 2 groups according to the presence or absence of angina prior to acute myocardial infarction. We assessed the presence of angina preceding acute myocardial infarction and risk factors, such as age >55 years, male sex, smoking, systemic arterial hypertension, lipid profile, diabetes mellitus, obesity, sedentary lifestyle, and familial history of ischemic heart disease. On coronary angiography, the severity of coronary heart disease and presence of left ventricular hypertrophy were assessed. RESULTS: Of the 104 patients studied, 72.1% were males, 90.4% were white, 73.1% were older than 55 years, and 53.8% were hypertensive. Acute myocardial infarction was the first manifestation of ischemic heart disease in 49% of the patients. The associated risk factors were systemic arterial hypertension (RR=0.19; 95% CI=0.06-0.59; P=0.04 and left ventricular hypertrophy (RR=0.27; 95% CI=0,.8-0.88; P=0.03. The remaining risk factors were not statistically significant. CONCLUSION: Prevalence of acute myocardial infarction as the first manifestation of ischemic heart disease is high, approximately 50%. Hypertensive individuals more frequently have symptoms preceding acute myocardial infarction, probably due to ventricular hypertrophy associated with high blood pressure levels.

  9. Early Aldosterone Blockade in Acute Myocardial Infarction: The ALBATROSS Randomized Clinical Trial.

    Science.gov (United States)

    Beygui, Farzin; Cayla, Guillaume; Roule, Vincent; Roubille, François; Delarche, Nicolas; Silvain, Johanne; Van Belle, Eric; Belle, Loic; Galinier, Michel; Motreff, Pascal; Cornillet, Luc; Collet, Jean-Philippe; Furber, Alain; Goldstein, Patrick; Ecollan, Patrick; Legallois, Damien; Lebon, Alain; Rousseau, Hélène; Machecourt, Jacques; Zannad, Faiez; Vicaut, Eric; Montalescot, Gilles

    2016-04-26

    Mineralocorticoid receptor antagonists (MRA) improve outcome in the setting of post-myocardial infarction (MI) heart failure (HF). The study sought to assess the benefit of an early MRA regimen in acute MI irrespective of the presence of HF or left ventricular (LV) dysfunction. We randomized 1,603 patients to receive an MRA regimen with a single intravenous bolus of potassium canrenoate (200 mg) followed by oral spironolactone (25 mg once daily) for 6 months in addition to standard therapy or standard therapy alone. The primary outcome of the study was the composite of death, resuscitated cardiac arrest, significant ventricular arrhythmia, indication for implantable defibrillator, or new or worsening HF at 6-month follow-up. Key secondary/safety outcomes included death and other individual components of the primary outcome and rates of hyperkalemia at 6 months. The primary outcome occurred in 95 (11.8%) and 98 (12.2%) patients in the treatment and control groups, respectively (hazard ratio [HR]: 0.97; 95% confidence interval [CI]: 0.73 to 1.28). Death occurred in 11 (1.4%) and 17 (2.1%) patients in the treatment and control groups, respectively (HR: 0.65; 95% CI: 0.30 to 1.38). In a non-pre-specified exploratory analysis, the odds of death were reduced in the treatment group (3 [0.5%] vs. 15 [2.4%]; HR: 0.20; 95% CI: 0.06 to 0.70) in the subgroup of ST-segment elevation MI (n = 1,229), but not in non-ST-segment elevation MI (p for interaction = 0.01). Hyperkalemia >5.5 mmol/l(-1) occurred in 3% and 0.2% of patients in the treatment and standard therapy groups, respectively (p < 0.0001). The study failed to show the benefit of early MRA use in addition to standard therapy in patients admitted for MI. (Aldosterone Lethal effects Blockade in Acute myocardial infarction Treated with or without Reperfusion to improve Outcome and Survival at Six months follow-up; NCT01059136). Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All

  10. Mortality after acute myocardial infarction according to income and education

    DEFF Research Database (Denmark)

    Rasmussen, Jeppe Nørgaard; Rasmussen, Søren; Gislason, Gunnar H

    2006-01-01

    OBJECTIVE: To study how income and educational level influence mortality after acute myocardial infarction (AMI). DESIGN AND SETTING: Prospective analysis using individual level linkage of registries in Denmark. PARTICIPANTS: All patients 30-74 years old hospitalised for the first time with AMI...... in Denmark in 1995-2002. MAIN OUTCOME MEASURES: Relative risk (RR) of 30 day mortality and long term mortality (31 days until 31 December 2003) associated with income (adjusted for education) or educational level (adjusted for income) and further adjusted for sex, age, civil status, and comorbidity. RESULTS...... of 30 day mortality and long term mortality among younger patients with low compared with high income was 1.54 (95% confidence interval 1.36 to 1.79) and 1.65 (1.45 to 1.85), respectively. The RR of 30 day and long term mortality among younger patients with low compared with high education was 1.24 (1...

  11. Recurrent Acute Myocardial Infarction in Patients with Immune Thrombocytopenic Purpura

    Directory of Open Access Journals (Sweden)

    Fengyi Shen

    2014-01-01

    Full Text Available Immune thrombocytopenic purpura (ITP, also known as idiopathic thrombocytopenic purpura, is an acquired immune-mediated disease of adults and children characterized by a transient or persistent decrease of platelets and, depending upon the degree of thrombocytopenia, an increased risk of bleeding. The use of standard treatments for acute myocardial infarction (AMI, such as antiplatelet agents and anticoagulants, pose serious problems in patients with ITP due to the potential higher risk of bleeding complications. There are no current guidelines available for management of ITP patients with AMI. In this brief review of the limited available literature, we discuss the proposed pathophysiological link between ITP and arterial thrombosis and the challenging medical and interventional treatment of these patients.

  12. Climate and environmental triggers of acute myocardial infarction.

    Science.gov (United States)

    Claeys, Marc J; Rajagopalan, Sanjay; Nawrot, Tim S; Brook, Robert D

    2017-04-01

    Over the past few decades, a growing body of epidemiological and clinical evidence has led to heightened concerns about the potential short- and long-term deleterious effects of the environment on cardiovascular health, including the risk for acute myocardial infarction (AMI). This review highlights the increased risk of AMI caused by exposure to air pollution and cold temperatures. These factors should be considered modifiable risk factors in the prevention of cardiovascular disease. The current body of knowledge about the biological mechanisms linking environmental changes to atherothrombotic events and the impact of climate change on cardiovascular health are discussed. Finally, recommendations for prevention and public policy are presented. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.

  13. Sleep i