WorldWideScience

Sample records for acute reperfused myocardial

  1. Assessment of myocardial viability using multidetector computed tomography in patients with reperfused acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kim, T. [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Choi, B.J. [Department of Cardiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Kang, D.K., E-mail: kdklsm@ajou.ac.kr [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of); Sun, J.S. [Department of Radiology, Ajou University School of Medicine, Suwon (Korea, Republic of)

    2012-08-15

    Aim: To assess the prognostic value of 64-section multidetector computed tomography (MDCT) to predict follow-up myocardial dysfunction and functional recovery after reperfusion therapy in patients with acute myocardial infarction (MI) as defined by echocardiography. Materials and methods: After reperfusion therapy for acute MI, 71 patients underwent two-phase contrast-enhanced MDCT and follow-up echocardiography. MDCT findings were compared with echocardiographic findings using kappa statistics. The areas under the receiver operating characteristic curves (AUCs) and the odds ratios (ORs) of early perfusion defects (EPD), delayed enhancement (DE), and residual perfusion defects (RPD) for predicting follow-up myocardial dysfunction and functional recovery were calculated on a segmental basis. Results: The presence of transmural EPD (EPD{sub TM}) or RPD showed good agreement (k = 0.611 and 0.658, respectively) with follow-up myocardial dysfunction, while subendocardial EPD (EPD{sub sub}) or subendocardial DE (DE{sub sub}) showed fair agreement with follow-up myocardial dysfunction (k = 0.235 and 0.234, respectively). The AUC of RPD (0.796) was superior (p < 0.001 and 0.031, respectively) to those of EPD{sub TM} (0.761) and DE{sub TM} (0.771). The presence of EPD{sub TM}, DE{sub TM}, and RPD were significant, independent positive predictors of follow-up myocardial dysfunction (OR = 6.4, 1.9, and 9.8, respectively). EPD{sub TM} was a significant, independent negative predictor of myocardial functional recovery (OR = 0.13). Conclusion: Abnormal myocardial attenuation on two-phase MDCT after reperfusion therapy may provide promising information regarding myocardial viability in patients with acute MI.

  2. Early reperfusion strategy for acute myocardial infarction:a need for clinical implementation

    Institute of Scientific and Technical Information of China (English)

    Yan ZHANG; Yong HUO

    2011-01-01

    Reperfusion is the key strategy in acute ST-segment elevation myocardial infarction (STEMI) care,and it is time-dependent.Shortening the time from symptom to reperfusion and choosing the optimal reperfusion strategy for STEMI patients are great challenges in practice.We need to improve upon the problems of low reperfusion rate,non-standardized treatment,and economic burden in STEMI care.This article briefly reviews the current status of reperfusion strategy in STEMI care,and also introduces what we will do to bridge the gap between the guidelines and implementation in the clinical setting through the upcoming China STEMI early reperfusion program.

  3. Conditioned blood reperfusion during angioplasty (CoBRA) treatment of acute myocardial infarction.

    Science.gov (United States)

    Patel, M B; Kilgore, K S; Ortolano, G A; Gryboski, C L; Qureshi, M A; Marcovitz, P; Naylor, K B; Park, J L; Wenz, B; Gikakis, N; Freedman, R J; Lucchesi, B R; O'Neill, W W

    2001-03-01

    Acute myocardial infarct (MI) results in ischemia distal to lesions which puts heart muscle at risk for reperfusion injury (RI). Neutrophils, platelets and complement are putative mediators of RI. Recent advances in filtration technology provide integrated neutrophil and platelet removal together with complement-attenuating properties in a single blood-conditioning device. The present study characterizes the properties of a blood-conditioning filter and describes its clinical effect when used in conjunction with active hemoperfusion for acute MI. The filter reduces leukocytes by 99.9998 +/- 0.0002% (pheart preparation. The deposition of membrane attack complex and the resultant functional myocardial impairments [reflected in hemodynamic and biochemical measurements, including developed pressure, coronary blood flow, lymph-derived myocardial creatine kinase (CK)] are significantly attenuated by blood conditioning. Integration of the blood-conditioning filter into an active hemoperfusion system during primary percutaneous transluminal coronary angioplasty (PTCA) for acute MI (n=8) did not delay the procedure or cause any complications. Reperfusion of occluded coronary arteries with 300 cm3 of conditioned blood led to significant improvement in echocardiographic global wall motion scores (in standard deviations) following treatment (-1.64 +/- 0.18 to -1.45 +/- 0.15, p=0.02). Initial reperfusion of totally occluded coronary arteries with conditioned blood leads to acutely improved ventricular function. Collectively, these data provide a strong indication for continued investigation of conditioned blood reperfusion in angioplasty following acute MI for the long-term effect upon recovery of salvagable myocardium.

  4. Usefulness of BMIPP SPECT to evaluate myocardial viability, contractile reserve and coronary stenotic progression after reperfusion in acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Katsunuma, Eita; Kurokawa, Shingo; Takahashi, Motoi; Fukuda, Naoto; Kurosawa, Toshiro; Izumi, Tohru [Kitasato Univ., Sagamihara, Kanagawa (Japan). School of Medicine

    2001-07-01

    Using combined {sup 123}I-BMIPP (BMIPP), {sup 201}Tl (Tl) and {sup 99m}Tc-PYP (PYP) myocardial SPECT imaging, risk areas of acute myocardial infarction were documented in the acute stage, and then these images were evaluated for how well they reflected muscle viability, contractile reserve and coronary stenotic progression subsequent to reperfusion therapy. Patients who only experienced a first attack of myocardial infarction were enrolled. In total, 36 cases who had had the occluded artery successfully reperfused were examined during the past year. They had no significant vessel disease except for the culprit single artery. The patients were comprised of 32 men and 4 women. The mean age was 59.5 years. All patients underwent coronary angiography and left ventricular (LV) angiography in the emergency room. BMIPP/Tl and PYP myocardial SPECT were conducted in the acute stage and chronic stage. In the chronic stage LV angiography was repeated to assess the improvement of LV wall motion. The response to postextrasystolic potentiation (PESP) testing was performed to estimate myocardial contractile reserve. The risk area of acute myocardial infarction (AMI) was documented by reduced BMIPP accumulation. The size of reduced BMIPP accumulation was larger than that of PYP accumulation. A BMIPP/Tl discrepancy and PYP accumulation were documented to assess myocardial viability. Both improvement in LV wall motion and augmentation of PESP response were more closely related to a BMIPP/Tl discrepancy in the presence or absence of PYP accumulation. Therefore, it would be possible to evaluate myocardial viability and contractile reserve by the BMIPP/Tl discrepancy. In patients with good viability, it is important to predict whether there is coronary stenotic progression or not. In this study, we demonstrated that most patients with improved BMIPP images had no significant progression at the site of intervention. Serial observation of BMIPP images from the acute stage to the chronic

  5. Arrhythmias following Revascularization Procedures in the Course of Acute Myocardial Infarction: Are They Indicators of Reperfusion or Ongoing Ischemia?

    Directory of Open Access Journals (Sweden)

    Ersan Tatli

    2013-01-01

    Full Text Available Objective. The most important step in the treatment of ST elevation myocardial infarction is to sustain myocardial blood supply as soon as possible. The two main treatment methods used today to provide myocardial reperfusion are thrombolytic therapy and percutaneous coronary intervention. In our study, reperfusion arrhythmias were investigated as if they are indicators of coronary artery patency or ongoing ischemia after revascularization. Methods. 151 patients with a diagnosis of acute ST elevation myocardial infarction were investigated. 54 patients underwent primary percutaneous coronary intervention and 97 patients were treated with thrombolytic therapy. The frequency of reperfusion arrythmias following revascularization procedures in the first 48 hours after admission was examined. The relation between reperfusion arrhythmias, ST segment regression, coronary artery patency, and infarct related artery documented by angiography were analyzed. Results. There was no statistically significant difference between the two groups in the frequency of reperfusion arrhythmias (P=0.355. Although angiographic vessel patency was higher in patients undergoing percutaneous coronary intervention, there was no significant difference between the patency rates of each group with and without reperfusion arrythmias. Conclusion. Our study suggests that recorded arrhythmias following different revascularization procedures in acute ST elevation myocardial infarction may not always indicate vessel patency and reperfusion. Ongoing vascular occlusion and ischemia may lead to various arrhythmias which may not be distinguished from reperfusion arrhythmias.

  6. Limitations of spontaneous reperfusion and conventional medical therapy to afford myocardial protection through antecedent angina pectoris in acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Hashimoto, Akiyoshi; Nakata, Tomoaki; Wakabayashi, Takeru; Yuda, Satoshi; Eguchi, Mariko; Sasao, Hisataka; Tsuchihashi, Kazufumi; Shimamoto, Kazuaki [Sapporo Medical Univ. (Japan)

    1999-10-01

    Despite the cardioprotective effect of rapid coronary reperfusion, the effects of spontaneous recanalization on myocardial viability and metabolism are unknown. We studied whether preinfarction angina affords cardioprotection when spontaneous coronary reperfusion occurred in acute infarct patients. Myocardial tomographies with thallium and I-123-labeled-{beta}-methyl-p-iodophenyl penta-decanoic acid (BMIPP) were performed in 27 acute myocardial infarct patients treated medically: 15 patients had preexisting angina before infarction (group A) and 12 did not (group B). Thallium and BMIPP abnormalities and regional function were quantified by a polar map and contrast ventriculography, respectively. There was no significant difference between thallium and BMIPP in the severity index in groups A and B (89{+-}97 vs. 85{+-}68, 97{+-}28 vs. 95{+-}27, respectively), and no significant difference between the groups in the thallium or BMIPP severity index. The ratio of the thallium severity index to that of BMIPP and the regional wall-motion abnormality index were identical in groups A and B. Both patient groups were divided into 2 subgroups based on the presence or absence of spontaneous coronary reperfusion: subgroups A1 and A2, and subgroups B1 and B2, respectively. There were no significant differences among the 4 subgroups in severity indexes for both tracers, the thallium/BMIPP ratio, or the asynergy score. The BMIPP severity index correlated significantly with that of thallium in all subgroups, but no significant difference between the regression lines was found. It is therefore unlikely that spontaneous coronary recanalization affords beneficial effects through preservation of myocardial viability in an ischemia-related zone, suggesting that the cardioprotective effect of preinfarction angina is a limited phenomenon in patients undergoing rapid coronary reperfusion. (author)

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

    Directory of Open Access Journals (Sweden)

    Hamed Ashrafzadeh Takhtfooladi

    2015-01-01

    Full Text Available Background: 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. Objective: This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. Methods: 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. Results: 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. Conclusion: From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model.

  8. 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.

  9. Towards optimalisation of mechanical reperfusion therapy for acute myocardial

    NARCIS (Netherlands)

    Ernst, Nicolette Maria Simone Karin Josephina

    2005-01-01

    This thesis adresses diverse aspects of daily clinical practice in a setting where all patients with accute myocardial infarction are treated with primary angioplasty. The importance of pre-hospital infarction-diagnosis and triage, the influence of pharmacological pre-treatment before primary angiop

  10. Influence of ambulance use on early reperfusion therapies for acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    SONG Li; HU Da-yi; YAN Hong-bing; YANG Jin-gang; SUN Yi-hong; LI Chao; LIU Shu-shan; WU Dong; FENG Qi

    2008-01-01

    Background Ambulance use expedites the definitive treatment of acute myocardial infarction (AMI). The aim of this study was to evaluate the effect of ambulance use on the administration of early reperfusion therapies for patients with AMI in Beijing, China.Methods Data were prospectively collected from 498 patients with ST-elevation myocardial infarction (STEMI) who were admitted within 12 hours of symptom onset to 19 hospitals in Beijing between November 1,2005 and December 31, 2006. The baseline characteristics of and the initial management of the ambulance users and the non-ambulance users were compared.Results Only 186 (37.3%) patients used an ambulance as transportation to the hospital. Ambulance users were, on average, older and at relatively higher risk on presentation than the non-ambulance users. After adjustment for patient and hospital characteristics, ambulance use was associated with a greater early reperfusion rate, mainly because of a greater incidence of primary percutaneous coronary intervention. In addition, ambulance users had a significantly shorter median door-to-balloon (120 compared with 145 minutes, P<0.001) and symptom onset-to-balloon (223 compared with 300 minutes, P<0.001) time than non-ambulance users.Conclusions Ambulances are underused by AMI patients in Beijing. Ambulance use may lead to more frequent and faster receipt of early reperfusion therapies. New public health strategies should be developed to facilitate an increased use of ambulances by AMI patients.

  11. Prediction of myocardial recovery by dobutamine magnetic resonance imaging and delayed enhancement early after reperfused acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Barmeyer, Achim A.; Muellerleile, Kai; Heuer, Mirko; Meinertz, Thomas; Lund, Gunnar K. [University Heart-Center, University Hospital Hamburg-Eppendorf, Clinic of Cardiology/Angiology, Hamburg (Germany); Stork, Alexander; Bansmann, Martin; Adam, Gerhard [University Hospital Hamburg-Eppendorf, Clinic of Diagnostic and Interventional Radiology, Hamburg (Germany); Bavastro, Markus [University Hospital Hamburg-Eppendorf, Clinic of Anaesthesiology, Hamburg (Germany)

    2008-01-15

    The purpose was to study dobutamine magnetic resonance cine imaging (DOB-MRI) and delayed myocardial contrast enhancement (DE) early after reperfused acute myocardial infarction (AMI) for the prediction of segmental myocardial recovery and to find the optimal dose of dobutamine. Fifty patients (56{+-}12 years, 42 males) with reperfused AMI underwent DOB-MRI and DE studies 3.5 (1-19) days after reperfusion. In DOB-MRI systolic wall thickening (SWT) was measured in 18 segments at rest and during dobutamine at 5, 10 and 20 {mu}g*kg{sup -1}*min{sup -1}. Dysfunctional segments were identified and the extent of DE was measured for each segment. Segmental recovery was examined after 8 (5-15) months. Two hundred-forty-eight segments were dysfunctional with presence of DE in 193. DOB-MRI showed the best prediction of recovery at 10 {mu}g*kg{sup -1}*min{sup -1} of dobutamine with sensitivity of 67%, specificity of 63% and accuracy of 66% using a cut-off value for SWT of 2.0 mm. DE revealed a sensitivity of 68%, specificity of 65% and accuracy of 67% using a cut-off value of 46%. Combined analysis of DOB-MRI and DE did not improve diagnostic performance. Early prediction of segmental myocardial recovery after AMI is possible with DOB-MRI and DE. No improvement is achieved by dobutamine >10 {mu}g*kg{sup -1}*min{sup -1} or a combination of DOB-MRI and DE. (orig.)

  12. Detection and evaluation of renal biomarkers in a swine model of acute myocardial infarction and reperfusion.

    Science.gov (United States)

    Duan, Su-Yan; Xing, Chang-Ying; Zhang, Bo; Chen, Yan

    2015-01-01

    The prevalence of type 1 cardiorenal syndrome (CRS) is increasing and strongly associated with long-term mortality. However, lack of reliable animal models and well-defined measures of renoprotection, made early diagnosis and therapy difficult. We previously successfully established the swine acute myocardial infarction (AMI) model of ischemia-reperfusion by blocking left anterior descending branch (LAD). Reperfusion was performed after 90-minute occlusion of the LAD. AMI was confirmed by ECG and left ventricular angiography (LVG). Then those 52 survived AMI reperfusion swine, including ventricular fibrillation-cardiac arrest after restoration of blood flow, were randomly divided into four groups (four/group) according to different interventions: resuscitation in room temperature, resuscitation with 500 ml saline in room temperature, resuscitation with 4°C 500 ml saline and normal control (with no intervention of resuscitation). Each group was further observed in four groups according to different time of resuscitation after ventricular arrhythmias: 1, 3, 5, 10-minute reperfusion after ventricular arrhythmias. Plasma and random urine were collected to evaluate renal function and test renal biomarkers of acute kidney injury (AKI). Our swine AMI model of ischemia-reperfusion provoked subclinical AKI with the elevation of the tubular damage biomarker, NGAL, IL-18 and L-FABP. Renal damage rapidly observed after hemodynamic instability, rather than observation after several hours as previously reported. The increasing rate of biological markers declined after interventions, however, its impact on the long-term prognosis remains to be further studied. These data show that elevation of tubular damage biomarkers without glomerular function loss may indicate appropriate timing for effective renoprotections like hypothermia resuscitation in type 1 CRS.

  13. The effects of tirofiban on acute non-ST segment elevation myocardial infarction patients not receiving early reperfusion intervention

    Institute of Scientific and Technical Information of China (English)

    张大鹏

    2014-01-01

    Objective To study the efficacy of tirofiban in patients with acute non-ST-segment elevation myocardial infarction(NSTEMI)without early reperfusion intervention.Methods A total of 151 NSTEMI patients without early reperfusion intervention were enrolled in the study and randomized to the tirofiban group(n=76)and the control group(n=75).Coronary angiography was performed at day 3 and day 7,while percutaneous coronary

  14. Quantitative myocardial perfusion measurement using CT perfusion: a validation study in a porcine model of reperfused acute myocardial infarction.

    Science.gov (United States)

    So, Aaron; Hsieh, Jiang; Li, Jian-Ying; Hadway, Jennifer; Kong, Hua-Fu; Lee, Ting-Yim

    2012-06-01

    We validated a CT perfusion technique with beam hardening (BH) correction for quantitative measurement of myocardial blood flow (MBF). Acute myocardial infarction (AMI) was created in four pigs by occluding the distal LAD for 1 h followed by reperfusion. MBF was measured from dynamic contrast enhanced CT (DCE-CT) scanning of the heart, with correction of cardiac motion and BH, before ischemic insult and on day 7, 10 and 14 post. On day 14 post, radiolabeled microspheres were injected to measure MBF and the results were compared with those measured by CT perfusion. Excised hearts were stained with 2,3,5-triphenyltetrazolium chloride (TTC) to determine the relationship between MBF measured by CT Perfusion and myocardial viability. MBF measured by CT perfusion was strongly correlated with that by microspheres over a wide range of MBF values (R = 0.81, from 25 to 225 ml min(-1) 100 g(-1)). While MBF in the LAD territory decreased significantly from 98.4 ± 2.5 ml min(-1) 100 g(-1) at baseline to 32.2 ± 9.1 ml min(-1) 100 g(-1), P 0.05). TTC staining confirmed incomplete infarction in the LAD territory and no infarction in the LCx territory. Microvascular obstruction in infarcted tissue resulted in no-reflow and hence persistently low MBF in the reperfused LAD territory which contained a mixture of viable and non-viable tissue. CT perfusion measurement of MBF was accurate and correlated well with histology and microspheres measurements.

  15. 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.

  16. New perspectives on the role of cardiac magnetic resonance imaging to evaluate myocardial salvage and myocardial hemorrhage after acute reperfused ST-elevation myocardial infarction.

    Science.gov (United States)

    Mangion, Kenneth; Corcoran, David; Carrick, David; Berry, Colin

    2016-07-01

    Cardiac magnetic resonance (CMR) imaging enables the assessment of left ventricular function and pathology. In addition to established contrast-enhanced methods for the assessment of infarct size and microvascular obstruction, other infarct pathologies, such as myocardial edema and myocardial hemorrhage, can be identified using innovative CMR techniques. The initial extent of myocardial edema revealed by T2-weighted CMR has to be stable for edema to be taken as a retrospective marker of the area-at-risk, which is used to calculate myocardial salvage. The timing of edema assessment is important and should be focused within 2 - 7 days post-reperfusion. Some recent investigations have called into question the diagnostic validity of edema imaging after acute STEMI. Considering the results of these studies, as well as results from our own laboratory, we conclude that the time-course of edema post-STEMI is unimodal, not bimodal. Myocardial hemorrhage is the final consequence of severe vascular injury and a progressive and prognostically important complication early post-MI. Myocardial hemorrhage is a therapeutic target to limit reperfusion injury and infarct size post-STEMI.

  17. 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

    registries. In countries where no such registries exist, data were based on best expert estimates. Data were collected on the use of STEMI reperfusion treatment and mortality, the numbers of cardiologists, and the availability of PPCI facilities in each country. Our survey provides a brief data summary...... of these countries. CONCLUSION: Large variations in reperfusion treatment are still present across Europe. Countries in Eastern and Southern Europe reported that a substantial number of STEMI patients are not receiving any reperfusion therapy. Implementation of the best reperfusion therapy as recommended......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...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2003-02-01

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

  19. Heart fatty acid binding protein and myoglobin after reperfusion of acute myocardial infarction.

    Science.gov (United States)

    Ozdemir, Murat; Durakoğlugil, Emre; Gülbahar, Ozlem; Turkoglu, Sedat; Sancak, Banu; Paşaoğlu, Hatice; Cengel, Atiye

    2007-10-01

    The aim of this study was to disclose the release kinetics of heart fatty acid binding protein (HFABP) and myoglobin in acute myocardial infarction (AMI) reperfused by primary percutaneous coronary intervention (PPCI) and to determine the influence of the quality of coronary flow post PPCI on the release properties of these markers. Twenty-four patients with AMI who underwent successful PPCI and had no evidence of reocclusion within the first 120 minutes were studied. Serum myoglobin and HFABP levels at baseline and at 15, 30, 45, 60, 90 and 120 minutes after reperfusion were measured. Corrected TIMI frame count (CTFC) in the relevant vessel post PPCI was used to categorize patients in group I (CTFC > 21) and group 2 (CTFC < or = 21). Biomarker ratios at each sampling point were calculated by dividing the serum level of the biomarker at the specific sampling time by its baseline level. Baseline myoglobin and HFABP levels rose significantly at 15 minutes (153 +/- 251.5 microg/L vs. 904.3 +/- 542.6 microg/L, 10.9 +/- 8 microg/L vs. 17.8 +/- 9.1 microg/L, both P < 0.0001) after successful PPCI. Group 2 patients tended to have higher biomarker ratios at each time point as compared to group I. Successful PPCI for AMI results in a significant increase of both HFABP and myoglobin levels within 15 minutes of vessel opening and the quality of flow in the infarction-related artery post PCI as evaluated by CTFC does not influence the release kinetics of these biomarkers.

  20. Changes of transmural heterogeneity of Cx43 expression in acute myocardial ischemia reperfusion

    Institute of Scientific and Technical Information of China (English)

    Jiang-Hua Zhong; Shi-Juan Lu; Xiao-Pan Chen; Qi Zuo; Zheng-Wang Liu; Ding-Jun Sun; Miao Wu

    2016-01-01

    Objective:To observe the change of transmural heterogeneity of Cx43 protein among three myocardial layers and explore physiological mechanisms of malignant ventricular arrhythmia (MVA) in myocardial ischemia reperfusion (MIR).Methods: Twenty rabbits were randomly divided into MIR group (n=10) which rabbits with MIR were made in and sham group (n=10). 90% monophasic action potential repolarization duration (APD90), transmural dispersion of repolarization (TDR) and Cx43 protein (Cx43-pro) and mRNA (Cx43-Cq) expression among three myocardial layers were measured in both groups.Results:Compared with APD90 and TDR among three myocardial layers in the sham group, those in the MIR group were significant increased (P<0.01), which showed that transmural dispersion of repolarization increased significantly in MIR. Compared to those in the sham group, all three myocardial Cx43-pro significantly decreased (P<0.05) and△Cx43-pro obviously increased (P<0.05) in the MIR group which indicated transmural expression heterogeneity of Cx43 protein enlarged in MIR. 3. Cx43-Cq in all myocardium were significantly reduced (P<0.05) and△Cx43-Cq was significantly increased (P<0.05) in the MIR group compared to those in the sham group, which proved that transmural heterogeneity of Cx43 mRNA raised in MIR.Conclusions:Transmural heterogeneity of Cx43 expression among three myocardial layers in MIR significantly increased, which may enlarge dispersion of repolarization and prone to MVA.

  1. 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.

  2. Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute myocardial infarction: Results from the Metocard-CNIC trial (Effect of Metoprolol in Cardioprotection during an Acute Myocardial Infarction)

    OpenAIRE

    Pizarro, Gonzalo; García Lunar, Inés; Martínez de Vega, Vicente; Cabrera Rodríguez, José Ángel

    2014-01-01

    The goal of this trial was to study the long-term effects of intravenous (IV) metoprolol administration before reperfusion on left ventricular (LV) function and clinical events. Early IV metoprolol during ST-segment elevation myocardial infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percutaneous coronary intervention (pPCI). The METOCARD-CNIC (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction) trial recruited 270 pat...

  3. Assessment of circumferential endocardial extent of myocardial edema and infarction in patients with reperfused acute myocardial infarction: a cardiovascular magnetic resonance study.

    Science.gov (United States)

    Ota, Shingo; Tanimoto, Takashi; Hirata, Kumiko; Orii, Makoto; Shiono, Yasutsugu; Shimamura, Kunihiro; Ishibashi, Kohei; Yamano, Takashi; Ino, Yasushi; Kitabata, Hironori; Yamaguchi, Tomoyuki; Kubo, Takashi; Imanishi, Toshio; Akasaka, Takashi

    2014-01-01

    T2 weighted (T2W) images on cardiovascular magnetic resonance (CMR) visualizes myocardial edema, which reflects the myocardial area at risk (AAR) in reperfused acute myocardial infarction (AMI). Late gadolinium enhancement (LGE) demonstrates myocardial infarction. LGE images cover the whole left ventricle, but T2W images are obtained from a few slices of the left ventricle due to the long sequence time, so the quantification of AAR of the entire left ventricle is difficult. We hypothesize that we can quantify AAR with only LGE images if there is a strong correlation between the circumferential endocardial extent of myocardial edema and infarction. Thirty patients with first AMI were enrolled. All patients underwent successfully reperfusion therapy and CMR was performed within the first week after the event. We measured the circumferential extent of edema and infarction on short-axis views (T2 angle and LGE angle), respectively. A total of 82 short-axis slices showed transmural edema on T2W images. Corresponding LGE images were analyzed for the circumferential extent of infarction. The median [interquartile range] of T2 angle and DE angle were 147° [116°-219°] and 134° [104°-200°] in patients with LAD culprit lesion, 91° [87°-101°] and 85° [80°-90°] in LCX, and 110° [94°-123°] and 104° [89°-118°] in RCA, respectively. T2 angle was well correlated with LGE angle (r = 0.99, P infarction in reperfused AMI. Thus, T2 weighted imaging can be skipped to quantify the amount of AAR.

  4. Usefulness of the presenting electrocardiogram in predicting successful reperfusion with streptokinase in acute myocardial infarction.

    Science.gov (United States)

    Wong, C K; French, J K; Aylward, P E; Frey, M J; Adgey, A A; White, H D

    1999-01-15

    The presenting electrocardiogram may contain information indicating the probability of successful reperfusion. The relation between 3 parameters in the presenting electrocardiogram (pathologic Q waves, T-wave inversion, and the slope of ST elevation) and Thrombolysis in Myocardial Infarction trial (TIMI) grade 3 flow in the infarct-related artery was assessed angiographically 90 minutes after beginning streptokinase in 362 patients. TIMI grade 3 flow was more common in patients without Q waves (55%) than in those with Q waves (35%; p wave inversion (50%) than in those with T-wave inversion (30%; p waves and T-wave inversion had TIMI grade 3 flow, compared with 50% of the remaining patients (p waves (p wave inversion (p = 0.06). Among patients treated after 3 hours, TIMI grade 3 flow was seen in 38% of those without versus 30% of those with Q waves (p = NS), and in 38% of those without versus 23% of those with T-wave inversion (p waves, the time from the onset of chest pain to treatment, and age were independent predictors of TIMI grade 3 flow. Pathologic Q waves in the presenting electrocardiogram provide valuable information as to the probability of achieving successful reperfusion following administration of streptokinase, and may be helpful for triage of patients to alternative reperfusion strategies, including percutaneous revascularization.

  5. Impact of reperfusion therapy and infarct localization on frequency of premature ventricular beats in acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Davor Horvat

    2015-08-01

    Full Text Available Aim To determine the impact of infarct localization and types of reperfusion therapy on the frequency of ventricular premature beats (VPBs in patients with acute myocardial infarction (AMI and reduced left ventricular ejection fraction (LVEF. Methods A total of 705 patients with acute ST elevation myocardial infarction (STEMI were divided according to the infarct localization (anteroseptal, anterolateral, inferior and posterior and reperfusion therapy (fibrinolysis or percutaneous coronary intervention with stenting into two groups: LVEF45% was a control group. The occurrence of VPBs10 per hour defined as a significant. Results In patients with fibrinolysis therapy and LVEF<45% significant number of VPBs were in anteroseptal (p=0.017, anterolateral (p<0.001 and posterior AMI (p<0.001, but in patients with percutaneous coronary intervention (PCI and LVEF<45% significant number of VPBs were only in anteroseptal AMI (p=0.001 localization. Conclusion In patients with reduced ejection fraction in AMI, treatment with PCI method has a better antiarrhythmic effect compared to fibrinolysis treatment.

  6. Non-invasive evaluation of myocardial reperfusion by transthoracic Doppler echocardiography and single-photon emission computed tomography in patients with anterior acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Celutkiene Jelena

    2011-05-01

    Full Text Available Abstract Background The study was designed to evaluate whether the preserved coronary flow reserve (CFR 72 hours after reperfused acute myocardial infarction (AMI is associated with less microvascular dysfunction and is predictive of left ventricular (LV functional recovery and the final infarct size at follow-up. Methods In our study, CFR was assessed by transthoracic Doppler echocardiography (TDE in 44 patients after the successful percutaneous coronary intervention during the acute AMI phase. CFR was correlated with contractile reserve assessed by low-dose dobutamine echocardiography and with the total perfusion defect measured by single-photon emission computed tomography 72 hours after reperfusion and at 5 months follow-up. The ROC analysis was performed to determine test sensitivity and specificity based on CFR. Categorical data were compared by an χ2 analysis, continuous variables were analysed with the independent Student's t test. In order to analyse correlation between CFR and the parameters of LV function and perfusion, the Pearson correlation analysis was conducted. The linear regression analysis was used to assess the relationship between CFR and myocardial contractility as well as the final infarct size. Results We estimated the CFR cut-off value of 1.75 as providing the maximal accuracy to distinguish between patients with preserved and impaired CFR during the acute AMI phase (sensitivity 91.7%, specificity 75%. Wall motion score index was better in the subgroup with preserved CFR as compared to the subgroup with reduced CFR: 1.74 (0.29 vs. 1.89 (0.17 (p Conclusion The early measurement of CFR by TDE can be of high value for the assessment of successful reperfusion in AMI and can be used to predict LV functional recovery, myocardial viability and the final infarct size.

  7. Primary PCI and Treatment of Reperfusion Injury in Acute Myocardial Infarction

    NARCIS (Netherlands)

    M.T. Dirksen (Maurits)

    2008-01-01

    textabstractAcute myocardial infarction (AMI) is responsible for the majority of (sudden) deaths and significant morbidity, thereby causing a major burden on health care. The prognosis of patients after an AMI is mainly determined by the size of the infarct, which is dependent of the area at risk (d

  8. High-throughput 13-parameter immunophenotyping identifies shifts in the circulating T-cell compartment following reperfusion in patients with acute myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Jedrzej Hoffmann

    Full Text Available RATIONALE: With the advent of primary PCI (PPCI, reperfusion is achieved in almost all patients presenting with acute myocardial infarction. However, despite multiple trials, reperfusion injury has not been successfully dealt with so far. In mouse models, CD4(+ T lymphocytes (T cells have been shown to be crucial instigators of reperfusion injury. OBJECTIVE: Our goal was to investigate the role of CD4(+ T cells during myocardial reperfusion following PPCI by developing a protocol for high-throughput multiplexed flow cytometric analysis and multivariate flow clustering. METHODS AND RESULTS: 13-parameter immunophenotyping and hierarchical cluster analysis (HCA identified a unique CD4(+CD57(+ T-cell population in PPCI patients that reflected acute proliferation in the CD4(+ T-cell compartment. CD4(+CCR7(+ T cells were specifically depleted from peripheral blood during the first 30 min of myocardial reperfusion after PPCI, suggesting a potential role for the chemokine receptor CCR7 in T-cell redistribution to either peripheral tissues or migration to the infarcted heart during ischemia/reperfusion following PPCI. CONCLUSIONS: High-throughput polychromatic flow cytometry and HCA are capable of objective, time and cost efficient assessment of the individual T-cell immune profile in different stages of coronary heart disease and have broad applications in clinical trials.

  9. Implications of myocardial reperfusion on survival in women versus men with acute myocardial infarction undergoing primary coronary intervention.

    Science.gov (United States)

    Meller, Stephanie M; Lansky, Alexandra J; Costa, Ricardo A; Soffler, Morgan; Costantini, Costantino O; Brodie, Bruce R; Cox, David A; Stuckey, Thomas D; Fahy, Martin; Grines, Cindy L; Stone, Gregg W

    2013-10-15

    We evaluated the effects of myocardial perfusion after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) on gender-based mortality rates. Research has demonstrated a gender-specific response of cardiomyocytes to ischemia and a potential increase in myocardial salvage in women compared with men. Myocardial blush grade (MBG), an angiographic surrogate of myocardial perfusion, is an independent predictor of early and late survival after AMI. Whether the incidence and prognosis of myocardial perfusion differs according to gender among patients with AMI undergoing PCI is unknown. MBG and short- and long-term mortality were evaluated in 1,301 patients (male = 935; female = 366) with AMI randomized to primary angioplasty ± abciximab versus stent ± abciximab. Following PCI, >96% of patients achieved final Thrombolysis In Myocardial Infarction 3 flow, of which MBG 2/3 was present in 58.3% of women versus 51.1% of men (p = 0.02). Worse MBG was an independent predictor of mortality in women at 30 days (7.4% for MBG 0/1 vs 2.4% for MBG 2/3, p = 0.04) and at 1-year (11.0% for MBG 0/1 vs 3.4% for MBG 2/3, p = 0.01); however, MBG was not associated with differences in mortality for men. In conclusion, impaired myocardial perfusion following PCI for AMI, indicated by worse MBG, is an independent predictor of early and late mortality in women but not in men. These findings imply an enhanced survival benefit from restoring myocardial perfusion for women compared with men during primary angioplasty and may have clinical implications for interventional strategies in women.

  10. Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers

    Science.gov (United States)

    2016-01-25

    Acute Myocardial Infarction (AMI); Acute Coronary Syndrome (ACS); ST Elevation (STEMI) Myocardial Infarction; Ischemic Reperfusion Injury; Non-ST Elevation (NSTEMI) Myocardial Infarction; Angina, Unstable

  11. Contemporary percutaneous reperfusion therapy for acute myocardial infarction in the elderly

    Institute of Scientific and Technical Information of China (English)

    Kimberly A. Skelding; Charanjit S. Rihal

    2005-01-01

    Elderly patients with acute myocardial infarction have not been specifically studied in the context of a large randomized clinical trial. Estimates of the efficacy of available treatments are gleaned from subset analyses of clinical trials, retrospective analysis and singlecenter experiences. In western countries the population is aging and a disproportionate number of myocardial infarctions occur in the elderly. Usage of appropriate therapy in this age group is becoming increasingly important given the potential for benefit but also the potential for harm. Recent publications have found steady improvement in outcomes in the elderly population utilizing contemporary interventions.

  12. Comparison of regional and global left ventricular function by serial echocardiograms after reperfusion in acute myocardial infarction.

    Science.gov (United States)

    Broderick, T M; Bourdillon, P D; Ryan, T; Feigenbaum, H; Dillon, J C; Armstrong, W F

    1989-01-01

    Fifty patients undergoing successful reperfusion therapy (percutaneous transluminal coronary angioplasty 20, thrombolysis 10, combined 20) for acute myocardial infarction were evaluated with serial two-dimensional echocardiograms performed early (less than 24 hours, mean 8 hours) and late (greater than 3 days, mean 6 days) after presentation. Treatment occurred within 12 hours of the onset of symptoms with most patients achieving reperfusion in less than 6 hours (mean 4.7 hours) from the onset of pain. Reperfusion was demonstrated short-term by angiography in 42 of 50 patients (84%). Four patients had clinical signs of reperfusion and subsequent angiographic confirmation. An additional four patients with "stuttering" infarct courses were treated late by percutaneous transluminal coronary angioplasty. Echocardiograms were analyzed for global performance by calculation of fractional area change at the papillary muscle level and ejection fraction (biplane Simpson's rule) in 18 patients in whom this analysis could be performed. Measurements of regional function included fractional shortening at the base (n = 37), regional wall motion index (n = 50) and percent of normal functioning myocardium (n = 50). Overall there was a significant improvement in regional wall scores and percent of functioning myocardium (regional wall motion index 1.73 to 1.43, p less than 0.001 and percent of functioning myocardium 0.61 to 0.70, p less than 0.001) but only a trend toward improvement when global function was assessed by ejection fraction (0.42 to 0.48, p less than 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)

  13. Study on Effect of Shenmai Injection Protecting Myocardium against Ischemia-Reperfusion Injury in Thrombolytic Therapy with Urokinase for Acute Myocardial Infarction Patient Evaluated by 99mTc-MIBI Myocardial Imaging

    Institute of Scientific and Technical Information of China (English)

    郭松鹏; 张言镇

    2001-01-01

    Objective: To evaluate the myocardial protecting effect of Shenmai injection (SMI) against ischemia/reperfusion injury in thrombolytic therapy with urokinase (UK) for acute myocardial infarction patients by 99mTc-MIBI myocardial imaging (SPECT). Methods: Five hundred and thirty-seven patients were divided into two groups randomly. The SMI group (n=292) was treated with thrombolytictreatment plus SMI and the control group (n=245) with thrombolytic treatment solely. Single photon emission computed tomography (SPECT) was carried out on the 7th day after thrombolysis to determine the ischemic myocardial area (IMA) and ejection fraction (EF) in both groups and compared. Results: The infarction related area (IRA) of reperfusion rate in the two groups was not different significantly (72.26% vs 72.65%, P >0.05). The IMA in patients of the SMI group, no matter with or without reperfused IRA (211 cases and 81 cases) respectively, was significantly lower than that in the control group (178 cases and 67 cases) respectively, P<0.01 and P<0.05 respectively. The EF value in the SMI group was significantly higher than that in the control group (P<0.01). Conclusion:Using SMI in early stage of thrombolytic treatment in acute myocardial infarction could significantly reduce IMA and increase EF. SMI showed good protective effect against myocardial ischemia/reperfusion injury in thrombolytic treatment.

  14. Study on Effect of Shenmai Injection Protecting Myocardium against Ischemia-Reperfusion Injury in Thrombolytic Therapy with Urokinase for Acute Myocardial Infarction Patient Evaluated by 99mTc-MIBI Myocardial Imaging

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To evaluate the myocardial protecting effect of Shenmai injection (SMI) against ischemia/reperfusion injury in thrombolytic therapy with urokinase (UK) for acute myocardial infarction patients by 99mTc-MIBI myocardial imaging (SPECT). Methods: Five hundred and thirty-seven patients were divided into two groups randomly. The SMI group (n=292) was treated with thrombolytictreatment plus SMI and the control group (n=245) with thrombolytic treatment solely. Single photon emission computed tomography (SPECT) was carried out on the 7th day after thrombolysis to determine the ischemic myocardial area (IMA) and ejection fraction (EF) in both groups and compared. Results: The infarction related area (IRA) of reperfusion rate in the two groups was not different significantly (72.26% vs 72.65%, P >0.05). The IMA in patients of the SMI group, no matter with or without reperfused IRA (211 cases and 81 cases) respectively, was significantly lower than that in the control group (178 cases and 67 cases) respectively, P<0.01 and P<0.05 respectively. The EF value in the SMI group was significantly higher than that in the control group (P<0.01). Conclusion:Using SMI in early stage of thrombolytic treatment in acute myocardial infarction could significantly reduce IMA and increase EF. SMI showed good protective effect against myocardial ischemia/reperfusion injury in thrombolytic treatment.

  15. Relation between Tc-99m-PYP and Tl-201 scintigraphic findings and left ventricular function in acute myocardial infarction with early reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Mori, Takao; Fukuzaki, Hisashi; Igarashi, Yuuichirou; Minamiji, Katsumi; Takarada, Akira; Imai, Naoaki; Fujino, Motohiro; Kurogane, Hiroyuki; Yoshida, Yutaka.

    1988-07-01

    The purpose of this study was to examine the significance of Tc-99m PYP uptake in the evaluation of myocardial salvage and reperfusion injury during early reperfusion in acute myocardial infarction. The subjects were 54 patients with initial myocardial infarction attributable to left anterior descending branch lesion in whom early reperfusion was attained by spontaneous recanalization (SR), intracoronary thrombolysis (ICT), and percutaneous transluminal angioplasty (PTCA). The radionuclide imaging appearances of the myocardium fell into four categories : I) small Tl-201 defect and faint Tc-99m PYP uptake ; II) small Tl-201 defect and intense Tc-99m PYP uptake ; III) large Tl-201 defect and faint Tc-99m PYP uptake ; and IV) large Tl-201 defect and intense Tc-99m PYP uptake. The incidences of I and II were higher in the group of SR patients than the group of ICT and PTCA patients. Features of left ventricular ejection fraction (LVEF) from the acute through the chronic stages were as follows : Category I - favorable LVEF through the stages ; Category II - improvement at chronic stage ; Category III - no consistent tendency for LVEF ; and Category IV - aggravation at chronic stage. In cases of early recanalization of acute myocardial infarction, Tc-99m PYP images combined with Tl-201 images may provide useful information on changes of cardiac function and salvage of the ischemic myocardium. (Namekawa, K.).

  16. 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

  17. Pharmacologic Effects of Cannabidiol on Acute Reperfused Myocardial Infarction in Rabbits: Evaluated With 3.0T Cardiac Magnetic Resonance Imaging and Histopathology.

    Science.gov (United States)

    Feng, Yuanbo; Chen, Feng; Yin, Ting; Xia, Qian; Liu, Yewei; Huang, Gang; Zhang, Jian; Oyen, Raymond; Ni, Yicheng

    2015-10-01

    Cannabidiol (CBD) has anti-inflammatory effects. We explored its therapeutic effects on cardiac ischemia-reperfusion injury with an experimental imaging platform. Reperfused acute myocardial infarction (AMI) was induced in rabbits with a 90-minute coronary artery occlusion followed by 24-hour reperfusion. Before reperfusion, rabbits received 2 intravenous doses of 100 μg/kg CBD (n = 10) or vehicle (control, n = 10). Evans blue was intravenously injected for later detection of the AMI core. Cardiac magnetic resonance imaging was performed to evaluate cardiac morphology and function. After euthanasia, blood troponin I (cTnI) was assessed, and the heart was excised and infused with multifunctional red iodized oil dye. The heart was sliced for digital radiography to quantify the perfusion density rate, area at risk (AAR), and myocardial salvage index, followed by histomorphologic staining. Compared with controls, CBD treatment improved systolic wall thickening (P < 0.05), significantly increased blood flow in the AAR (P < 0.05), significantly decreased microvascular obstruction (P < 0.05), increased the perfusion density rate by 1.7-fold, lowered the AMI core/AAR ratio (P < 0.05), and increased the myocardial salvage index (P < 0.05). These improvements were associated with reductions in serum cTnI, cardiac leukocyte infiltration, and myocellular apoptosis (P < 0.05). Thus, CBD therapy reduced AMI size and facilitated restoration of left ventricular function. We demonstrated that this experimental platform has potential theragnostic utility.

  18. 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.

  19. 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.)

  20. Antiarrhythmic activity of n-tyrosol during acute myocardial ischemia and reperfusion.

    Science.gov (United States)

    Chernyshova, G A; Plotnikov, M B; Smol'yakova, V I; Golubeva, I V; Aliev, O I; Tolstikova, T G; Krysin, A P; Sorokina, I V

    2007-06-01

    Antiarrhythmic activity of n-tyrosol was demonstrated on the model of early occlusion and reperfusion arrhythmia. The preparation reduces the incidence of ventricular tachycardia and fibrillation, increases the percent of animals without ventricular arrhythmia, and moderates the severity of developing ventricular arrhythmias.

  1. 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

    Background 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. Methods and Results 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. Conclusions 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

  2. Iloprost and vitamin C attenuates acute myocardial injury induced by suprarenal aortic ischemia-reperfusion in rabbits.

    Science.gov (United States)

    Iriz, E; Iriz, A; Take, G; Ozgul, H; Oktar, L; Demirtas, H; Helvacioglu, F; Arslan, M

    2015-01-01

    The aim of this study was to evaluate antioxidant and cytoprotective effects of iloprost and Vitamin C in a distant organ after abdominal aorta ischemia-reperfusion injury. Twenty-eight New Zealand rabbits weighing 2,400-2,800 g were used for this study. The rabbits were divided into four equal groups. These groups are control group, sham group, iloprost group, and iloprost+vitamin C group. Suprarenal aorta was occluded with a vascular clamp. Following 30 minutes of ischemia, the vascular clamp was removed. Rabbits in group 3 received 10 ng/kg/min iloprost and those in group 4 received 10 ng/kg/min iloprost and 10 mg/kg vitamin C. At the end of the reperfusion period, the rabbits were sacrificed by a high intraperitoneal dose of xylazine+ketamine injection. Myocardial tissue samples were taken for electron microscopic analysis. We evaluated SOD, MDA and catalase in myocardial tissue samples. Iloprost and iloprost+vitamin C groups significantly reduced the oxidative stress markers in tissue samples (pvitamin C administration (pvitamin C showed an attenuation of ischemia-reperfusion injury in distant organs (Tab. 3, Fig. 4, Ref. 30).

  3. Prognostic value and determinants of a hypointense infarct core in T2-weighted cardiac magnetic resonance in acute reperfused ST-elevation-myocardial infarction.

    Science.gov (United States)

    Eitel, Ingo; Kubusch, Konrad; Strohm, Oliver; Desch, Steffen; Mikami, Yoko; de Waha, Suzanne; Gutberlet, Matthias; Schuler, Gerhard; Friedrich, Matthias G; Thiele, Holger

    2011-07-01

    A hypointense core of infarcted myocardium in T2-weighted cardiovascular MRI (CMR) has been used as a noninvasive marker for intramyocardial hemorrhage. However, the clinical significance of such findings not yet been established. The aim of this study was to evaluate determinants and prognostic impact of a hypointense infarct core in T2-weighted CMR images, studied in patients after acute, reperfused ST-elevation-myocardial infarction. We analyzed 346 patients with ST-elevation-myocardial infarction undergoing primary angioplasty core in T2-weighted images, and late microvascular obstruction. Patients were categorized into 2 groups defined by the presence or absence of a hypointense core. The primary end point of the study was occurrence of major adverse cardiovascular events defined as death, reinfarction, and congestive heart failure within 6 months after infarction. A hypointense core was present in 122 (35%) patients and was associated with larger infarcts, greater amount of microvascular obstruction, less myocardial salvage, and impaired left ventricular function (P core was a strong univariable predictor of major adverse cardiovascular events (hazard ratio, 2.59; confidence interval, 1.27 to 5.27) and was significantly associated with an increased major adverse cardiovascular events rate (16.4% versus 7.0%, P = 0.006) 6 months after infarction. A hypointense infarct core within the area at risk of reperfused infarcted myocardium in T2-weighted CMR is closely related to infarct size, microvascular obstruction, and impaired left ventricular function, with subsequent adverse clinical outcome.

  4. 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...

  5. Intracoronary adenosine improves myocardial perfusion in late reperfused myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    Background Myocardial perfusion associates with clinical syndromes and prognosis.Adenosine could improve myocardial perfusion of acute myocardial infarction within 6 hours,but few data are available on late perfusion of myocardial infarction (MI).This study aimed at quantitatively evaluating the value of intracoronary adenosine improving myocardial perfusion in late reperfused MI with myocardial contrast echocardiography(MCE).Methods Twenty-six patients with anterior wall infarcts were divided randomly into 2 groups:adenosine group(n=12) and normal saline group(n=14).Their history of myocardial infarction was about 3-12 weeks.Adenosine or normalsaline was given when the guiding wire crossed the lesion through percutaneous coronary intervention(PCI),then the balloon was dilated and stent(Cypher/Cypher select)was implanted at the lesion.Contrast pulse sequencing MCE with Sonovue contrast via the coronary route was done before PCI and 30 minutes after PCI.Video densitometry and contrast filled-blank area were calculated with the CUSQ off-line software.Heart function and cardiac events were followed up within 30 days.Results Perfusion in the segments of the criminal occlusive coronary artery in the adenosine group was better than that in the saline group(5.71±0.29 vs 4.95±1.22,P<0.05).Ischemic myocardial segment was deminished significantly afterPCI,but the meliorated area was bigger in the adenosine group than in the saline group((1.56±0.60)cm2 vs(1.02±0.56) cm2,P<0.05).The video densitometry in critical segments was also improved significantly in the adenosine group (5.53±0.36 vs 5.26±0.35,P<0.05).Left ventricular ejection fraction(LVEF)was improved in all patients after PCI,but EF was not significant between the two groups((67±6)% vs(62±7)%,P>0.05).There was no in-hospital or 30-day major adverse cardiac event(MACE)in the adenosine group but 3 MACE in the saline group in 30 days after PCI.Conclusions Adenosine could improve myocardial microvascular

  6. Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute myocardial infarction: results from the METOCARD-CNIC trial (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction).

    Science.gov (United States)

    Pizarro, Gonzalo; Fernández-Friera, Leticia; Fuster, Valentin; Fernández-Jiménez, Rodrigo; García-Ruiz, José M; García-Álvarez, Ana; Mateos, Alonso; Barreiro, María V; Escalera, Noemí; Rodriguez, Maite D; de Miguel, Antonio; García-Lunar, Inés; Parra-Fuertes, Juan J; Sánchez-González, Javier; Pardillos, Luis; Nieto, Beatriz; Jiménez, Adriana; Abejón, Raquel; Bastante, Teresa; Martínez de Vega, Vicente; Cabrera, José A; López-Melgar, Beatriz; Guzman, Gabriela; García-Prieto, Jaime; Mirelis, Jesús G; Zamorano, José Luis; Albarrán, Agustín; Goicolea, Javier; Escaned, Javier; Pocock, Stuart; Iñiguez, Andrés; Fernández-Ortiz, Antonio; Sánchez-Brunete, Vicente; Macaya, Carlos; Ibanez, Borja

    2014-06-10

    The goal of this trial was to study the long-term effects of intravenous (IV) metoprolol administration before reperfusion on left ventricular (LV) function and clinical events. Early IV metoprolol during ST-segment elevation myocardial infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percutaneous coronary intervention (pPCI). The METOCARD-CNIC (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction) trial recruited 270 patients with Killip class ≤II anterior STEMI presenting early after symptom onset (<6 h) and randomized them to pre-reperfusion IV metoprolol or control group. Long-term magnetic resonance imaging (MRI) was performed on 202 patients (101 per group) 6 months after STEMI. Patients had a minimal 12-month clinical follow-up. Left ventricular ejection fraction (LVEF) at the 6 months MRI was higher after IV metoprolol (48.7 ± 9.9% vs. 45.0 ± 11.7% in control subjects; adjusted treatment effect 3.49%; 95% confidence interval [CI]: 0.44% to 6.55%; p = 0.025). The occurrence of severely depressed LVEF (≤35%) at 6 months was significantly lower in patients treated with IV metoprolol (11% vs. 27%, p = 0.006). The proportion of patients fulfilling Class I indications for an implantable cardioverter-defibrillator (ICD) was significantly lower in the IV metoprolol group (7% vs. 20%, p = 0.012). At a median follow-up of 2 years, occurrence of the pre-specified composite of death, heart failure admission, reinfarction, and malignant arrhythmias was 10.8% in the IV metoprolol group versus 18.3% in the control group, adjusted hazard ratio (HR): 0.55; 95% CI: 0.26 to 1.04; p = 0.065. Heart failure admission was significantly lower in the IV metoprolol group (HR: 0.32; 95% CI: 0.015 to 0.95; p = 0.046). In patients with anterior Killip class ≤II STEMI undergoing pPCI, early IV metoprolol before reperfusion resulted in higher long-term LVEF, reduced incidence of severe LV systolic dysfunction

  7. 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

  8. Calpain system and its involvement in myocardial ischemia and reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Christiane; Neuhof; Heinz; Neuhof

    2014-01-01

    Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction.

  9. Assessment of coronary reperfusion in patients with myocardial infarction using fatty acid binding protein concentrations in plasma

    NARCIS (Netherlands)

    M.J.M. de Groot; A.M.M. Muijtjens; M.L. Simoons (Maarten); W.T. Hermens (Wim); J.F.C. Glatz

    2001-01-01

    textabstractOBJECTIVE: To examine whether successful coronary reperfusion after thrombolytic treatment in patients with confirmed acute myocardial infarction can be diagnosed from the plasma marker fatty acid binding protein (FABP), for either acute clinical decision making or retrospective purposes

  10. The Effects of Oxygen Therapy on Myocardial Salvage in ST Elevation Myocardial Infarction Treated with Acute Percutaneous Coronary Intervention: The Supplemental Oxygen in Catheterized Coronary Emergency Reperfusion (SOCCER) Study.

    Science.gov (United States)

    Khoshnood, Ardavan; Carlsson, Marcus; Akbarzadeh, Mahin; Bhiladvala, Pallonji; Roijer, Anders; Bodetoft, Stefan; Höglund, Peter; Zughaft, David; Todorova, Lizbet; Erlinge, David; Ekelund, Ulf

    2015-01-01

    Despite a lack of scientific evidence, oxygen has long been a part of standard treatment for patients with acute myocardial infarction (AMI). However, several studies suggest that oxygen therapy may have negative cardiovascular effects. We here describe a randomized controlled trial, i.e. Supplemental Oxygen in Catheterized Coronary Emergency Reperfusion (SOCCER), aiming to evaluate the effect of oxygen therapy on myocardial salvage and infarct size in patients with ST elevation myocardial infarction (STEMI) treated with a primary percutaneous coronary intervention (PCI). One hundred normoxic STEMI patients accepted for a primary PCI are randomized in the ambulance to either standard oxygen therapy or no supplemental oxygen. All patients undergo cardiovascular magnetic resonance imaging (CMR) 2-6 days after the primary PCI, and a subgroup of 50 patients undergo an extended echocardiography during admission and at 6 months. All patients are followed for 6 months for hospital admission for heart failure and subjective perception of health. The primary endpoint is the myocardial salvage index on CMR. Even though oxygen therapy is a part of standard care, oxygen may not be beneficial for patients with AMI and is possibly even harmful. The results of the present and concurrent oxygen trials may change international treatment guidelines for patients with AMI or ischemia.

  11. 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.)

  12. 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

  13. Effect of intravenous FX06 as an adjunct to primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction results of the F.I.R.E. (Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury) trial

    DEFF Research Database (Denmark)

    Atar, Dan; Petzelbauer, Peter; Schwitter, Jürg

    2009-01-01

    by mitigating reperfusion injury. METHODS: In all, 234 patients presenting with acute ST-segment elevation myocardial infarction were randomized in 26 centers. FX06 or matching placebo was given as intravenous bolus at reperfusion. Infarct size was assessed 5 days after myocardial infarction by late gadolinium...... enhanced cardiac magnetic resonance imaging. Secondary outcomes included size of necrotic core zone and microvascular obstruction at 5 days, infarct size at 4 months, left ventricular function, troponin I levels, and safety. RESULTS: There were no baseline differences between groups. On day 5......: In this proof-of-concept trial, FX06 reduced the necrotic core zone as one measure of infarct size on magnetic resonance imaging, while total late enhancement was not significantly different between groups. The drug appears safe and well tolerated. (Efficacy of FX06 in the Prevention of Myocardial Reperfusion...

  14. 急性ST段抬高型心肌梗死再灌注治疗的急缓之择%Balance the Emergency or Delay Treatment in Reperfusion Strategies for Acute ST-segment Elevation Myocardial Infarction

    Institute of Scientific and Technical Information of China (English)

    刘海伟; 韩雅玲

    2012-01-01

    Reperfusion is the most efficient treatment for acute ST-segment elevation myocardial infarction(STEMI). Reperfusion mainly includes primary percutaneous coronary intervention( PCI) and fibrinolysis treatment. It is best to combine the conditions of patients and the hospital -level factor to select the optimal reperfusion strategies, which could extend benefits and improve long-term outcomes for STEMI patients.%急性ST段抬高型心肌梗死(STEMI)最有效治疗方法是再灌注治疗,主要包括直接经皮冠状动脉介入治疗(PCI)和溶栓治疗.只有结合患者、医疗机构的实际情况,合理选择再灌注治疗方案,才能使STEMI患者获益最大化,改善其长期预后.

  15. Effects of reperfusion arrhythmias and myocardial connexin 43 by Compound Astragalus Mixture Nourishing Heart in a rat model of acute myocardial ischemic reperfusion injury%复方黄芪养心合剂对大鼠缺血再灌注心肌缝隙连接蛋白43的影响

    Institute of Scientific and Technical Information of China (English)

    陈启兰; 龚一萍; 祝光礼; 齐国安; 赫小龙; 任兴昌; 王骋

    2013-01-01

    目的:观察复方黄芪养心合剂对SD大鼠缺血再灌注心肌细胞缝隙连接蛋白43(Cx43)分布的改变和表达的影响.方法:应用复方黄芪养心合剂按每天14g/kg剂量、琥珀酸美托洛尔缓释片按每天(MSSRT) 9.5mg/kg剂量灌胃2周后,对SD大鼠行冠状动脉左前降支结扎30min后再灌注60min造成心肌缺血再灌注(I/R)损伤模型,记录Ⅱ导联心电图,采用免疫组织化学法(IHC)观察心肌细胞Cx43分布的改变;运用Image Pro Plus 6.0图像分析软件对Cx43的表达进行半定量分析.结果:Cx43平均光密度(AOD)I/R组心肌内膜下缺血区Cx43的AOD显著低于假手术组(P<0.01),且MSSRT组、复方组较1/R组升高(P<0.05).结论:对冠状动脉左前降支结扎术后再灌注SD大鼠,复方黄芪养心合剂对心肌细胞Cx43分布的改变有改善作用,有促进心肌内膜下缺血区域Cx43表达的作用,其作用与MSSRT相近.%Objective: To evaluate the effects of Compound Astragalus Mixture Nourishing Heart (CAMNH) antiarrhythmia and myocardial connexin 43 (Cx43) in a rat model of acute myocardial ischemic reperfusion injury. Methods: Myocardial infarction (MI) was induced by ligating left anterior descending coronary artery (LAD) for 30 minutes, followed by reperfusion of 60 minutes in rats. Rats were treated with CAMNH (14g·kg-1·d-1) or metoprolol succinate sustained-release tablets (MSSRT, 9.5mg·kg-1d-1) for 14 days before MI. The distribution of myocardial Cx43 was observed by Immunohistochemistry (IHC), and the expression of myocardial Cx43, which were represented by average optical density (AOD), was measured by Image Pro Plus 6.0. Results: The expression of myocardial Cx43 in infarction region was significantly reduced, disordered and even all disappearing, the expression of myocardial Cx43 from infarction region into ischemic region and normal region had a gradual recovery of transitional variability. Ischemia/reperfusion(I/R) group vs sham-operated (SO

  16. 急性STEMI再灌注治疗策略选择的再思考%The Rethinking of Reperfusion Strategy in Acute ST Segment Elevation Myocardial Infarction

    Institute of Scientific and Technical Information of China (English)

    徐泽升; 辛兴利

    2012-01-01

    Primary percutaneous coronary intervention (PCI) and thrombolysis are two commonly used reperfusion methods in acute ST segment elevation myocardial infarction (STEMI). Primary PCI though a state -of -the -art technique is too complicated to apply for everyone of STEMI in practice. Thrombolysis, though limited in its effectiveness and posing a risk of bleeding, can be administered quickly and performed relatively easy. We should choose proper method between thrombolysis therapy with mechanical treatment to open the infarction-related artery (IRA) early, consistently and thoroughly.%静脉溶栓和直接经皮冠状动脉介入术是急性STEMI再灌注治疗的两种主要方法,既要发挥化学性药物和物理性机械再灌注治疗各自治疗的优势,又要二者有机地结合,实现梗死相关冠脉的早期、有效、持续的开通.

  17. Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction.

    Directory of Open Access Journals (Sweden)

    Maurits R Hollander

    Full Text Available Microvascular injury (MVI after coronary ischemia-reperfusion is associated with high morbidity and mortality. Both ischemia and reperfusion are involved in MVI, but to what degree these phases contribute is unknown. Understanding the etiology is essential for the development of new potential therapies.Rats were divided into 3 groups receiving either 30 minutes ischemia, 90 minutes ischemia or 30 minutes ischemia followed by 60 minutes reperfusion. Subsequently hearts were ex-vivo perfused in a Langendorff-model. Fluorescence and electron microscopy was used for analysis of capillary density, vascular permeability and ultrastructure. Most MVI was observed after 30 minutes ischemia followed by 60 minutes reperfusion. In comparison to the 30' and 90' ischemia group, wall thickness decreased (207.0±74 vs 407.8±75 and 407.5±71, p = 0.02. Endothelial nuclei in the 30'-60' group showed irreversible damage and decreased chromatin density variation (50.5±9.4, 35.4±7.1 and 23.7±3.8, p = 0.03. Cell junction density was lowest in the 30'-60' group (0.15±0.02 vs 2.5±0.6 and 1.8±0.7, p<0.01. Microsphere extravasation was increased in both the 90' ischemia and 30'-60' group.Ischemia alone for 90 minutes induces mild morphological changes to the coronary microcirculation, with increased vascular permeability. Ischemia for 30 minutes, followed by 60 minutes of reperfusion, induces massive MVI. This shows the direct consequences of reperfusion on the coronary microcirculation. These data imply that a therapeutic window exists to protect the microcirculation directly upon coronary revascularization.

  18. Activation of Poly(ADP-Ribose) Polymerase by Myocardial Ischemia and Coronary Reperfusion in Human Circulating Leukocytes

    OpenAIRE

    Tóth-Zsámboki, Emese; Horváth, Eszter; Vargova, Katarina; Pankotai, Eszter; Murthy, Kanneganti; Zsengellér, Zsuzsanna; Bárány, Tamás; Pék, Tamás; Fekete, Katalin; Kiss, Róbert Gábor; Préda, István; Lacza, Zsombor; Gerö, Domokos; SzabÓ, Csaba

    2006-01-01

    Reactive free radical and oxidant production leads to DNA damage during myocardial ischemia/reperfusion. Consequent overactivation of poly(ADP-ribose) polymerase (PARP) promotes cellular energy deficit and necrosis. We hypothesized that PARP is activated in circulating leukocytes in patients with myocardial infarction and reperfusion during primary percutaneous coronary intervention (PCI). In 15 patients with ST segment elevation acute myocardial infarction, before and after primary PCI and 2...

  19. Efficacy of Clopidrogel on Reperfusion and High-Sensitivity C-Reactive Protein in Patients with Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Mehmet Akbulut

    2009-01-01

    Full Text Available We investigated the effects of clopidogrel on reperfusion and inflammatory process in STEMI. A total of 175 STEMI patients with similar clinical characteristics were included to this study. One was the standard pharmacological reperfusion therapy group (group 1, n : 90, who received 300 mg aspirin, 70 U/kg bolus, and 12 U/kg/hr continuous infusion of unfractioned heparin and accelerated t-PA. Clopidogrel 450 mg loading and 75 mg/d thereafter was added to standard reperfusion therapy in the other group (group 2, n : 85. The ST-segment resolution, CK-MB, and high-sensitive CRP (hs-CRP parameters were measured. Complete ST resolution was observed in 32 patients (36.8% in group 1 and 53 patients (63.8% in group 2 (<.001. Also in the first 24 hours, the CK-MB levels of patients in group 1 were significantly higher than those of group 2 (=.001. The hs-CRP values were greater in group 1 than group 2 at 48th hour (gruop 1: 9.4±0.1 mg/L, group 2: 3.7±1.4 mg/L; =.000. We concluded that adding clopidogrel to standard treatment in STEMI patients provided early reperfusion and suppression of inflammatory response.

  20. 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 electrocardiographic acuteness score is better than historical timing for predicting myocardial salvage and prognosis in patients with anterior AMI treated with fibrinolysis or primary percutaneous coronary intervention. METHODS: One hundred seventy-five patients with anterior infarct without electrocardiogram (ECG...... the Aldrich score to determine the initially predicted myocardial infarct size and the Selvester score to determine the final QRS-estimated myocardial infarct size. RESULTS: The mean amount of myocardium salvage depended on ECG timing (43% [+/-38%] for "early" vs 1% [+/-56%] for "late"; P

  1. A New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-Inflammation in a Rat Model.

    Directory of Open Access Journals (Sweden)

    Kazuhiro Nagaoka

    Full Text Available There is an unmet need to develop an innovative cardioprotective modality for acute myocardial infarction (AMI, for which the effectiveness of interventional reperfusion therapy is hampered by myocardial ischemia-reperfusion (IR injury. Pretreatment with statins before ischemia is shown to reduce MI size in animals. However, no benefit was found in animals and patients with AMI when administered at the time of reperfusion, suggesting insufficient drug targeting into the IR myocardium. Here we tested the hypothesis that nanoparticle-mediated targeting of pitavastatin protects the heart from IR injury.In a rat IR model, poly(lactic acid/glycolic acid (PLGA nanoparticle incorporating FITC accumulated in the IR myocardium through enhanced vascular permeability, and in CD11b-positive leukocytes in the IR myocardium and peripheral blood after intravenous treatment. Intravenous treatment with PLGA nanoparticle containing pitavastatin (Pitavastatin-NP, 1 mg/kg at reperfusion reduced MI size after 24 hours and ameliorated left ventricular dysfunction 4-week after reperfusion; by contrast, pitavastatin alone (as high as 10 mg/kg showed no therapeutic effects. The therapeutic effects of Pitavastatin-NP were blunted by a PI3K inhibitor wortmannin, but not by a mitochondrial permeability transition pore inhibitor cyclosporine A. Pitavastatin-NP induced phosphorylation of Akt and GSK3β, and inhibited inflammation and cardiomyocyte apoptosis in the IR myocardium.Nanoparticle-mediated targeting of pitavastatin induced cardioprotection from IR injury by activation of PI3K/Akt pathway and inhibition of inflammation and cardiomyocyte death in this model. This strategy can be developed as an innovative cardioprotective modality that may advance currently unsatisfactory reperfusion therapy for AMI.

  2. Core-shell hybrid liposomal vesicles loaded with panax notoginsenoside: preparation, characterization and protective effects on global cerebral ischemia/reperfusion injury and acute myocardial ischemia in rats

    Directory of Open Access Journals (Sweden)

    Zhang J

    2012-08-01

    Full Text Available Jing Zhang,1,* Xizhen Han,1,* Xiang Li,2 Yun Luo,1 Haiping Zhao,1 Ming Yang,1 Bin Ni,1 Zhenggen Liao11Key Laboratory of Modern Preparation of TCM, Ministry of Education, 2National Pharmaceutical Engineering Center for Solid Preparation in Chinese Herbal Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang, People's Republic of China*These authors contributed equally to this workPurpose: Novel panax notoginsenoside-loaded core-shell hybrid liposomal vesicles (PNS-HLV were developed to resolve the restricted bioavailability of PNS and to enhance its protective effects in vivo on oral administration.Methods: Physicochemical characterizations of PNS-HLV included assessment of morphology, particle size and zeta potential, encapsulation efficiency (EE%, stability and in vitro release study. In addition, to evaluate its oral treatment potential, we compared the effect of PNS-HLV on global cerebral ischemia/reperfusion and acute myocardial ischemia injury with those of PNS solution, conventional PNS-loaded nanoparticles, and liposomes.Results: In comparison with PNS solution, conventional PNS-loaded nanoparticles and liposomes, PNS-HLV was stable for at least 12 months at 4°C. Satisfactory improvements in the EE% of notoginsenoside R1, ginsenoside Rb1, and ginsenoside Rg1 were shown with the differences in EE% shortened and the greater controlled drug release profiles were exhibited from PNS-HLV. The improvements in the physicochemical properties of HLV contributed to the results that PNS-HLV was able to significantly inhibit the edema of brain and reduce the infarct volume, while it could markedly inhibit H2O2, modified Dixon agar, and serum lactate dehydrogenase, and increase superoxide dismutase (P < 0.05.Conclusion: The results of the present study imply that HLV has promising prospects for improving free drug bioactivity on oral administration.Keywords: liposomes, nanoparticles, panax notoginsenoside, physicochemical properties

  3. Relation between plasma brain natriuretic peptide, serum indexes of collagen type I turnover, and left ventricular remodeling after reperfused acute myocardial infarction.

    Science.gov (United States)

    Cerisano, Giampaolo; Pucci, Paolo Domenico; Sulla, Antonio; Tommasi, Mariasilvia; Raspanti, Silvia; Santoro, Giovanni Maria; Antoniucci, David

    2007-03-01

    The aim of the study is to investigate the relation between plasma brain natriuretic peptide (BNP), collagen type I turnover, and left ventricular (LV) remodeling after primary angioplasty. Echo-Doppler, BNP, carboxy-terminal telopeptide of procollagen type I (ICTP), C-terminal propeptide of procollagen type I (PICP), and their ratio PICP/ICTP (as an index of coupling between the synthesis and degradation of collagen type I) were evaluated at days 1 and 3 and months 1 and 6 after primary angioplasty in 56 consecutive patients with a first large acute myocardial infarction (AMI). During the 6 months after AMI, a direct relation was shown between BNP and ICTP (day 1, r = 0.54, p = 0.000; day 3, r = 0.64, p = 0.000; month 1, r = 0.64, p = 0.000; month 6, r = 0.41, p = 0.005) and BNP and PICP/ICTP (day 1, r = -0.54, p = 0.003; day 3, r = -0.58, p = 0.000; month 1, r = -0.50, p = 0.000; month 6, r = -0.30, p = 0.043), but not between BNP and PICP. Using analysis of covariance, relations between BNP and ICTP and PICP/ICTP were independent from infarct size. Patients with LV remodeling had significantly higher plasma ICTP and BNP levels and lower PICP/ICTP than patients without LV remodeling. Day-1 ICTP independently predicted 6-month remodeling (exp beta = 2.14, 95% confidence interval 1,120 to 3,550, p = 0.01). In conclusion, a relation exists between plasma BNP collagen type I turnover and LV remodeling after reperfused AMI.

  4. 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...

  5. Distinct effects of acute pretreatment with lipophilic and hydrophilic statins on myocardial stunning, arrhythmias and lethal injury in the rat heart subjected to ischemia/reperfusion.

    Science.gov (United States)

    Čarnická, S; Adameová, A; Nemčeková, M; Matejíková, J; Pancza, D; Ravingerová, T

    2011-01-01

    Although both lipophilic and more hydrophilic statins share the same pathway of the inhibition of HMG-CoA reductase, their pleiotropic cardioprotective effects associated with the ability to cross cellular membranes, including membranes of heart cells, may differ. To test this hypothesis, isolated rat hearts were Langendorff-perfused either with simvastatin (S, 10 micromol/l) or pravastatin (P, 30 micromol/l), 15 min prior to ischemia. Control untreated hearts (C) were perfused with perfusion medium only. Postischemic contractile dysfunction, reperfusion-induced ventricular arrhythmias and infarct size were investigated after exposure of the hearts to 30-min global ischemia and 2-h reperfusion. Both lipophilic S and hydrophilic P reduced the severity of ventricular arrhythmias (arrhythmia score) from 4.3 +/- 0.2 in C to 3.0 +/- 0 and 2.7 +/- 0.2 in S and P, respectively, (both P statins indicating a different ability to cross cardiac membranes may underlie their distinct cardioprotective effects on myocardial stunning and lethal injury induced by ischemia/reperfusion.

  6. INVIVO EFFECT OF BRADYKININ DURING ISCHEMIA AND REPERFUSION - IMPROVED ELECTRICAL STABILITY 2 WEEKS AFTER MYOCARDIAL-INFARCTION IN THE PIG

    NARCIS (Netherlands)

    TOBE, TJM; DELANGEN, CDJ; TIO, RA; BEL, KJ; MOOK, PH; WESSELING, H

    1991-01-01

    In this study, the effect of bradykinin or saline infusion during ischemia and reperfusion on electrical stability, 2 weeks after myocardial infarction, was assessed. Acute myocardial infarction was induced in 21 pigs by a transluminal occlusion of the left coronary artery with a catheter balloon, i

  7. Effects of ischemic postconditioning on myocardial apoptosis and infarction in rabbits with acute myocardial ischemia and reperfusion%缺血后处理对缺血再灌注大鼠心肌梗死和心肌细胞凋亡的作用

    Institute of Scientific and Technical Information of China (English)

    李源; 陶凌; 臧益民; 高峰

    2002-01-01

    AIM To observe the effects of ischemic postconditioning (IPC) on cardiomyocyte apoptosis and myocardial infarct size in myocardial ischemia/reperfusion rabbits. METHODS Rabbit acute myocardial ischemia/reperfusion model was used and the heart was conditioned either pre-or post-myocardial ischemia followed by reperfusion. Cardiomyocyte apoptosis and myocardial infarct size were determined by in situ TDT-mediated dUTP nick end labeling (TUNEL) and Evan's blue-TTC dual staining, respectively. RESULTS Compared with those in the control group, both cardiomyocyte apoptotic index and myocardial infarct size were significantly reduced in IPC group [apoptotic index: (15±7)% vs (30±12)% of control, P<0.05; infarction:(13±5)% vs (27±7)% of control, P<0.01, respectively]. No significant difference was found between ischemic preconditioning (IP) and IPC groups. CONCLUSION Ischemic postconditioning, like ischemic preconditioning, exerts an anti-apoptotic effect, which may contribute partly to the ultimate reduction of myocardial infarction in acute myocardial ischemia-reperfusion.%目的观察在体情况下缺血后处理(IPC)对兔心肌梗死范围及缺血心肌细胞凋亡的影响,并与缺血预处理(IP)心脏保护作用比较. 方法采用兔心肌缺血/再灌注模型,在缺血后、再灌注前多次短暂再灌/停灌处理. 以Even's blue-TTC法检测心肌梗死范围,TUNEL方法检测缺血心肌细胞凋亡. 结果与对照组相比,缺血后处理明显减小心肌梗死范围(12.5±5.4% vs对照组26.7±6.7%, P<0.01),缺血区心肌凋亡指数明显下降(14.6±7.4 vs对照组30.4±12.3, P<0.05). 结论对于已缺血心肌,再灌前予多次短暂复灌、停灌处理具有与IP类似缩小心梗范围作用,IPC对缺血心肌的保护效应可能与其抑制缺血心肌细胞凋亡有关.

  8. 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

  9. Rat experimental model of myocardial ischemia/reperfusion injury: an ethical approach to set up the analgesic management of acute post-surgical pain.

    Science.gov (United States)

    Ciuffreda, Maria Chiara; Tolva, Valerio; Casana, Renato; Gnecchi, Massimiliano; Vanoli, Emilio; Spazzolini, Carla; Roughan, John; Calvillo, Laura

    2014-01-01

    During the past 30 years, myocardial ischemia/reperfusion injury in rodents became one of the most commonly used model in cardiovascular research. Appropriate pain-prevention appears critical since it may influence the outcome and the results obtained with this model. However, there are no proper guidelines for pain management in rats undergoing thoracic surgery. Accordingly, we evaluated three analgesic regimens in cardiac ischemia/reperfusion injury. This study was strongly focused on 3R's ethic principles, in particular the principle of Reduction. Rats undergoing surgery were treated with pre-surgical tramadol (45 mg/kg intra-peritoneal), or carprofen (5 mg/kg sub-cutaneous), or with pre-surgical administration of carprofen followed by 2 post-surgery tramadol injections (multi-modal group). We assessed behavioral signs of pain and made a subjective evaluation of stress and suffering one and two hours after surgery. Multi-modal treatment significantly reduced the number of signs of pain compared to carprofen alone at both the first hour (61±42 vs 123±47; p<0.05) and the second hour (43±21 vs 74±24; p<0.05) post-surgery. Tramadol alone appeared as effective as multi-modal treatment during the first hour, but signs of pain significantly increased one hour later (from 66±72 to 151±86, p<0.05). Carprofen alone was more effective at the second hour post-surgery when signs of pain reduced to 74±24 from 113±40 in the first hour (p<0.05). Stress behaviors during the second hour were observed in only 20% of rats in the multimodal group compared to 75% and 86% in the carprofen and tramadol groups, respectively (p<0.05). Multi-modal treatment with carprofen and tramadol was more effective in preventing pain during the second hour after surgery compared with both tramadol or carprofen. Our results suggest that the combination of carprofen and tramadol represent the best therapy to prevent animal pain after myocardial ischemia/reperfusion. We obtained our results

  10. Antioxidative and cardioprotective effects of total flavonoids extracted from Dracocephalum moldavica L. against acute ischemia/reperfusion-induced myocardial injury in isolated rat heart.

    Science.gov (United States)

    Jiang, Jiangtao; Yuan, Xuan; Wang, Ting; Chen, Hongmei; Zhao, Hong; Yan, Xinyan; Wang, Zhiping; Sun, Xiling; Zheng, Qiusheng

    2014-03-01

    This study evaluates antioxidative and cardioprotective effects of total flavonoids extracted from Dracocephalum moldavica L. (DML). The total flavonoids showed remarkable scavenging effects against 1,1-diphenyl-2-picrylhydrazyl, hydroxyl and superoxide anion radicals in vitro. Compared with the ischemia/reperfusion (I/R) group as demonstrated by the use of improved Langendorff retrograde perfusion technology, the total flavonoids (5 μg/mL) pretreatment improved the heart rate and coronary flow, rised left ventricular developed pressure and decreased creatine kinase, lactate dehydrogenase levels in coronary flow. The infarct size/ischemic area at risk of DML-treated hearts was smaller than that of I/R group; the superoxide dismutase activity and glutathione/glutathione disulfide ratio increased and malondialdehyde content reduced obviously (P total flavonoids treatment groups. In conclusion, the total flavonoids possess obvious protective effects on myocardial I/R injury, which may be related to the improvement of myocardial oxidative stress states.

  11. Effectiveness of Panax ginseng on Acute Myocardial Ischemia Reperfusion Injury Was Abolished by Flutamide via Endogenous Testosterone-Mediated Akt Pathway.

    Science.gov (United States)

    Pei, Luo; Shaozhen, Hou; Gengting, Dong; Tingbo, Chen; Liang, Liu; Hua, Zhou

    2013-01-01

    Mechanisms for Panax ginseng's cardioprotective effect against ischemia reperfusion injury involve the estrogen-mediated pathway, but little is known about the role of androgen. A standardized Panax ginseng extract (RSE) was orally given with or without flutamide in a left anterior descending coronary artery ligation rat model. Infarct size, CK and LDH activities were measured. Time-related changes of NO, PI3K/Akt/eNOS signaling, and testosterone concentration were also investigated. RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE. NO was increased by RSE and reached a peak after 15 min of ischemia; however, flutamide cotreatment suppressed this elevation. Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE. RSE completely reversed the dropping of endogenous testosterone level induced by I/R injury. Flutamide plus RSE treatment not only abolished RSE's effect but also produced a dramatic change on endogenous testosterone level after pretreatment and ischemia. Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

  12. 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.

  13. Late reperfusion of a totally occluded infarct-related artery increases granulocyte-colony stimulation factor and reduces stroma-derived factor-1alpha blood levels in patients with ongoing ischemia after acute myocardial infarction.

    Science.gov (United States)

    Kuo, Li-Tang; Chen, Shih-Jen; Cherng, Wen-Jin; Yang, Ning-I; Lee, Chen-Chin; Cheng, Chi-Wen; Verma, Subodh; Wang, Chao-Hung

    2009-07-01

    After acute myocardial infarction (AMI), reopening of a totally occluded infarct-related artery (IRA) at a subacute stage is still controversial in symptom-free patients. However, in patients with persistent ischemic symptoms and inadequate collaterals to the infarct area, recanalization is thought to provide beneficial effects. In addition to augmenting myocardial perfusion, we hypothesized that the benefit of recanalization involves the manipulation of circulating stem cell-mobilizing cytokines. This study included 30 patients with a totally occluded IRA and ongoing ischemic symptoms (the study group) and 30 patients with a partially occluded IRA (the control group). All patients underwent successful angioplasty and/or stenting. Before and immediately after the coronary intervention, blood granulocyte-colony-stimulating factor (G-CSF), stem-cell factor (SCF), vascular endothelial growth factor (VEGF), and stroma-derived factor-1 (SDF-1alpha) were measured. After recanalization, G-CSF levels significantly increased in the study group compared to the control group (P=0.03). SDF-1alpha levels in the study group decreased relative to the controls (P=0.02). However, no significant changes in VEGF or SCF levels between the two groups were found. In the multivariate analysis, reopening of a totally occluded IRA was independently and significantly associated with changes in G-CSF and SDF-1alpha levels after recanalization. In conclusion, our data suggest that the benefits of late reperfusion of a totally occluded IRA in patients with ongoing myocardial ischemia may involve mechanisms associated with stem cell-mobilizing and plaque-stabilizing cytokines. This study provides the rationale to investigate serial changes in cytokines and the numbers of circulating progenitors after reperfusion in the future.

  14. 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

    INTRODUCTION: 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...... following pPCI in patients with AMI. MATERIAL AND METHODS: The IMPACT trial is a multicentre, randomised, double-blinded, placebo-controlled study. We wish to include 2 × 20 patients with ST-elevation myocardial infarctions undergoing pPCI within six hours from symptom onset. The primary end......-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...

  15. 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

    INTRODUCTION: 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...... following pPCI in patients with AMI. MATERIAL AND METHODS: The IMPACT trial is a multicentre, randomised, double-blinded, placebo-controlled study. We wish to include 2 × 20 patients with ST-elevation myocardial infarctions undergoing pPCI within six hours from symptom onset. The primary end......-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...

  16. Myocardial bridging as a cause of acute myocardial infarction: a case report

    Directory of Open Access Journals (Sweden)

    Emiroglu Yunus

    2002-09-01

    Full Text Available Abstract Background Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation. Case presentation A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI. Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints. Conclusions Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.

  17. Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury

    Directory of Open Access Journals (Sweden)

    Nicolosi Alfred C

    2009-12-01

    control and GdCl3 treated rats. Likewise, IL-8 levels increased throughout the 3 hour time period in the Sham group. There was no difference in IL-8 detected in the myocardium after 120 min reperfusion between groups. In contrast, after 120 min reperfusion GdCl3 decreased the myocardial tissue levels of macrophage secreted cytokines, GM-CSF and IL-1. Conclusion GdCl3 treatment prior to ischemia and reperfusion injury decreased circulating monocytes and neutrophils, macrophage secreted cytokines, and leukocyte infiltration into injured myocardium. These results suggest GdCl3 decreased monoctye and neutrophil migration and activation and may be a novel treatment for inflammation during ischemia and reperfusion.

  18. 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.

  19. Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Xia Yin

    2012-01-01

    Full Text Available Ischemic preconditioning (IPC or postconditioning (Ipost is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.

  20. Elevated Plasma IL-38 Concentrations in Patients with Acute ST-Segment Elevation Myocardial Infarction and Their Dynamics after Reperfusion Treatment

    Directory of Open Access Journals (Sweden)

    Yucheng Zhong

    2015-01-01

    Full Text Available Objective. Recent studies suggest that IL-38 is associated with autoimmune diseases. Furthermore, IL-38 is expressed in human atheromatous plaque. However, the plasma levels of IL-38 in patients with ST-segment elevation myocardial infarction (STEMI have not yet to be investigated. Methods. On admission, at 24 h, at 48 h, and at 7 days, plasma IL-38, C-reactive protein (CRP, cardiac troponin I (cTNI, and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP levels were measured and IL-38 gene in peripheral blood mononuclear cells (PBMCs was detected in STEMI patients. Results. The results showed that plasma IL-38 levels and IL-38 gene expression in PBMCs were significantly increased in STEMI patients compared with control group and were time dependent, peaked at 24 h. In addition, plasma IL-38 levels were dramatically reduced in patients with reperfusion treatment compared with control group. Similar results were also demonstrated with CRP, cTNI, and NT-proBNP levels. Furthermore, IL-38 levels were found to be positively correlated with CRP, cTNI, and NT-proBNP and be weakly negatively correlated with left ventricular ejection fraction (LVEF in STEMI patients. Conclusions. The results indicate that circulating IL-38 is a potentially novel biomarker for patients with STEMI and IL-38 might be a new target for MI study.

  1. Ischemic ''memory image'' in acute myocardial infarction of {sup 123}I-BMIPP after reperfusion therapy. A comparison with {sup 99m}Tc-pyrophosphate and {sup 201}Tl dual-isotope SPECT

    Energy Technology Data Exchange (ETDEWEB)

    Mochizuki, Teruhito; Miyagawa, Masao; Sugawara, Yoshifumi; Kikuchi, Takanori; Ikezoe, Junpei [Ehime Univ., Matsuyama (Japan). School of Medicine; Murase, Kenya [Osaka Univ., Suita (Japan). Medical School; Higashino, Hiroshi [Ehime Imabari Hospital (Japan)

    2002-12-01

    Ischemic ''memory image'' is a phenomenon of {sup 123}I-15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) in which an area at risk of acute myocardial infarction (AMI), could be detected as a defect in a couple of weeks even after successful reperfusion therapy. The purpose of this study was to clarify the incidence of the ischemic ''memory image'' of {sup 123}I-BMIPP in patients with AMI by comparing {sup 99m}Tc-pyrophosphate(PYP) and {sup 201}Tl dual-isotope SPECT. Materials consisted of 14 patients with successfully reperfused AMI and 20 patients with old myocardial infarction (OMI). All AMI patients underwent PYP/Tl dual-isotope SPECT within 1 week after the onset of AMI, and BMIPP SPECT was performed within 1 week after the PYP/Tl dual-isotope SPECT. The extent and severity of the defect of BMIPP and Tl were visually scored into four grades: 0=no defect to 3=large or severe defect. These scores were compared. PYP positive AMI lesions were concordant with BMIPP defects (13/14). In AMI, both the extent and severity scores of BMIPP were higher than {sup 201}Tl (p<0.001). Differences (BMIPP-Tl) of extent and severity scores were greater in AMI than in OMI (p<0.001). In conclusion, the ischemic ''memory image'' obtained by means of the BMIPP is a common phenomenon (13/14) in AMI, and helpful in evaluating the area at risk. (author)

  2. Protective effect of Shenfu injection on myocardial mitochondria injured by ischemia-reperfusion in rabbits

    Institute of Scientific and Technical Information of China (English)

    CAO Jun; ZHENG Chuan-dong; ZHANG Guang-xin; ZHANG You-jun; MIN Su

    2005-01-01

    @@ The main active components of Shenfu injection (SFI), an extract of traditional Chinese herbs, are ginsenoside and higenamine. Ginsenoside can improve ischemic myocardium metabolism, scavenge free radicals, protect myocardial ultrastructure and reduce Ca2+ overload. Higenamine can enhance heart contractility, improve coronary circulation and decrease the effect of acute myocardial ischemia. SFI was found to have had some cardiac protective effect during cardiopulmonary bypass.1,2 SFI was added into St. Thomas crystal cardioplegic solution in this study to investigate the protective effect of SFI on ischemic-reperfused rabbit heart and to observe the influence on mitochondrial oxygen free radical (OFR), Ca2+ and mitochondrial ultrastructure.

  3. Iloprost reduces myocardial edema in a rat model of myocardial ischemia reperfusion.

    Science.gov (United States)

    Caliskan, A; Yavuz, C; Karahan, O; Yazici, S; Guclu, O; Demirtas, S; Mavitas, B

    2014-05-01

    Myocardial ischemia severely reduces myocyte longevity and function. Extensive interstitial edema and cell damage occur as a result of myocardial reperfusion injury. Current therapies are directed at prevention of ischemia-induced damage to cardiac tissue. Iloprost is a novel pharmaceutical agent for the treatment of ischemia. Twenty rats were segregated into four experimental groups. The procedure control group consisted of four rats undergoing a sham operation. The remaining 16 rats were divided into two equal groups. The first group (control group) received a continuous intravenous infusion of physiological serum immediately prior to the procedure. Iloprost was administered by a continuous intravenous infusion into the right jugular vein at an infusion rate of 100 ng/kg/min for 30 minutes prior to reperfusion in the experimental group (study group). Following the infusion treatments, ligation of the left coronary artery was conducted for 30 minutes to induce myocardial ischemia. The rats were euthanized 24 hours after reperfusion and cardiac tissue was harvested from all specimens for analysis. Histological examination revealed three myocardial tissue specimens with grade II damage and five myocardial tissue specimens with grade III reperfusion injury in the control group. However, the study group consisted of two grade III myocardial tissue specimens, five grade II myocardial tissue specimens and one grade I myocardial tissue specimen. Moreover, a statistically significant reduction in myocardial edema was observed in the study group (p=0.022). Our results support the hypothesis that iloprost enhances protection against cardiac ischemia reperfusion injury. This protective effect may be associated with vasodilation, antioxidant or anti-edema mechanisms.

  4. Cardioprotective effect of liposomal prostaglandin E1 on a porcine model of myocardial infarction reperfusion no-reflow

    Institute of Scientific and Technical Information of China (English)

    Jia-hui LI; Peng YANG; Ai-li LI; Yong WANG; Yuan-nan KE; Xian-lun LI

    2011-01-01

    Abstract:Objective:To evaluate whether liposomal prostaglandin E1 (lipo-PGE1) can decrease reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI).Methods:Twenty-two male Chinese mini-swines were randomized into three groups:six in a sham-operation group,and eight each in the control and lipo-PGE1 groups.The distal part of the left anterior descending coronary artery (LAD) in the latter two groups was completely occluded for 2 h,and then reperfused for 3 h.Lipo-PGE1 (1 pg/kg) was injected 10 min before LAD occlusion until reperfusion for 1 h in the lipo-PGE1 group.Hemodynamic data and proinflammatory cytokines were examined before AMI,2 h after occlusion,and 1,2,and 3 h after reperfusion.Myocardial contrast echocardiography (MCE) and double staining were performed to evaluate the myocardial no-reflow area (NRA).Results:Left ventricular systolic pressure and end-diastolic pressure significantly improved in the lipo-PGE1 group after reperfusion compared with the control group and also 2 h after AMI (P<0.05 for both).MCE and double staining both showed that lipo-PGE1 decreased reperfusion NRA after AMI (P<0.05,P<0.01).Lipo-PGE1 decreased serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) after myocardial infarction reperfusion (P<0.05 for both).Conclusions:Lipo-PGE1 is cardioprotective in our porcine model of myocardial infarction reperfusion no-reflow,decreasing NRA and attenuating the inflammatory response.

  5. [The role of free radicals in the myocardial reperfusion injuries and in the development of endogenous adaptation].

    Science.gov (United States)

    Rőth, Erzsébet

    2015-11-22

    The reperfusion of acute ischaemic myocardium is essential for myocardial salvage, so-called "gold standard" therapy, however it can result in serious damage to the myocardium. Functional alterations occur, including depressed contractile function and decreased coronary flow as well as altered vascular reactivity. Over several decades it has been demonstrated that oxygen radical formation is greatly increased in the post-ischaemic heart and serves as a critical central mechanism of ischaemic-reperfusion injury. However it has been demonstrated that free radicals play an important role in the endogenous adaptation phenomenon of the heart, too. Ischaemic preconditioning is a cellular adaptive response of the heart to stress, which provides the most potent endogenous protection against reperfusion arrhytmias, stunning and infarction. Post-conditioning defined as brief periods of ischaemia and reperfusion during the very early minutes of reperfusion stimulates endogenous adaptation. Post-conditioning may also attenuate the damage to endothelial cells and cardiomyocytes from oxidants, cytokines, proteases and inflammatory cells.

  6. Dephosphorylation of cardiomyocyte Cx43 is associated with myocardial ischemia and reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Zhijuan Cao; Xuan Xu; Linli Que; Qi Chen; Yuehua Li

    2009-01-01

    Objective:Myocardial ischemia/reperfusion(I/R) injury is the leading cause of death in the world. However, the details of the mechanism of its pathophysioiogy are still unknown. The present study was designed to investigate the role of connexin 43(Cx63) in acute models of myocardial I/R injury. Methods: Male C57BL/6 mice were subjected to myocardial ischemia(45 rain) followed by reperfusion(4 hrs) in vivo. The whole operation was monitored using a two-lead ECG. Hearts were harvested and the level of protein was assessed by western blot analysis. Haematoxylin and Eosin(HE) staining was used to detect the extent of neutrophil infiltration. The expression level of IL-6 was detected by ELISA. Results: A murine myocardial I/R injury model was constructed successfully. Phosphorylated Cx43 decreased 83.45% while non-phosphorylated Cx43 increased 1.62- fold in the myocardium after I/R injury. Neutrophil infiltration and the expression of the inflammatory cytokine IL-6 increased in the myocardium following I/R. Conclusion: During myocardial I/R injury, cardiomyocyte Cx43 is dephosphorylated, and this may be associated with an inflammatory response.

  7. Contribution of calpains to myocardial ischaemia/reperfusion injury.

    Science.gov (United States)

    Inserte, Javier; Hernando, Victor; Garcia-Dorado, David

    2012-10-01

    Loss of calcium (Ca(2+)) homeostasis contributes through different mechanisms to cell death occurring during the first minutes of reperfusion. One of them is an unregulated activation of a variety of Ca(2+)-dependent enzymes, including the non-lysosomal cysteine proteases known as calpains. This review analyses the involvement of the calpain family in reperfusion-induced cardiomyocyte death. Calpains remain inactive before reperfusion due to the acidic pHi and increased ionic strength in the ischaemic myocardium. However, inappropriate calpain activation occurs during myocardial reperfusion, and subsequent proteolysis of a wide variety of proteins contributes to the development of contractile dysfunction and necrotic cell death by different mechanisms, including increased membrane fragility, further impairment of Na(+) and Ca(2+) handling, and mitochondrial dysfunction. Recent studies demonstrating that calpain inhibition contributes to the cardioprotective effects of preconditioning and postconditioning, and the beneficial effects obtained with new and more selective calpain inhibitors added at the onset of reperfusion, point to the potential cardioprotective value of therapeutic strategies designed to prevent calpain activation.

  8. Myocardial ischemia/reperfusion impairs neurogenesis and hippocampal-dependent learning and memory.

    Science.gov (United States)

    Evonuk, Kirsten S; Prabhu, Sumanth D; Young, Martin E; DeSilva, Tara M

    2017-03-01

    The incidence of cognitive impairment in cardiovascular disease (CVD) patients has increased, adversely impacting quality of life and imposing a significant economic burden. Brain imaging of CVD patients has detected changes in the hippocampus, a brain region critical for normal learning and memory. However, it is not clear whether adverse cardiac events or other associated co-morbidities impair cognition. Here, using a murine model of acute myocardial ischemia/reperfusion (I/R), where the coronary artery was occluded for 30min followed by reperfusion, we tested the hypothesis that acute myocardial infarction triggers impairment in cognitive function. Two months following cardiac I/R, behavioral assessments specific for hippocampal cognitive function were performed. Mice subjected to cardiac I/R performed worse in the fear-conditioning paradigm as well as the object location memory behavioral test compared to sham-operated mice. Reactive gliosis was apparent in the hippocampal subregions CA1, CA3, and dentate gyrus 72h post-cardiac I/R as compared with sham, which was sustained two months post-cardiac I/R. Consistent with the inflammatory response, the abundance of doublecortin positive newborn neurons was decreased in the dentate gyrus 72h and 2months post-cardiac I/R as compared with sham. Therefore, we conclude that following acute myocardial infarction, rapid inflammatory responses negatively affect neurogenesis, which may underlie long-term changes in learning and memory.

  9. Risk Factors of Reperfusion Failure following Primary Angioplasty for ST-Segment Elevation Myocardial Infarction (STEMI

    Directory of Open Access Journals (Sweden)

    HamidReza Sanati

    2015-10-01

    Full Text Available Background: Although  percutaneous  coronary  intervention  (PCI  improves  outcomes  compared  to  thrombolysis,  a substantial number of ST-elevation myocardial infarction (STEMI patients do not achieve optimal myocardial reperfusion. This study was designed to evaluate factors related to suboptimal myocardial reperfusion after primary PCI in patients with STEMI.Methods: Totally, 155 patients (124 men; mean age = 56.6 ± 11.03 years, range = 31- 85 years with STEMI undergoing primary PCI were retrospectively studied. Additionally, the relationships between the occurrence of reperfusion failure and variables such as age, sex, cardiac risk factors, family history, Body Mass Index, time of symptom onset, ejection fraction, previous PCI, coronary artery bypass graft surgery or previous myocardial infarction, and angiographic data were analyzed. Results: Procedural success was 97.1% and complete ST resolution occurred in 43.2%. Age; cardiac risk factors; family history; body mass index; previous MI, coronary artery bypass graft surgery, or PCI; and use of thrombectomy device and GPIIb/IIIa inhibitor were not the determining factors (p value > 0.05. According to our multivariate analysis, time of symptom onset (OR [95% CI]: 045 [0.2 to 0.98]; p value = 0.044 and ejection fraction (OR [95% CI]:0.37 [0.26 to .091]; p value = 0.050 had reverse and male gender had direct significant associations with failed reperfusion (OR [95%CI]:0.34 [0.11 to 1.08]; p value = 0.068. More degrees of ST resolution occurred when the right coronary artery was the culpritvessel (p value = 0.001. The presence of more than three cardiac risk factors was associated with failed reperfusion (p value= 0.050.Conclusion: Considering the initial risk profile of patients with acute STEMI, including time of symptom onset and ejection fraction, as well as the accumulation of cardiac risk factors in a given patient, we could predict failed myocardial reperfusion to design a

  10. MG132 Inhibits Myocardial Ischemia-reperfusion Injury by Regulating Apoptotic Pathway

    Institute of Scientific and Technical Information of China (English)

    Dai Cuilian; Luo Kailiang; Chen Zhangrong

    2007-01-01

    Objectives To administrated proteasome inhibitor-MG-132 prior to reperfusion in rat myocardial ischemia-reperfusion model to determine whether MG-132 could reduce myocytic apoptosis. Methods and results MG-132 (0.75 mg/kg in 2 ml DMSO) injection 5 min prior to reperfusion resulted significant reduction of myocardial reperfusion injury. This effect was accompanied by reduced polymorphonuclear neutrophils(PMN) infiltration in myocardial region surrounding the myocardial infarct, reduced apoptosis in cardiac myocytes, reduced NF-κB activation, as determined by electron microscopy, histology, immunohistochemistry, the terminal deoxynucleotidyl transferase-mediated nick endlabeling (TUNEL) method, reverse transcription-polymerase chain reaction. Functional effects of MG-132 on PMN accumulation, activation of nuclear factor kappa B(p65 mRNA and protein levels ), and apoptosis were characterized in rat myocardial tissue. MG132 time-dependently inhibited myocardial p65 mRNA expression and reduced myocardial apoptotic index (AI) after reperfusion for 2 h, 6 h and 24 h ( P<0.01 ). Moreover, MG-132 time-dependently decreased Bax protein levels, while increased Bcl-2 protein levels in ischemic and reperfused myocardium ( P<0.05 ), its effect peaked after reperfusion for 24 h. Conclusions Our results demonstrate that MG-132 reduced myocardial reperfusion injury by inhibiting myosytic apoptotic cell death and blocking activation of NF-κB, down-regulating Bax expression and up-regulating Bcl-2 expression as well as elevating Bcl-2/Bax ratio.

  11. Ablation of cereblon attenuates myocardial ischemia-reperfusion injury.

    Science.gov (United States)

    Kim, Jooyeon; Lee, Kwang Min; Park, Chul-Seung; Park, Woo Jin

    2014-05-16

    Cereblon (CRBN) was originally identified as a target protein for a mild type of mental retardation in humans. However, recent studies showed that CRBN acts as a negative regulator of AMP-activated protein kinase (AMPK) by binding directly to the AMPK catalytic subunit. Because AMPK is implicated in myocardial ischemia-reperfusion (I-R) injury, we reasoned that CRBN might play a role in the pathology of myocardial I-R through regulation of AMPK activity. To test this hypothesis, wild-type (WT) and crbn knockout (KO) mice were subjected to I-R (complete ligation of the coronary artery for 30 min followed by 24h of reperfusion). We found significantly smaller infarct sizes and less fibrosis in the hearts of KO mice than in those of WT mice. Apoptosis was also significantly reduced in the KO mice compared with that in WT mice, as shown by the reduced numbers of TUNEL-positive cells. In parallel, AMPK activity remained at normal levels in KO mice undergoing I-R, whereas it was significantly reduced in WT mice under the same conditions. In rat neonatal cardiomyocytes, overexpression of CRBN significantly reduced AMPK activity, as demonstrated by reductions in both phosphorylation levels of AMPK and the expression of its downstream target genes. Collectively, these data demonstrate that CRBN plays an important role in myocardial I-R injury through modulation of AMPK activity.

  12. Optimal timing of hypothermia in relation to myocardial reperfusion.

    Science.gov (United States)

    Götberg, Matthias; van der Pals, Jesper; Götberg, Michael; Olivecrona, Göran K; Kanski, Mikael; Koul, Sasha; Otto, Andreas; Engblom, Henrik; Ugander, Martin; Arheden, Håkan; Erlinge, David

    2011-09-01

    Two previous clinical trials investigating hypothermia as an adjunct therapy for myocardial infarction have failed. Recently a pilot study has demonstrated a significant reduction in infarct size. The aims of this study were to elucidate the effects of hypothermia on reperfusion injury and to investigate the optimal hypothermia protocol for a future clinical trial. Pigs (40-50 kg) were anesthetized and a normal pig temperature of 38°C was established utilizing an endovascular temperature modulating catheter. The pigs were randomized to a combination hypothermia group (1,000 ml of 4°C saline solution and endovascular cooling, n = 8), or to normothermic controls (n = 8). A PCI balloon was then inflated in the LAD for 40 min (control) or 45 min with hypothermia induced during the last 5 min. Furthermore, hypothermia induced by cold saline alone (n = 8), and prolonged combination hypothermia during reperfusion (n = 7) were also examined. Infarct size and area at risk were determined ex vivo after 4 h of reperfusion using gadolinium-enhanced MRI and Tc-99-tetrofosmin SPECT, respectively. All pigs in the combination hypothermia group were cooled to <35°C within 5 min. Combination hypothermia reduced IS/AAR by 18% compared with normothermic controls despite 5 min longer ischemic time (61 ± 5 vs. 74 ± 4%, p = 0.03). Cold saline did not reduce IS/AAR. Prolonging hypothermia treatment after onset of reperfusion by an additional 45 min over that used in a previous paper did not confer any additional benefit. The cardioprotective effects of hypothermia treatment are due to an attenuation of myocardial injury during both ischemia and reperfusion. The results suggest that a hypothermia protocol using a cold saline infusion and endovascular cooling enables hypothermia to be induced in a clinical setting without delaying reperfusion therapy.

  13. Amelioration of ischemia/reperfusion-induced myocardial infarction by the 2-alkynyladenosine derivative 2-octynyladenosine (YT-146).

    Science.gov (United States)

    Sasamori, Jun; Aihara, Kazuyuki; Yoneyama, Fumiya; Sato, Isamu; Kogi, Kentaro; Takeo, Satoshi

    2006-04-01

    The present study was aimed at determining whether the novel adenosine A2-agonist YT-146 may have cardioprotective effects against ischemia-reperfusion injury. Anesthetized open-chest dogs underwent 90-min occlusion of the left anterior descending artery and subsequent 300-min reperfusion. The animals were randomly assigned to receive vehicle, 3, or 10 microg/kg YT-146 or ischemic preconditioning (4 episodes of 5 min occlusion followed by 5 min of reperfusion). Blood pressure, heart rate, and regional myocardial blood flow throughout the experiment were measured, as was the myocardial infarct size after reperfusion. The infarct size of the vehicle-treated dog was 56.2% +/- 2.7% (n = 5), whereas that of 3 or 10 microg/kg YT-146-treated dog was smaller (ie, 29.5% +/- 8.7% or 20.2% +/- 7.0%, respectively; n = 5). The infarct size of the dog treated with 10 microg/kg YT-146 was reduced to a degree similar to that of the ischemic preconditioning (19.2% +/- 6.3%, n = 5). YT-146 at both doses elicited a dose-dependent increase in acute hyperemic coronary flow immediately after reperfusion. The cardioprotective effect may be attributed to the limitation of the infarct size, probably via A2-receptor-mediated coronary artery dilatation during the early period of reperfusion.

  14. 芬太尼预处理对兔心肌缺血再灌注后心肌梗死范围及心功能的影响%Effects of pretreatment with fentanyl on myocardial infarction size and cardiac function in rabbits with acute myocardial ischemia reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    郑向明; 孟凡民; 王春亭

    2012-01-01

    Objective To study the myocardial protective effect of pretreatment with fentanyl on rabbits with acute myocardial ischemia reperfusion injury.Methods Twenty-four male New Zealand White rabbits were randomly divided into 3 groups:group C ( acute myocardial ischemia reperfusion injury group),group F ( fentanyl group) and group N-F ( naloxone-fentanyl group),with 8 cases in each group.All rabbits experienced 30 min of regional ischemia through the occlusion of the left anterior descending coronary artery( LAD),followed by 120 min of reperfusion.The rabbits in C group were only subjected to the above ischemia/reperfusion (I/R) sequence.The rabbits in Group F were intravenously injected with fentany1 0.15 mg/kg at 15 minutes before the coronary occlusion.The rabbits in Group N-F were intravenously injected with naloxone 3 mg/kg,followed by 70 μg/(kg · min) infusion before reperfusion and were intravenously injected with fentanyl 0.15 mg/kg at 15 min before myocardial ischemia.Heart rate(HR),left ventricular systolic pressure( LVSP),left ventricular end diastolic pressure( LVEDP),maximum positive and minimum negative left ventricular pressure derivatives ( + dp/dt and-dp/dt) were continuously monitored and recorded at baseline ( T0 ),30 min after ischemia( T1 ),and 10 min ( T2 ),30 min(T3 ),120 min(T4) after reperfusion during I/R process.After 120 min reperfusion,hearts were removed for the measurement of myocardial ischemia and infarction size.Results Compared with the baseline(T0),LVSP,± dp/dt decreased whereas LVEDP increased significantly during T1-T4 (P <0.05 ).There were no significant differences in homodynamic parameters between group C and group N F ( P > 0.05 ).In F group,the LVSP and + dp/dt were significantly higher than those of group C and group N-F after 30 min in reperfusion ( P < 0.05 ) and the infarction size and weight were smaller (P <0.01 ).Conclusions Pretreatment with fentanyl has protective effect against ischemia/reperfusion injury

  15. Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era.

    Science.gov (United States)

    Dominguez-Rodriguez, Alberto; Abreu-Gonzalez, Pedro; Reiter, Russel J

    2014-03-26

    In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification of several promising pharmacological (cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proof-of-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease.

  16. Heparins with reduced anti-coagulant activity reduce myocardial reperfusion injury.

    Science.gov (United States)

    Barry, William H; Kennedy, Thomas P

    2011-05-01

    Heparin which is desulfated at the 2-O and 3-O positions (ODSH) has reduced anti-coagulant properties, and reduced interaction with heparin antibodies. Because of the reduced anti-coagulant effect, ODSH can be safely administered to animals and humans intravenously at doses up to 20 mg/kg, resulting in a serum concentration of up to 250µg/ml. Administration of ODSH causes a 35% reduction in infarct size in dogs and pigs subjected to coronary artery occlusion and reperfusion when given 5 min before reperfusion. ODSH has anti-inflamatory effects, manifest as a decrease in neutrophil infiltration into ischemic tissue at high doses, but this effect does not entirely account for the reduction in infarct size. ODSH decreases Na(+) and Ca(2+) loading in isolated cardiac myocytes subjected to simulated ischemia. This effect appears due to an ODSH-induced reduction in an enhanced Na(+) influx via the Na channel in the membrane of cardiac myocyes caused by oxygen radicals generated during ischemia and reperfusion. Reduction in Na(+) influx decreases Ca(2+) loading by reducing Ca2(+) influx via Na/Ca exchange, thus reducing Ca(2+) - dependent reperfusion injury. ODSH does not appear to interact with antibodies to the heparin/platelet factor 4 complex, and does not cause heparin-induced thrombocytopenia. Because of these therapeutic and safety considerations, ODSH would appear to be a promising heparin derivative for prevention of reperfusion injury in humans undergoing thrombolytic or catheter-based reperfusion for acute myocardial infarction. The review article discussed the use of heparin and the discussion of some of the important patents, including: US6489311; US7478358; PCTUS2008070836 and PCTUS2009037836.

  17. Remote postconditioning induced by brief pulmonary ischemia and reperfusion attenuates myocardial reperfusion injury in rabbits

    Institute of Scientific and Technical Information of China (English)

    TANG Yan-hua; XU Jian-jun; LI Ju-xiang; CHENG Xiao-shu

    2011-01-01

    Background The lung is one of the most important organs that are sensitive to ischemia. We hypothesized that remote postconditioning (RPostC) induced by brief occlusion and reperfusion of the pulmonary artery could attenuate myocardial reperfusion injury.Methods Thirty rabbits were randomized into three groups. Group ischemia-reperfusion (IR) (n=10) were anesthetized rabbits subjected to 30-minute occlusion of the left anterior descending coronary artery followed by 180-minute reperfusion. Group RPostC (n=10) had the left pulmonary artery blocked for five minutes followed by a 5-minute reperfusion, and the left anterior descending coronary artery (LAD) occluded for 30 minutes with a 180-minute reperfusion. Group L-Nw-nitro-L-arginine methylester (L-NAME) + RPostC (n=10) had the left pulmonary artery blocked for five minutes followed by a 5-minute reperfusion and intravenous infusion of L-NAME (10 mg/kg), and the LAD occluded for 30 minutes with a 180-minute reperfusion. Blood samples were taken for levels of creatine kinase (CK),superoxide dismutase (SOD) and malondialdehyde (MDA) at three different time points. At the end of the experiment,tissue samples of the infarcted region were harvested to calculate the cardiomyocyte apoptosis index (Al) by TUNEL. A piece of left and right lung tissue was harvested to evaluate the damage to the lung.Results After reperfusion for 180 minutes, the concentration of CK was lower in group RPostC, (4.79±0.27) U/ml, than that in group IR, (6.23±0.55) U/ml (P <0.01), and group L-NAME + RPsotC, (5.86±0.42) U/ml (P <0.01). The concentration of MDA was lower in group RPostC, (6.06±0.36) nmol/ml, than that in group IR, (11.41±0.91) nmol/ml (P <0.01), and group L-NAME + RPostC, (11.06±0.62) nmol/ml (P<0.01). The activity of SOD was higher in group RPostC,(242.34±25.02) U/ml, than that in group IR, (148.05±18.24) U/ml (P<0.01), and group L-NAME + RPostC, (160.66±9.55) U/ml (P<0.01). The apoptosis index was lower in

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

    Directory of Open Access Journals (Sweden)

    A. L. Alyavi

    2009-01-01

    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. 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.

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

    DEFF Research Database (Denmark)

    Diemar, Sarah S; Sejling, Anne-Sophie; Iversen, Kasper K;

    2015-01-01

    OBJECTIVE: 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 myocar...... glycaemic level and measures of myocardial infarction, rates of ventricular fibrillation and subsequent premature death in the setting of acute ischaemia and reperfusion.......OBJECTIVE: 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...

  1. 急性心肌梗死患者冠状动脉内抽吸物成分与再灌注水平的关系%Relationship between myocardial reperfusion and intracoronary aspiration ingredients in patients with acute myocardial infarction undergone primary percutaneous coronary intervention

    Institute of Scientific and Technical Information of China (English)

    李怀东; 曾惠; 骆丽; 张立新; 郭金成

    2014-01-01

    Objective To study the relationship between myocardial reperfusion and intracoronary aspiration ingredients in patients with acute ST-segment elevation myocardial infarction( STEMI) undergone primary percutaneous coronary intervention ( PCI ) . Methods Aspiration catheter was used in 150 consecutive patients(96 males and 54 females) with STEMI undergoing primary PCI. Filtered, aspirated materials were fixed in formalin for 24 hours. Histological sections were prepared and stained with hematoxylin and eosin for examination. According to the pathological findings, patients were divided into 3 groups:thrombus group, plaque group and mixed group. Clinical data and myocardial reperfusion were analyzed and compared among the three groups. Results Aspiration catheter was successfully reached the lesion in 97. 3% ( 146/150 ) of the patients, and no materials obtained in 15 cases. Effective thrombus aspiration was done in 87. 33% (131 of 150) of the patients. The rates of coronary flow less than TMP class 3 in criminal vessel were 43. 86% (25/57),14. 81% (4/27) and 17. 02% (8/47) in thrombus group, plaque group and mixed group, respectively. Multivariate and non-conditional Logistic analysis showed that plaque components were closely related with the level of myocardial reperfusion after primary PCI ( OR:3. 412,P=0. 011). Conclusions Intracoronary aspiration plays an important role in improving myocardial reperfusion in patients with STEMI undergone primary PCI.%目的:通过对急性ST段抬高型心肌梗死( STEMI)患者急诊经皮冠状动脉介入治疗( PCI)术中的抽吸物成分进行病理分析,研究不同抽吸物成分与心肌水平再灌注的关系。方法连续入选STEMI并行急诊PCI的患者150例,其中男性96例,女性54例。术者根据术中情况进行血栓抽吸。抽吸物用福尔马林固定后24 h内送病理科,行光学显微镜检查。根据病理检查结果将患者分为3组:血栓组、斑块组、混合组。分析3组

  2. 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...

  3. Physiologically tolerable insulin reduces myocardial injury and improves cardiac functional recovery in myocardial ischemic/reperfused dogs.

    Science.gov (United States)

    Zhang, Hang-Xiang; Zang, Yi-Min; Huo, Jian-Hua; Liang, Shao-Jun; Zhang, Hai-Feng; Wang, Yue-Min; Fan, Qian; Guo, Wen-Yi; Wang, Hai-Chang; Gao, Feng

    2006-12-01

    This study was designed to examine whether physiologically tolerable insulin, which maintains lower blood glucose, can protect the myocardium against ischemia/reperfusion (I/R) injury in a preclinical large animal model. Adult dogs were subjected to 50 minutes of myocardial ischemia (80% reduction in coronary blood flow) followed by 4 hours of reperfusion and treated with vehicle, glucose-insulin-potassium (GIK; glucose, 250 g/L; insulin, 60 U/L; potassium, 80 mmol/L), GK, or low-dose insulin (30 U/L) 10 minutes before reperfusion. Treatment with GIK exerted significant cardioprotective effects as evidenced by improved cardiac function, improved coronary blood flow, reduced infarct size, and myocardial apoptosis. In contrast, treatment with GK increased blood glucose level and aggravated myocardial I/R injury. It is interesting that treatment with insulin alone at the dose that reduced blood glucose to a clinically tolerable level exerted significant cardioprotective effects that were comparable to that seen in the GIK-treated group. This low-dose insulin had no effect on coronary blood flow after reperfusion but markedly reduced coronary reactive hyperemia and switched myocardial substrate uptake from fat to carbohydrate. Our results suggest that lower glucose supply to the ischemic myocardium at early reperfusion may create a "metabolic postconditioning" and thus reduce myocardial ischemia/reperfusion injury after prolonged reperfusion.

  4. 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.

  5. Acute myopericarditis masquerading as acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Wen Tian; Zixin Zhang; Xiaojuan Bai; Dingyin Zeng; Guoxian Qi

    2008-01-01

    Patients with abrupt onset of chest pain, ischemic ECG abnormalities and elevated levels of cardiac markers could be given a diagnosis of acute myocardial infarction. However, some other diseases should be taken into consideration in this clinical setting when coronary arteries are proven to be normal. Here we report a case of acute myopericarditis with clinical presentation of myocardial infarction and normal coronary anatomy. The Herpes Simplex Virus Ⅱ was considered as the organism causing myopericarditis and the patient was recovered by the treatment with valacicloavir. A precise diagnosis is a prerequisite of successful treatment and favorable prognosis.

  6. Phosphomimetic modulation of eNOS improves myocardial reperfusion and mimics cardiac postconditioning in mice.

    Directory of Open Access Journals (Sweden)

    Terrence Pong

    Full Text Available OBJECTIVE: Myocardial infarction resulting from ischemia-reperfusion injury can be reduced by cardiac postconditioning, in which blood flow is restored intermittently prior to full reperfusion. Although key molecular mechanisms and prosurvival pathways involved in postconditioning have been identified, a direct role for eNOS-derived NO in improving regional myocardial perfusion has not been shown. The objective of this study is to measure, with high temporal and spatial resolution, regional myocardial perfusion during ischemia-reperfusion and postconditioning, in order to determine the contribution of regional blood flow effects of NO to infarct size and protection. METHODS AND RESULTS: We used myocardial contrast echocardiography to measure regional myocardial blood flow in mice over time. Reperfusion after myocardial ischemia-reperfusion injury is improved by postconditioning, as well as by phosphomimetic eNOS modulation. Knock-in mice expressing a phosphomimetic S1176D form of eNOS showed improved myocardial reperfusion and significantly reduced infarct size. eNOS knock-out mice failed to show cardioprotection from postconditioning. The size of the no-reflow zone following ischemia-reperfusion is substantially reduced by postconditioning and by the phosphomimetic eNOS mutation. CONCLUSIONS AND SIGNIFICANCE: Using myocardial contrast echocardiography, we show that temporal dynamics of regional myocardial perfusion restoration contribute to reduced infarct size after postconditioning. eNOS has direct effects on myocardial blood flow following ischemia-reperfusion, with reduction in the size of the no-reflow zone. These results have important implications for ongoing clinical trials on cardioprotection, because the degree of protective benefit may be significantly influenced by the regional hemodynamic effects of eNOS-derived NO.

  7. 高迁移率族蛋白B1对心肌缺血再灌注损伤保护作用的初步临床研究%Cardioprotective effect of high mobility group protein B1 against myocardial ischemia-reperfusion injury in acute myocardial infarction patients

    Institute of Scientific and Technical Information of China (English)

    刘宇; 曹清心; 张燕; 赵仙先

    2012-01-01

    目的 随着急性心肌梗死(acute myocardial infarction,AMI)发病率的不断增加,以及再灌注治疗的广泛开展,缺血再灌注损伤(ischemical reperfusion injury,IRI)已经引起了广泛关注,但尚未找到一种能有效减轻IRI的治疗方法.近年来,国内外基于动物模型的研究发现:高迁移率族蛋白B1(high mobility group box 1 protein,HMGB1)可能在IRI过程中发挥着中枢作用,并且目前有关AMI患者经经皮冠状动脉内介入术(percutaneous coronary intervention,PCI)血浆中HMGB1浓度变化及其机制的研究还鲜见报道.文中初步探讨HMGB1是否参与AMI患者PCI中心肌IRI过程,及其在此过程中产生的心肌保护作用和可能机制.方法 采用酶联免疫吸附法,分别测定17例经冠状动脉造影术(coronary arteriography,CAG)检查正常的健康志愿者(对照组),41例AMI经急诊PCI治疗患者(AMI手术组)术前即刻、术后24h和48h血浆中HMGB1和血管内皮生长因子(vascular endothelial growth factor,VEGF)变化水平,并记录AMI手术组梗死相关血管(infarction related artery,IRA)开通即刻出现的再灌注心律失常(reperfusion arrhythmia,RA)类型、术后24h脑钠肽(brain natriuretic peptide,BNP)水平、住院期间不良临床事件(心力衰竭、心源性猝死)及其他基本临床数据.结果 AMI手术组患者在IRA开通即刻均观察到RA;术后24h HMGB1水平明显高于术前即刻及术后48h(P<0.05),并且各时间点HMGB1水平与VEGF水平呈正相关(P<0.05);AMI手术组院内出现不良临床事件与无不良事件的患者相比较,各时间点HMGB1水平明显降低(P<0.05).结论 HMGB1参与了AMI患者行PCI手术中IRI的过程;HMGB1水平对于AMI患者的远期预后有一定预测作用;HMGB1可能通过促进VEGF的分泌而参与梗死后心肌的修复过程,并可能通过此作用对改善心功能、保护心肌细胞产生一定作用.%Objective With the increasing incidence of acute myocardial infarction

  8. Oxygen free radicals in myocardial ischemia and reperfusion

    NARCIS (Netherlands)

    A.M.M. van der Kraaij

    1989-01-01

    textabstractIn patients with acute myocardial infarction, death normally results from rhythmic disturbances or pump failure. Over the past 3 decades, the mortality rate from this disease has been substantially reduced predominantly by vigorous treatment of dysrhythmias using modern monitoring techni

  9. 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

    2017-03-21

    Myocardial reperfusion decreases glucose oxidation and uncouples glucose oxidation from glycolysis. Therapies that increase glucose oxidation lessen myocardial ischemia/reperfusion injury. However, the regulation of glucose uptake during reperfusion remains poorly understood. Here we found that glucose uptake was remarkably diminished in myocardium following reperfusion in Sprague-Dawley rats as detected by 18F-labeled and fluorescent-labeled glucose analogs, even though GLUT1 was upregulated by 3 folds and GLUT4 translocation remained unchanged compared with those of sham 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 ischemia/reperfusion injury. In vitro data in neonatal myocytes showed that PDK4 overexpression decreased glucose uptake, while its knockdown increased glucose uptake, suggesting a role of PDK4 in regulating glucose uptake. Moreover, inhibition of PDK4 increased myocardial glucose uptake with concomitant enhancement of cardiac insulin sensitivity following myocardial ischemia/reperfusion. These results showed that the suppressed glucose oxidation mediated by PDK4 contributes to the reduced glucose uptake in 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 ischemia/reperfusion injury. Copyright © 2017, American Journal of Physiology-Endocrinology and Metabolism.

  10. Mechanism of the protective effects of noninvasive limbs preconditioning on myocardial ischemia-reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    CHEN Xiao-guang; WU Bin-yang; WANG Jun-ke; BAI Tao

    2005-01-01

    Background This study aimed at assessing the effect of noninvasive limb preconditioning on myocardial infarct size, and determining whether nitric oxide and neurogenic pathway play an important role in the mechanism of acute remote ischemic preconditioning (IPC).Methods Forty Wistar rats were randomly divided into four experimental groups. In Group Ⅰ, the rats underwent 30-minute occlusion of the left anterior descending coronary artery, and 120-minute reperfusion. In Group PL, the rats underwent four cycles of 5-minute occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group Ⅰ. In Group PL-N and Group PL-H, we administered L-nitro-arginine methyl ester (L-NAME) 10 mg/kg or hexamethonium chloride 20 mg/kg intravenously, 10 minutes before IPC. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. Results There were no statistically significant differences in mean arterial pressure and heart rate among these groups at any time point during the experiment (P>0.05). The myocardial infarct size (IS) was decreased significantly in Group PL and Group PL-H compared with Group Ⅰ, and the IS/AAR was 34.5%±7.6%, 35.9%±8.6% and 58.5%±8.5%, respectively (P0.05).Conclusions Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. Nitric oxide plays an important role in the mechanism of acute remote IPC, in which the neurogenic pathway is not involved.

  11. Cardioprotective Effects of Total Flavonoids Extracted from Xinjiang Sprig Rosa rugosa against Acute Ischemia/Reperfusion-Induced Myocardial Injury in Isolated Rat Heart.

    Science.gov (United States)

    Hou, Xuejiao; Han, Jichun; Yuan, Changsheng; Ren, Huanhuan; Zhang, Ya; Zhang, Tao; Xu, Lixia; Zheng, Qiusheng; Chen, Wen

    2016-01-01

    This study evaluated the antioxidative and cardioprotective effects of total flavonoids extracted from Xinjiang sprig Rosa rugosa on ischemia/reperfusion (I/R) injury using an isolated Langendorff rat heart model. The possible mechanism of Xinjiang sprig rose total flavonoid (XSRTF) against I/R injury was also studied. XSRTF (5, 10, and 20 µg/mL) dissolved in Krebs-Henseleit buffer was administered to isolated rat heart. The XSRTF showed remarkable scavenging effects against 1,1-diphenyl-2-picrylhydrazyl, hydroxyl, and superoxide anion radicals in vitro. XSRTF pretreatment improved the heart rate, increased LVDP, and decreased CK and LDH levels in coronary flow. This pretreatment also increased SOD activity and GSH/GSSG ratio but decreased MDA, TNF-α, and CRP levels and IL-8 and IL-6 activities. The infarct size and cell apoptosis in the hearts from the XSRTF-treated group were lower than those in the hearts from the I/R group. Therefore, the cardioprotective effects of XSRTF may be attributed to its antioxidant, antiapoptotic, and anti-inflammatory activities.

  12. Humanized cobra venom factor decreases myocardial ischemia-reperfusion injury.

    Science.gov (United States)

    Gorsuch, W Brian; Guikema, Benjamin J; Fritzinger, David C; Vogel, Carl-Wilhelm; Stahl, Gregory L

    2009-12-01

    Cobra venom factor (CVF) is a complement activating protein in cobra venom, which functionally resembles C3b, and has been used for decades for decomplementation of serum to investigate the role of complement in many model systems of disease. The use of CVF for clinical practice is considered impractical because of immunogenicity issues. Humanization of CVF was recently demonstrated to yield a potent CVF-like molecule. In the present study, we demonstrate that mice treated with recombinant humanized CVF (HC3-1496) are protected from myocardial ischemia-reperfusion (MI/R) injuries with resultant preservation of cardiac function. Also, C3 deposition in the myocardium following MI/R was not observed following treatment with HC3-1496. HC3-1496 led to complement activation and depletion of C3, but preserved C5 titers. These data suggest, unlike CVF, HC3-1496 does not form a C5 convertase in the mouse, similar to recent studies in human sera/plasma. These results suggest that humanized CVF (HC3-1496) protects the ischemic myocardium from reperfusion injuries induced by complement activation and represents a novel anti-complement therapy for potential clinical use.

  13. Cellular recruitment in myocardial ischaemia/reperfusion injury.

    Science.gov (United States)

    Bonaventura, Aldo; Montecucco, Fabrizio; Dallegri, Franco

    2016-06-01

    Myocardial infarction (MI) is strictly linked to atherosclerosis. Beyond the mechanical narrowing of coronary vessels lumen, during MI a great burden of inflammation is carried out. One of the crucial events is represented by the ischaemia/reperfusion injury, a complex event involving inflammatory cells (such as neutrophils, platelets, monocytes/macrophages, lymphocytes and mast cells) and key activating signals (such as cytokines, chemokines and growth factors). Cardiac repair following myocardial infarction is dependent on a finely regulated response involving a sequential recruitment and the clearance of different subsets of inflammatory cells. This narrative review was based on the works detected on PubMed and MEDLINE up to November 2015. Infarct healing classically follows three overlapping phases: the inflammatory phase, in which the innate immune pathways are activated and inflammatory leucocytes are recruited in order to clear the wound from dead cells; the proliferative phase, characterized by the suppression of pro-inflammatory signalling and infiltration of 'repairing' cells secreting matrix proteins in the injured area; and the maturation phase, which is associated with the quiescence and the elimination of the reparative cells together with cross-linking of the matrix. All these phases are timely regulated by the production of soluble mediators, such as cytokines, chemokines and growth factors. Targeting inflammatory cell recruitment early during reperfusion and healing might be promising to selectively inhibit injury and favour repair. This approach might substantially improve adverse postischaemic left ventricle remodelling, characterized by dilation, hypertrophy of viable segments and progressive dysfunction. © 2016 Stichting European Society for Clinical Investigation Journal Foundation.

  14. 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.

  15. NADPH oxidase inhibitor apocynin attenuates ischemia/reperfusion induced myocardial injury in rats

    Institute of Scientific and Technical Information of China (English)

    罗秀菊

    2013-01-01

    Objective To explore the role of NADPH oxidase inhibitor apocynin on ischemia/reperfusion(I/R)-induced myocardial injury. Methods Male SD rat hearts were divided into the normal control group; sham group;I/R group(1 h ischemia followed by 3 h reperfusion); I/R+ apocynin group(50 mg/kg,administrated at 30 min

  16. Role of general practitioner in the management of acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Beeleonie Beeleonie

    2005-12-01

    Full Text Available Acute myocardial infarction (AMI has been the leading cause of death in Western countries, as well as in Indonesia. Delay in diagnosis and incorrect early management often result in failure of thrombolytic reperfusion. General practitioner (GP as the primary care, needs to be equipped with the ability to diagnose and moreover to manage AMI. A case of fail thrombolytic management in a 47 years old man after seven hours of angina typical chest pain, after previously managed by GP, is being reported. (Med J Indones 2005; 14:249-52Keywords: acute myocardial infarction, reperfusion, general practitioner

  17. Combined VEGF gene transfer and erythropoietin in ovine reperfused myocardial infarction.

    Science.gov (United States)

    Olea, Fernanda D; De Lorenzi, Andrea; Cortés, Claudia; Cuniberti, Luis; Fazzi, Lucía; Flamenco, María del Pilar; Locatelli, Paola; Cabeza Meckert, Patricia; Bercovich, Andrés; Laguens, Rubén; Crottogini, Alberto

    2013-05-10

    In reperfused acute myocardial infarction (RAMI), cardioprotective treatments may enhance myocardial salvage and hence reduce the area of necrosis. Based on studies showing that plasmid-mediated vascular endothelial growth factor (pVEGF) gene transfer reduces infarct size by combining angio-arteriogenic and cardiomyogenic effects and that erythropoietin (EPO) exerts anti-apoptotic actions in animal models of AMI, we aimed to assess if their association would reduce infarct size to a larger extent than any of them individually in a large mammalian model of RAMI. Adult sheep subjected to 90-minute coronary artery occlusion received upon reperfusion intramyocardial pVEGF 3.8 mg plus intravenous EPO 1000 IU/kg (n=8), pVEGF (n=8), EPO (n=8) or placebo (n=8). Fifteen days after treatment, infarct size was smaller in the 3 treatment groups (pVEGF+EPO: 8 ± 1 %; pVEGF: 16 ± 5 %; EPO: 13 ± 4 %) compared to placebo (25 ± 7 %, p<0.001). However, in the EPO+VEGF group infarct size was significantly smaller than in the groups receiving EPO or VEGF individually (p<0.05). DNA fragmentation, a hallmark of late apoptosis, was significantly lower in sheep receiving EPO. The combined treatment, while not affecting global left ventricular performance, improved regional peri-infarct function and prevented over-time expansion of the post-infarct perfusion defect. Combined pVEGF and EPO treatment might be clinically useful to enhance the benefits of early revascularization in patients with acute myocardial infarction. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  18. Newer thrombolytic drugs for acute myocardial infarction.

    Science.gov (United States)

    Reddy, D S

    1998-01-01

    Arterial thrombosis is the underlying cause of a wide variety of cardiovascular diseases such as myocardial infarction, stroke and pulmonary thromboembolism. All the currently used thrombolytic agents are plasminogen activators, which are very efficient in restoring the blood flow. The fibrinolytic system comprises an inactive proenzyme plasminogen, that is converted by plasminogen activators to the enzyme plasmin, that degrades fibrin. Despite the widespread use of established thrombolytic agents such as streptokinase, tissue-plasminogen activator and urokinase, all these agents suffer from a number of inadequacies including resistance to reperfusion, occurrence of acute coronary reocclusion and bleeding complications. The quest continues for thrombolytic agents with a higher potency, specific thrombolytic activity and fibrin selectivity. Several lines of research towards improvement of thrombolytic agents are being explored including the construction of mutants and variants of plasminogen activators, chimeric plasminogen activators and conjugates of plasminogen activators with monoclonal antibodies. Newer molecules such as pro-urokinase, saruplase, alteplase, K1K2Pu and staphylokinase have shown promise in animal models of arterial and venous thrombosis and also in pilot scale clinical studies in patients with myocardial infarction. However, more clinical trials are needed to determine whether these novel recombinant thrombolytic agents shows improved efficacy and fibrin specificity with minimal bleeding tendencies.

  19. 丹参多酚酸盐对急性心肌梗死患者介入治疗术后心肌组织灌注影响的临床研究%Effect of polydanshinolate on myocardial reperfusion after percutaneous coronary interventions in patients with acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    刘洋; 邓兵; 许嘉鸿; 李艳延; 徐文俊; 蒋金法

    2010-01-01

    Objective To compare the effect of percutaneons coronary interventions (PCI) combined with polydanshinolate on myocardial reperfusion with PCI combined with regular medicine in patients with acute myocardi-al infrarction ,and whether polydanshinolate would decrease no-reflow,improve the myocardial micro-circulation and the ventricular remodeling and clinical end-point events at the sixth month. Methods Random,parallel control and prospective clinical design was used in the current study. Sixty eligible patients for PCI, who were diagnosed as first-time acute myocardial infrarction with ST stage increasing,were recruited in the study with informed consent. All par-ticipants were divided into two groups randomly. Group A was treated with PCI combined with polydanshinolate, group B was treated with PCI combined with regular medicine. The participants were followed up for six months. The resolution of the sum of ST segment elevation (sum STR) ,corrected TIMI frame count (CTFC) and myocardial con-trast echocardiography (MCE) were used to assess myocardial perfusion. Bleeding events, heart function and major adverse cardiac events (MACE) were observed during hospitalization and follow-up visit. Results No significant difference was observed between two groups on the clinical condition and the results of emergency CAG and PCI. Compared to group B,the incidence of TIMI grade 3 was significantly higher in group A (90.0% vs 63.3% ,χ~2 = 4.565, P=0.0326). Sum STR one hour after PCI in group A was siguificanfly higher than that in group B (80.0% vs 50.0%, χ~2=4.689, P=0.0304). CTFC after PCI also differed significantly between the two groups (24.1±8.3 vs 33.4±15.9 respectively,P=0.0062). Localized myocardial blood flow 48 hours after PCI showed no significant difference between the two groups (P>0.05), whereas both increased at the 7th day after PCI (5.85±1.26 vs 2.09±1.85,t=9.2008,P0.05). The incidences of cardiovascular events and severe heart failure during

  20. Cholinergic anti-inflammatory pathway: a possible approach to protect against myocardial ischemia reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    XIONG Jun; XUE Fu-shan; YUAN Yu-jing; WANG Qiang; LIAO Xu; WANG Wei-li

    2010-01-01

    Objective A general review was made of studies involving: (1) the concept and mechanism of the cholinergic anti-inflammatory pathway (CAP), (2) the important role of inflammatory response in myocardial ischemia reperfusion (I/R)injury and (3) the evidence and mechanisms by which CAP may provide protection against myocardial I/R injury.Data sources The data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1987 to 2009. The search terms were "vagal nerve stimulation", "myocardial ischemia reperfusion injury","nicotine acetylcholine receptor" and "inflammation".Study selection (1) Clinical and experimental evidence that the inflammatory response induced by reperfusion enhances myocardial I/R injury. (2) Clinical and laboratory evidence that the CAP inhibits the inflammation and provides protection against myocardial I/R injury.Results The myocardial I/R injury is really an inflammatory process characterized by recruitment of neutrophils into the ischemic myocardium and excessive production of pro-inflammatory cytokines. Because the CAP can modulate the inflammatory response by decreasing the production and release of pro-inflammatory cytokines, it can provide protection against myocardial I/R injury.Conclusions The CAP can inhibit the inflammatory response induced by reperfusion and protect against myocardial I/R injury. It represents an exciting opportunity to develop new and novel therapeutics to attenuate the myocardial I/R injury.

  1. Protection effects of Sigmart for no-reflow or myocardial reperfusion injury after undergoing PCI surgery

    Institute of Scientific and Technical Information of China (English)

    Xiao-Peng Wu; Xuan-Qi Wang; Lei-Sen Han; Chong-Zhen Wang; Yin-Juan Mao; Wei-Jie Li

    2015-01-01

    Objective:To study the protection effects of Sigmart for lack of reflow or myocardial myocardial reperfusion injury after undergoing PCI surgery.Methods: A total of 150 patients undergoing PCI surgery were selected and divided into control group and observation group with 75 cases in each group. After undergoing the surgery, both groups were given low molecular heparin 4 100 IU for 3 d, 100 mg + aspirin + atorvastatin 20 mg + clopidogrel 75 mg. 5 mL of blood specimen were collected for detection of troponin I (TnI), myocardial enzyme spectrum (CK, CK-MB) level to evaluate myocardial myocardial reperfusion injury after undergoing PCI surgery. Also electrocardiogram (ECG) were detected. Six months after the surgery, effects of Sigmart for lack of reflow or myocardial myocardial reperfusion injury after undergoing PCI surgery were evaluated.Results: 1, 6, 12, 24 h after the surgery, TnI, Mb, CK-Mb levels of were significant different from those before undergoing the surgery, and these levels of the observation group were significant higher than that of the control group. ST segment elevation at 2, 12, and 24 h after undergoing the surgery were significant obvious than that of the control group. According to the follow up, incidence of comprehensive end point event was significant higher than that of the control group. SAQ and SF-36 scores of the two groups were significant different. Conclusion: Sigmart shows good protection effects for lack of reflow or myocardial myocardial reperfusion injury after undergoing PCI surgery.

  2. Infant acute myocarditis mimicking acute myocardial infarction

    Science.gov (United States)

    Tilouche, Samia; Masmoudi, Tasnim; Sahnoun, Maha; Chkirbène, Youssef; Mestiri, Sarra; Boughamoura, Lamia; Ben Dhiab, Mohamed; Souguir, Mohamed Kamel

    2016-01-01

    Myocarditis is an inflammatory disease of the myocardium with heterogeneous clinical manifestations and progression. In clinical practice, although there are many methods of diagnosis of acute myocarditis, the diagnosis remains an embarrassing dilemma for clinicians. The authors report the case of 9-month-old infant who was brought to the Pediatric Emergency Department with sudden onset dyspnea. Examination disclosed heart failure and resuscitation was undertaken. The electrocardiogram showed an ST segment elevation in the anterolateral leads with a mirror image. Cardiac enzyme tests revealed a significant elevation of troponin and creatine phosphokinase levels. A diagnosis of acute myocardial infarction was made, and heparin therapy was prescribed. The infant died on the third day after admission with cardiogenic shock. The autopsy showed dilatation of the ventricles and massive edema of the lungs. Histological examinations of myocardium samples revealed the presence of a marked lymphocytic infiltrate dissociating myocardiocytes. Death was attributed to acute myocarditis. The authors call attention to the difficulties of differential diagnosis between acute myocarditis and acute myocardial infarction especially in children, and to the important therapeutic implications of a correct diagnosis. PMID:28210569

  3. The tole of ischemic preconditioning in acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Ristić Anđelka

    2005-01-01

    Full Text Available Introduction Ischemic preconditioning is a phenomenon in which brief episodes of ischemia and reperfusion increase myocardial tolerance and substantially reduce the infarction size. Case report Two patients with acute left anterior descending artery occlusion received fibrinolytic therapy within 6 hours of symptom onset, but nevertheless developed myocardial infarctions of different size. The first patient, without a history of preinfarction angina, developed a large anterior infarction, because there was no time for ischemic preconditioning or development of coronary collateral vessels. The second patient, with a 4-day history of preinfarction angina, had a more favorable outcome-he developed apical necrosis, with greater myocardial viability in the infarct-related area. Conclusion The beneficial effects of angina occurring 24-48h before infarction are resulting from ischemic preconditioning, which reduces cardiac mortality, infarct size and occurrence of life-threatening ventricular arrhythmias. .

  4. Nanoparticle-Mediated Delivery of Irbesartan Induces Cardioprotection from Myocardial Ischemia-Reperfusion Injury by Antagonizing Monocyte-Mediated Inflammation

    Science.gov (United States)

    Nakano, Yasuhiro; Matoba, Tetsuya; Tokutome, Masaki; Funamoto, Daiki; Katsuki, Shunsuke; Ikeda, Gentaro; Nagaoka, Kazuhiro; Ishikita, Ayako; Nakano, Kaku; Koga, Jun-Ichiro; Sunagawa, Kenji; Egashira, Kensuke

    2016-07-01

    Myocardial ischemia-reperfusion (IR) injury limits the therapeutic effect of early reperfusion therapy for acute myocardial infarction (AMI), in which the recruitment of inflammatory monocytes plays a causative role. Here we develop bioabsorbable poly-lactic/glycolic acid (PLGA) nanoparticles incorporating irbesartan, an angiotensin II type 1 receptor blocker with a peroxisome proliferator-activated receptor (PPAR)γ agonistic effect (irbesartan-NP). In a mouse model of IR injury, intravenous PLGA nanoparticles distribute to the IR myocardium and monocytes in the blood and in the IR heart. Single intravenous treatment at the time of reperfusion with irbesartan-NP (3.0 mg kg‑1 irbesartan), but not with control nanoparticles or irbesartan solution (3.0 mg kg‑1), inhibits the recruitment of inflammatory monocytes to the IR heart, and reduces the infarct size via PPARγ-dependent anti-inflammatory mechanisms, and ameliorates left ventricular remodeling 21 days after IR. Irbesartan-NP is a novel approach to treat myocardial IR injury in patients with AMI.

  5. Efficacy of pre-hospital use of glycoprotein IIb/IIIa inhibitors in ST-segment elevation myocardial infarction before mechanical reperfusion in a rapid-transfer network (from the Acute Myocardial Infarction Registry of Brittany).

    Science.gov (United States)

    Auffret, Vincent; Oger, Emmanuel; Leurent, Guillaume; Filippi, Emmanuelle; Coudert, Isabelle; Hacot, Jean Philippe; Castellant, Philippe; Rialan, Antoine; Delaunay, Régis; Rouault, Gilles; Druelles, Philippe; Boulanger, Bertrand; Treuil, Josiane; Avez, Bertrand; Bedossa, Marc; Boulmier, Dominique; Le Guellec, Marielle; Le Breton, Hervé

    2014-07-15

    Previous studies investigating prehospital use of glycoprotein IIb/IIIa inhibitors (GPIs) in patients with ST-segment elevation myocardial infarction reached conflicting conclusions. The benefit of this strategy in addition to in-ambulance loading of dual-antiplatelet therapy remains controversial. The aim of this study was to analyze data from a prospective registry of patients with ST-segment elevation myocardial infarctions admitted 2 hours after symptom onset, of whom only 12.7% reached the primary end point. There was no significant difference between groups in the rate of in-hospital major adverse cardiac events. In conclusion, prehospital GPI use in patients with ST-segment elevation myocardial infarctions<12 hours after symptom onset scheduled for PPCI neither improved pre-PPCI infarct-related artery patency nor reduced in-hospital major adverse cardiac events.

  6. Pharmacological preconditioning with hyperbaric oxygen: can this therapy attenuate myocardial ischemic reperfusion injury and induce myocardial protection via nitric oxide?

    Science.gov (United States)

    Yogaratnam, Jeysen Zivan; Laden, Gerard; Guvendik, Lavent; Cowen, Mike; Cale, Alex; Griffin, Steve

    2008-09-01

    Ischemic reperfusion injury (IRI) is an inevitable part cardiac surgery such as coronary artery bypass graft (CABG). While ischemic hypoxia and the ensuing normoxic or hyperoxic reperfusion are critical to the initiation and propagation of IRI, conditioning myocardial cells to an oxidative stress prior to IRI may limit the consequences of this injury. Hyperbaric oxygen (HBO2) is a modality of treatment that is known to generate an oxidative stress. Studies have shown that treatment with HBO2 postischemia and reperfusion is useful in ameliorating myocardial IRI. Moreover, preconditioning the myocardium with HBO2 before reperfusion has demonstrated a myocardial protective effect by limiting the infarct size post ischemia and reperfusion. Current evidence suggests that HBO2 preconditioning may partly attenuate IRI by stimulating the endogenous production of nitric oxide (NO). As NO has the capacity to reduce neutrophil sequestration, adhesion and associated injury, and improve vascular flow, HBO2 preconditioning induced NO may play a role in providing myocardial protection during interventions that involve an inevitable episode of IRI. This current opinion review article attempts to suggest that HBO2 may be used to pharmacologically precondition and protect the myocardium from the effects of IRI that is known to occur during cardiac surgery.

  7. Hyperglycemia is an important predictor of impaired coronary flow before reperfusion therapy in ST-segment elevation myocardial infarction

    NARCIS (Netherlands)

    Timmer, [No Value; Ottervanger, JP; de Boer, MJ; Hoorntje, JCA; Gosselink, ATM; Suryapranata, H; Zijlstra, F; van't Hof, AWJ; Dambrink, Jan Hendrik Everwijn

    2005-01-01

    OBJECTIVES This study was designed to investigate whether elevated glucose is associated with impaired Thrombolysis In Myocardial Infarction (TIMI) flow before primary percutaneous coronary intervention (PCI). BACKGROUND Reperfusion before primary PCI in patients with ST-segment elevation myocardial

  8. Thrombus aspiration in acute myocardial infarction:Rationale and indication

    Institute of Scientific and Technical Information of China (English)

    Gennaro; Sardella; Rocco; Edoardo; Stio

    2014-01-01

    Reperfusion of myocardial tissue is the main goal of primary percutaneous coronary intervention(PPCI) with stent implantation in the treatment of acute ST-segment elevation myocardial infarction(STEMI). Although PPCI has contributed to a dramatic reduction in cardiovascular mortality over three decades, normal myocardial perfusion is not restored in approximately one-third of these patients. Several mechanisms may contribute to myocardial reperfusion failure, in particular distal embolization of the thrombus and plaque fragments. In fact, this is a possible complication during PPCI, resulting in microvascular obstruction and no-reflow phenomenon. The presence of a visible thrombus at the time of PPCI in patients with STEMI is associated with poor procedural and clinical outcomes. Aspiration thrombectomy during PPCI has been proposed to prevent embolization in order to improve these outcomes. In fact, the most recent guidelines suggest the routine use of manual aspiration thrombectomy during PPCI(class Ⅱa) to reduce the risk of distal embolization. Even though numerous international studies have been reported, there are conflicting results on the clinical impact of aspiration thrombectomy during PPCI. In particular, data on long-term clinical outcomes are still inconsistent. In this review, we have carefully analyzed literature data on thrombectomy during PPCI, taking into account the most recent studies and meta-analyses.

  9. 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.

  10. 《简明心肌梗死图解》对急性心肌梗死患者再灌注决定时间的影响%Influence of illustration of myocardial infarction on decision time of reperfusion therapy in patients with acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    韩兰唐; 曹树军; 胡硕强; 俞晓薇; 杨红英; 王文斌; 韩琦

    2014-01-01

    目的:探讨《简明心肌梗死图解》对急性ST段抬高心肌梗死( STEMI)患者再灌注治疗决定时间的影响。方法将2013年6月至2014年6月期间就诊于首都医科大学大兴医院适合急诊经皮冠状动脉介入治疗( PCI)的急性STEMI患者随机分为常规组和图解组;常规组采用目前临床常用的方法向患者和患者家属交代病情;图解组在常规方法的基础上借助《简明心肌梗死图解》向患者及其亲属进行简明扼要的STEMI医学知识紧急培训,帮助其迅速了解STEMI的发病机制和再灌注治疗的重要性;两组患者均在做出再灌注治疗决定并签署急诊PCI知情同意书后,尽快施行急诊PCI,并收住冠心病监护病房进一步治疗。结果图解组( n=49)患者的再灌注决定时间、进门-首次球囊扩张时间均明显短于常规组( n=50)[(15.1±11.5)min比(25.9±12.9)min,(105.7±28.4)min比(117.1±29.2)min,P均<0.05]。结论简明心肌梗死图解可以缩短STEMI患者再灌注治疗决定时间、缩短进门-首次球囊扩张时间。%Objective To explore the influence of illustration of acute ST-elevation myocardial infarction( STEMI)on decision time of reperfusion therapy in patients with acute STEMI. Methods Patients with acute STEMI and in line with the primary PCI indication were randomly divided into conventional group and illustration group from June 2013 to June 2014 period in department of cardiology of Daxing hospital of Capital Medical University. All patients signed informed consent after making reperfusion therapy decisions,and implementing interventional treatment as soon as possible and admitted to CCU. Results The decision time and door-to-balloon time of illustration group( n=49 )was significantly shorter than that of the conventional group(n=50)[(15.1 ±11.5)min vs.(25.9 ±12.9)min,(105.7 ±28.4)min vs.(117.1 ±29.2)min,P<0. 05]. Conclusion The illustration of acute

  11. 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%, p<0.05) and improved left ventricular ejection fraction (LVEF) (GLA 53.13±1.11% vs. Control 49.99±1.25%, p<0.05) and left ventricular fractional shortening (LVFS) (28.34±0.71% vs. Control 25.11±0.74%, p<0.05) in mice subjected to myocardial ischemia-reperfusion. GLA also attenuated microvascular thrombosis (P<0.05) and increased the phosphorylation of pro-survival kinase AKT (P<0.05) and GSK-3β (P<0.05) in the myocardium upon reperfusion injury. Conclusions Administration of GLA before reperfusion ameliorates myocardial ischemia-reperfusion injury in mice. The cardio-protective roles of GLA may be mediated through the attenuation of microvascular thrombosis. PMID:27716735

  12. Diltiazem in acute myocardial infarction treated with thrombolytic agents : a randomised placebo-controlled trial

    NARCIS (Netherlands)

    Boden, WE; van Gilst, WH; Scheldewaert, RG; Starkey, IR; Carlier, MF; Julian, DG; Whitehead, A; Bertrand, ME; Col, JJ; Pedersen, OL; Lie, KI; Santoni, JP; Fox, KM

    2000-01-01

    Background Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion. We postulated that this agent would reduce cardiac events in patients after a

  13. 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...

  14. Cardiomyocyte-specific overexpression of an active form of Rac predisposes the heart to increased myocardial stunning and ischemia-reperfusion injury

    Science.gov (United States)

    Talukder, M. A. Hassan; Elnakish, Mohammad T.; Yang, Fuchun; Nishijima, Yoshinori; Alhaj, Mazin A.; Velayutham, Murugesan; Hassanain, Hamdy H.

    2013-01-01

    The GTP-binding protein Rac regulates diverse cellular functions including activation of NADPH oxidase, a major source of superoxide production (O2·−). Rac1-mediated NADPH oxidase activation is increased after myocardial infarction (MI) and heart failure both in animals and humans; however, the impact of increased myocardial Rac on impending ischemia-reperfusion (I/R) is unknown. A novel transgenic mouse model with cardiac-specific overexpression of constitutively active mutant form of Zea maize Rac D (ZmRacD) gene has been reported with increased myocardial Rac-GTPase activity and O2·− generation. The goal of the present study was to determine signaling pathways related to increased myocardial ZmRacD and to what extent hearts with increased ZmRacD proteins are susceptible to I/R injury. The effect of myocardial I/R was examined in young adult wild-type (WT) and ZmRacD transgenic (TG) mice. In vitro reversible myocardial I/R for postischemic cardiac function and in vivo regional myocardial I/R for MI were performed. Following 20-min global ischemia and 45-min reperfusion, postischemic cardiac contractile function and heart rate were significantly reduced in TG hearts compared with WT hearts. Importantly, acute regional myocardial I/R (30-min ischemia and 24-h reperfusion) caused significantly larger MI in TG mice compared with WT mice. Western blot analysis of cardiac homogenates revealed that increased myocardial ZmRacD gene expression is associated with concomitant increased levels of NADPH oxidase subunit gp91phox, O2·−, and P21-activated kinase. Thus these findings provide direct evidence that increased levels of active myocardial Rac renders the heart susceptible to increased postischemic contractile dysfunction and MI following acute I/R. PMID:23161879

  15. A Role for Photobiomodulation in the Prevention of Myocardial Ischemic Reperfusion Injury: A Systematic Review and Potential Molecular Mechanisms.

    Science.gov (United States)

    Liebert, Ann; Krause, Andrew; Goonetilleke, Neil; Bicknell, Brian; Kiat, Hosen

    2017-02-09

    Myocardial ischemia reperfusion injury is a negative pathophysiological event that may result in cardiac cell apoptosis and is a result of coronary revascularization and cardiac intervention procedures. The resulting loss of cardiomyocyte cells and the formation of scar tissue, leads to impaired heart function, a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation is a novel cardiac intervention that has displayed therapeutic effects in reducing myocardial ischemia reperfusion related myocardial injury in animal models. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models has implicated multiple molecular interactions. A systematic review was conducted to identify the strength of the evidence for the therapeutic effect of photobiomodulation and to summarise the current evidence as to its mechanisms. Photobiomodulation in animal models showed consistently positive effects over a range of wavelengths and application parameters, with reductions in total infarct size (up to 76%), decreases in inflammation and scarring, and increases in tissue repair. Multiple molecular pathways were identified, including modulation of inflammatory cytokines, signalling molecules, transcription factors, enzymes and antioxidants. Current evidence regarding the use of photobiomodulation in acute and planned cardiac intervention is at an early stage but is sufficient to inform on clinical trials.

  16. A Role for Photobiomodulation in the Prevention of Myocardial Ischemic Reperfusion Injury: A Systematic Review and Potential Molecular Mechanisms

    Science.gov (United States)

    Liebert, Ann; Krause, Andrew; Goonetilleke, Neil; Bicknell, Brian; Kiat, Hosen

    2017-01-01

    Myocardial ischemia reperfusion injury is a negative pathophysiological event that may result in cardiac cell apoptosis and is a result of coronary revascularization and cardiac intervention procedures. The resulting loss of cardiomyocyte cells and the formation of scar tissue, leads to impaired heart function, a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation is a novel cardiac intervention that has displayed therapeutic effects in reducing myocardial ischemia reperfusion related myocardial injury in animal models. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models has implicated multiple molecular interactions. A systematic review was conducted to identify the strength of the evidence for the therapeutic effect of photobiomodulation and to summarise the current evidence as to its mechanisms. Photobiomodulation in animal models showed consistently positive effects over a range of wavelengths and application parameters, with reductions in total infarct size (up to 76%), decreases in inflammation and scarring, and increases in tissue repair. Multiple molecular pathways were identified, including modulation of inflammatory cytokines, signalling molecules, transcription factors, enzymes and antioxidants. Current evidence regarding the use of photobiomodulation in acute and planned cardiac intervention is at an early stage but is sufficient to inform on clinical trials. PMID:28181487

  17. Assessment of inflammation with a very small iron-oxide particle in a murine model of reperfused myocardial infarction.

    Science.gov (United States)

    Protti, Andrea; Dong, Xuebin; Andia, Marcelo E; Yu, Bin; Dokukina, Kate; Chaubey, Sanjay; Phinikaridou, Alkystis; Vizcay-Barrena, Gema; Taupitz, Matthias; Botnar, Rene M; Shah, Ajay M

    2014-03-01

    To investigate a very small iron-oxide particle (VSOP) in a mouse model of acute ischemia-reperfusion to access the mechanism of such particles in areas of myocardial inflammation. Animals were injected with VSOP at several time points, in a mouse model of acute myocardial infarction (MI), before and after MI. MRI was used to localize areas of VSOP enhancement, evaluate VSOP areas extension, and determine the related T2* values. Histology, electron microscopy, macrophage counting, and Evan's Blue staining were also performed. We found that areas of VSOP uptake decreased from 1 to 8 days post-MI while the related T2* values increased. T2* and VSOP areas, defined from MRI data, correlated well between 1 and 3 days post-MI but not at 7 days after injection. Histological analysis and electron microscopy showed colocalization of macrophages with areas of VSOP staining. However, there was no correlation between number of macrophages and the extension of the VSOP areas achieved by MR. We found that only areas of increased permeability (assessed by Evan's Blue staining) showed colocalization of macrophages and VSOP uptake. This study demonstrates that VSOP allows the assessment of myocardial inflammation associated with increased permeability during infarct healing in a mouse model of ischemia-reperfusion. Copyright © 2013 Wiley Periodicals, Inc.

  18. 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

    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...... 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...

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

    Science.gov (United States)

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

    2016-01-01

    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 (clinical serologic biomarkers.

  20. 99mTc-MIBI心肌显像评价参麦注射液对急性心肌梗死溶栓再灌注心肌的保护作用%Study on Effect of Shenmai Injection in Protecting Myocardium against Ischemia-Reperfusion Injury in Thrombolytic Therapy with Urokinase for Acute Myocardial Infarction Patients Evaluated by 99mTc-MIBI Myocardial Imaging

    Institute of Scientific and Technical Information of China (English)

    郭松鹏; 张言镇

    2001-01-01

    Objective: To evaluate the myocardial protecting effect ofShenmai injection (SMI) against ischemia/reperfusion injury in thrombolytic therapy with urokinase (UK) for acute myocardial infarction patients by 99m Tc-MIBI myocardial imaging (SPECT). Methods: Five hundred and thirty-seven patients were randomly divided into two groups. The SMI group (n=292) was treated with thrombolytic treatment plus SMI and the control group (n=245) with thrombolytic treatment only. Single photon emission computerized tomography (SPECT) was carried out on the 7th day after thrombolysis to determine the ischemic myocardial area (IMA) and ejection fraction (EF) in both groups and compared. Results: The reperfusion rate of infarction related area (IRA) in the two groups was not different significantly (72.26% vs 72.65%, P>0.05). The IMA in patients of the SMI group, no matter with or without reperfused IRA (211 cases and 81 cases) respectively, was significantly lower than that in the control group (178 cases and 67 cases) respectively, P<0.01 and P<0.05 respectively. The EF value in the SMI group was significantly higher than that in the control group (P<0.01). Conclusion: Using SMI in early stage of thrombolytic treatment in acute myocardial infarction could significantly reduce IMA and increase EF. SMI showed good protective effect against myocardial ischemia/reperfusion injury in thrombolytic treatment.%目的:用99m锝-甲氰基异丁基晴心肌灌注断层显像(SPECT),评价参麦注射液对急性心肌梗死(AMI)尿激酶(UK)溶栓治疗再灌注心肌保护作用的临床疗效。方法:537例AMI患者随机分为两组,参麦组(292例)采用UK溶栓疗法和参麦注射液治疗,对照组(245例)只使用UK溶栓疗法。于溶栓治疗后第7日进行SPECT检测。对两组心肌缺血面积(IMA)和左室射血分数(EF)的变化进行对比研究。结果:参麦组和对照组梗塞相关血管(IRA)再通率之间差异无显著性(分别为72.26%

  1. 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.)

  2. Pharmacokinetics of ligustrazine ethosome patch in rats and anti-myocardial ischemia and anti-ischemic reperfusion injury effect

    Directory of Open Access Journals (Sweden)

    Liu X

    2011-07-01

    Full Text Available Xingyan Liu1, Hong Liu1, Zhaowu Zeng2, Weihua Zhou3, Jianqiang Liu2, Zhiwei He11China-America Cancer Research Institute, Guangdong Medical College, 2Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College, Dongguan, Guangdong, 3Yichun University, Yichun, Jiangxi, People's Republic of ChinaAbstract: The objective of this study was to investigate the pharmacokinetics of the ligustrazine ethosome patch and antimyocardial ischemia and anti-ischemic reperfusion injury effect. Male Sprague Dawley rats were divided randomly into 3 groups: Group A (intragastric ligustrazine, Group B (transdermal ligustrazine ethosome patch, and Group C (conventional transdermal ligustrazine patch. After treatment, samples of blood and of various tissues such as heart, liver, spleen, lung, kidney, brain, and muscle samples were taken at different time points. Drug concentration was measured with HPLC, and the drug concentration–time curve was plotted. Pharmacokinetic software 3p97 was applied to calculate pharmacokinetic parameters and the area under the drug concentration–time curve (AUC in various tissues. The rat model of acute myocardial ischemia was constructed with intravenous injection of pituitrin and the model of myocardial ischemia-perfusion injury was constructed by tying off the left anterior descending coronary artery of rats to observe the effect of ligustrazine ethosome patches on ischemic myocardium and ischemia-reperfusion injury. Results showed that AUC was highest in the transdermal drug delivery group of ligustrazine ethosome patch. There were significant differences in whole blood viscosity, plasma viscosity, hematocrit, red blood cell aggregation index, and deformation index between ligustrazine the ethosome patch group and ischemic control group (P < 0.01. Moreover, ligustrazine ethosome patches could reduce the scope of myocardial infarction induced by long-term ischemia. Ligustrazine ethosome patches

  3. Effect and mechanism of salvianolic acid B on the myocardial ischemia-reperfusion injury in rats

    Institute of Scientific and Technical Information of China (English)

    Ling Xue; Zhen Wu; Xiao-Ping Ji; Xia-Qing Gao; Yan-Hua Guo

    2014-01-01

    Objective: To investigate the effect of salvianolic acid B on rats with myocardial ischemia-reperfusion injury. Methods: SD rats were randomly divided into five groups (n=10 in each group): A sham operation group, B ischemic reperfusion group model group, C low dose salvianolic acid B group, D median dose salvianolic acid B group, E high dose salvianolic acid B group. One hour after establishment of the myocardial ischemia-reperfusion model, the concentration and the apoptotic index of the plasma level of myocardial enzymes (CTnⅠ, CK-MB), SOD, MDA, NO, ET were measured. Heart tissues were obtained and micro-structural changes were observed. Results: Compared the model group, the plasma CTnⅠ, CK-MB, MDA and ET contents were significantly increased, NO, T-SOD contents were decreased in the treatment group (group C, D, and E) (P<0.05); compared with group E, the plasma CTnⅠ, CK-MB, MDA and ET levels were increased, the NO, T-SOD levels were decreased in groups C and D (P<0.05). Infarct size was significantly reduced, and the myocardial ultrastructural changes were improved significantly in treatment group. Conclusions: Salvianolic acid B has a significant protective effect on myocardial ischemia-reperfusion injury. It can alleviate oxidative stress, reduce calcium overload, improve endothelial function and so on.

  4. 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...

  5. Speckle tracking imaging in evaluation of radial strain of subendocardial and epicardial myocardium in canine acute myocardial ischemia and reperfusion%斑点追踪技术评价犬急性心肌缺血及再灌注心内膜下心肌和心外膜下心肌径向应变

    Institute of Scientific and Technical Information of China (English)

    宋平梅; 任卫东; 马春燕; 王秀芹; 乔伟

    2013-01-01

    Objective To evaluate the radial strain function of subendocardial and epicardial myocardium in acute myocardial ischemia and reperfusion canine with speckle tracking imaging. Methods The first diagonal branch of left coronary artery of 20 adult healthy hybrid dogs were ligated. Radial strain of subendocardial and epicardial myocardium at basal, apical and papillary muscle level were compared by speckle tracking imaging before ligation, ligation immediately, 60,120, 180 min after ligation, reperfusion immediately, and 60, 120 min after reperfusion, respectively. Results Radial strain of basal level elevated by compensatory role in canine acute ischemic process. Radial strain of apical and papillary muscle level decreased obviously. Myocardial reverse movement was even found at apical level. In acute ischemia and reperfusion process, subendocardial myocardium was more sensitive to ischemia. After reperfusion, radial strain of subendocardial and epicardial myocardium at apical and papillary muscle level were still lower than that in basic status. Conclusion Speckle tracking imaging can objectively quantify regional and overall heart function and transmural extent of myocardial infarction in canine.%目的 应用斑点追踪技术检测犬急性心肌缺血及再灌注不同时间点心内膜下心肌和心外膜下心肌的径向应变.方法 选取20只健康成年杂种犬,结扎左冠状动脉第一对角支,分别对结扎前、结扎即刻、60、120和180 min及再灌注即刻、60和120 min基底水平、乳头肌水平和心尖水平心内膜下和心外膜下心肌的径向应变进行比较.结果 在急性缺血过程中,基底水平心肌起代偿作用,其径向应变上升;乳头肌水平和心尖水平心肌下降明显,心尖水平心肌甚至出现反向运动.在急性缺血及再灌注过程中,心内膜下心肌对缺血更加敏感.再灌注后,乳头肌水平和心尖水平心内膜下和心外膜下心肌及跨壁的径向应变

  6. Effects of ischemic preconditioning and iloprost on myocardial ischemia-reperfusion damage in rats.

    Science.gov (United States)

    Ay, Yasin; Kara, Ibrahim; Aydin, Cemalettin; Ay, Nuray Kahraman; Teker, Melike Elif; Senol, Serkan; Inan, Bekir; Basel, Halil; Uysal, Omer; Zeybek, Rahmi

    2013-01-01

    This study investigates the effects of cardiac ischemic preconditioning and iloprost on reperfusion damage in rats with myocardial ischemia/reperfusion. 38 male Wistar Albino rats used in this study were divided into 5 groups. The control group (Group 1) (n=6), ischemia/reperfusion (IR) group (Group 2) (n=8), cardiac ischemic preconditioning (CIP) group (Group 3) (n=8), iloprost (ILO) group (Group 4) (n=8), and cardiac ischemic preconditioning + iloprost (CIP+ILO) group (Group 5) (n=8). Pre-ischemia, 15 minutes post-ischemia, 45 minutes post-reperfusion, mean blood pressure (MBP), and heart rates (HR) were recorded. The rate-pressure product (RPP) was calculated. Post-reperfusion plasma creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), troponin (cTn) vlaues, and infarct size/area at risk (IS/AAR) were calculated from myocardial tissue samples. Arrhythmia and ST segment elevations were evaluated during the ischemia and reperfusion stages. Although the MBP, HR, RPP values, biochemical parameters of CK-MB and LDH levels, IS/AAR rates, ST segment elevation values were found to be similar in CIP and CIP+ILO groups and the IR and ILO groups (p>0.05), CIP-containing group values had a positively meaningful difference (pILO group. While mild-moderate findings of damage were observed in Group 3 and Group 5, severely findings of damage were releaved in Group 2 and Group 4. The arrhythmia score of the ILO group was meaningfully lower (F: 41.4, p<0.001) than the IR group. We can conclude that the effects of myocardial reperfusion damage can be reduced by cardiac ischemic preconditioning, intravenous iloprost reduced the incidence of ventricular arrhythmia associated with reperfusion, and its use with CIP caused no additional changes.

  7. 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.

  8. 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...

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

    Institute of Scientific and Technical Information of China (English)

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

    2012-01-01

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

  10. Residual Myocardial Iron Following Intramyocardial Hemorrhage During the Convalescent Phase of Reperfused ST-Segment–Elevation Myocardial Infarction and Adverse Left Ventricular Remodeling

    Science.gov (United States)

    Bulluck, Heerajnarain; Rosmini, Stefania; Abdel-Gadir, Amna; White, Steven K.; Bhuva, Anish N.; Treibel, Thomas A.; Fontana, Marianna; Ramlall, Manish; Hamarneh, Ashraf; Sirker, Alex; Herrey, Anna S.; Manisty, Charlotte; Yellon, Derek M.; Kellman, Peter; Moon, James C.

    2016-01-01

    Background— The presence of intramyocardial hemorrhage (IMH) in ST-segment–elevation myocardial infarction patients reperfused by primary percutaneous coronary intervention has been associated with residual myocardial iron at follow-up, and its impact on adverse left ventricular (LV) remodeling is incompletely understood and is investigated here. Methods and Results— Forty-eight ST-segment–elevation myocardial infarction patients underwent cardiovascular magnetic resonance at 4±2 days post primary percutaneous coronary intervention, of whom 40 had a follow-up scan at 5±2 months. Native T1, T2, and T2* maps were acquired. Eight out of 40 (20%) patients developed adverse LV remodeling. A subset of 28 patients had matching T2* maps, of which 15/28 patients (54%) had IMH. Eighteen of 28 (64%) patients had microvascular obstruction on the acute scan, of whom 15/18 (83%) patients had microvascular obstruction with IMH. On the follow-up scan, 13/15 patients (87%) had evidence of residual iron within the infarct zone. Patients with residual iron had higher T2 in the infarct zone surrounding the residual iron when compared with those without. In patients with adverse LV remodeling, T2 in the infarct zone surrounding the residual iron was also higher than in those without (60 [54–64] ms versus 53 [51–56] ms; P=0.025). Acute myocardial infarct size, extent of microvascular obstruction, and IMH correlated with the change in LV end-diastolic volume (Pearson’s rho of 0.64, 0.59, and 0.66, respectively; P=0.18 and 0.62, respectively, for correlation coefficient comparison) and performed equally well on receiver operating characteristic curve for predicting adverse LV remodeling (area under the curve: 0.99, 0.94, and 0.95, respectively; P=0.19 for receiver operating characteristic curve comparison). Conclusions— The majority of ST-segment–elevation myocardial infarction patients with IMH had residual myocardial iron at follow-up. This was associated with

  11. Acute myocardial involvement after heroin inhalation

    Directory of Open Access Journals (Sweden)

    Ritu Karoli

    2012-01-01

    Full Text Available Amongst the illicit drugs cocaine, amphetamines and cannabis have been studied and documented well to cause myocardial infarction by different mechanisms but there is very sparse data available on myocardial involvement after heroin abuse. We report a young man who developed acute myocardial injury after heroin inhalation and alcohol binge drinking. Heroin induced cardio toxic effect and vasospasm compounded by alcohol were suspected to be the cause of this.

  12. Acute Myocardial Infarction Quality of Care: The Strong Heart Study

    Science.gov (United States)

    Best, Lyle G.; Butt, Amir; Conroy, Britt; Devereux, Richard B.; Galloway, James M.; Jolly, Stacey; Lee, Elisa T.; Silverman, Angela; Yeh, Jeun-Liang; Welty, Thomas K.; Kedan, Ilan

    2014-01-01

    Objectives Evaluate the quality of care provided patients with acute myocardial infarction and compare with similar national and regional data. Design Case series. Setting The Strong Heart Study has extensive population-based data related to cardiovascular events among American Indians living in three rural regions of the United States. Participants Acute myocardial infarction cases (72) occurring between 1/1/2001 and 12/31/2006 were identified from a cohort of 4549 participants. Outcome measures The proportion of cases that were provided standard quality of care therapy, as defined by the Healthcare Financing Administration and other national organizations. Results The provision of quality services, such as administration of aspirin on admission and at discharge, reperfusion therapy within 24 hours, prescription of beta blocker medication at discharge, and smoking cessation counseling were found to be 94%, 91%, 92%, 86% and 71%, respectively. The unadjusted, 30 day mortality rate was 17%. Conclusion Despite considerable challenges posed by geographic isolation and small facilities, process measures of the quality of acute myocardial infarction care for participants in this American Indian cohort were comparable to that reported for Medicare beneficiaries nationally and within the resident states of this cohort. PMID:21942161

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

    Science.gov (United States)

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

    2013-12-01

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

  14. [Antioxidant and cardioprotective effects of N-tyrosol in myocardial ischemia with reperfusion in rats].

    Science.gov (United States)

    Smol'iakova, V I; Chernyshova, G A; Plotnikov, M B; Aliev, O I; Krasnov, E A

    2010-01-01

    We demonstrated in experiments on rats with left coronary artery occlusion that intravenous administration of 20 mg/kg n-tyrosol during ischemia limited manifestations of oxidative stress in myocardial tissue during early post reperfusion period: content of diene and triene conjugates lowered 16 and 20%, respectively. This was associated with higher preservation of cardiomyocytes and reduction of the infarction zone.

  15. Protection of Puerarin on Oxidative Stress Induced by Acute Myocardial Ischemia-Reperfusion Injury in Rats in Cardiopulmonary Bypass%葛根素对大鼠体外循环后心肌缺血再灌注损伤的保护作用及抗氧化应激机制的探讨

    Institute of Scientific and Technical Information of China (English)

    巩红岩; 秦元旭; 王更富; 王庆志

    2012-01-01

    目的:探讨葛根素对大鼠体外循环后心肌缺血再灌注损伤(myocardial ischemia-reperfusion injury,MIRI)的保护作用及抗氧化应激机制.方法:取健康雄性SD大鼠75只,随机分为5组:即假手术组(给予等体积的生理盐水)、MIRI模型组(给予等体积的生理盐水)、葛根素低、中、高剂量组(2,5,10 mg·kg-13个剂量).于再灌注开始时在储血槽内加入稀释葛根素10mL.在全麻手术下制造大鼠体外循环模型后,随即阻断大鼠升主动脉造成心肌缺血30 min然后开放升主动脉后再灌注180 min造成大鼠心肌缺血再灌注损伤模型(灌注24 h,用于测定心肌梗死面积).实验组和对照组分别给予葛根素和生理盐水.实验完成后留取大鼠心脏标本,观察大鼠心肌缺血区的心肌细胞凋亡情况;收集血清测定其抗氧化应激的指标:超氧化物歧化酶(SOD),丙二醛(MDA),谷胱甘肽(GSH),谷胱甘肽过氧化物酶(GSH-Px).结果:与模型组相比,葛根素的应用减少了MIRI大鼠的心肌细胞凋亡、心梗面积和血清中丙二醛的含量,增加了血清中超氧化物歧化酶、谷胱甘肽过氧化物酶的活性和谷胱甘肽的含量,并且随着剂量的增加保护效果尤为明显.结论:葛根素对MIRI大鼠具有抗氧化应激的作用,它能够剂量依赖性的减少心肌细胞凋亡,最终减少心肌梗死面积.%Objective: To investigate the protective mechanism of puerarin on acute myocardial ischemia -reperfusion injury( MIRI) in rats, and to explain the antioxidative mechanism involved. Method: Rat MIRI model was induced by ischemia for 30 min and reperfusion for 180 min. At the end of the 3 h reperfusion period (or 24 h for infarct. Size ), myocardial infarct size, myocardial apoptosis and the activity of antioxidative enzymes were measured. Result: Puerarin reduced infarct size, myocardial apoptosisand the serum level of malondialdehyde, increased the activity of superoxide dismutase and glutathione

  16. Quantitative T2 mapping for detecting myocardial edema after reperfusion of myocardial infarction: validation and comparison with T2-weighted images.

    Science.gov (United States)

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

    2013-06-01

    This study evaluates the clinical usefulness of T2 mapping for the detection of myocardial edema in the re-perfused acute myocardial infarction (MI). Cardiac MRIs were reviewed in 20 patients who had acute MI after reperfusion therapy. The regional T2 values and T2-weighted image (T2WI) signal intensities (SI) were measured in the infarcted and remote zones of the myocardium. Patients were divided into three groups according to the signal patterns of the infarcted myocardium on the T2WIs. The T2 values of the infarcted zones were compared on the T2 maps among the three groups. Validation of the T2 values was performed in the normal myocardium of seven healthy volunteers. There were no significant differences in mean T2WI-SI or T2 values in the normal myocardium of healthy volunteers compared to the remote myocardium of acute MI patients (p > 0.05). Mean SI on the T2WIs was significantly higher in the infarcted myocardium (81.3 ± 37.6) than in the remote myocardium (63.8 ± 18.1) (p infarcted myocardium, compared to the remote myocardium. The T2 maps showed that T2 values in the infarcted myocardium had mostly increased, regardless of group, with values of 71 ± 9 ms in group 1, 64.9 ± 7.4 ms in group 2, and 61.4 ± 8.5 ms in group 3. T2 mapping is superior to T2WI for detecting areas of high SI in the infarcted myocardium. Therefore, quantitative T2 mapping sequences may be more useful and reliable in identifying myocardial edema in the infarcted myocardium than T2WI.

  17. Salidroside attenuates myocardial ischemia-reperfusion injury via PI3K/Akt signaling pathway.

    Science.gov (United States)

    Xu, Mao-Chun; Shi, Hai-Ming; Gao, Xiu-Fang; Wang, Hao

    2013-01-01

    To investigate the cardioprotective effects of salidroside on myocardial ischemia-reperfusion injury (IRI) in rabbits and the underlying action mechanisms in PI3K/Akt signaling pathway, a rabbit ischemia/reperfusion model was created by ligating the left anterior descending coronary arterial branch for 30 min and by releasing the ligature to allow reperfusion for 120 min. Salidroside or salidroside+PI3K inhibitor (LY294002) was administered via intracoronary injections at the onset of reperfusion. Apoptosis of cardiomyocytes was assessed by terminal dUTP nick-end labeling assay, and the expression of apoptosis-related proteins was observed by immunohistochemistry. The expressions of total Akt and phosphorylated Akt (p-Akt) were detected by western blot analysis. The results showed that intracoronary injection of salidroside at the onset of reperfusion markedly reduced the apoptosis of cardiomyocytes, significantly increasing Bcl-2 and p-Akt proteins expressions and decreasing Bax and caspase-3 expressions in the hearts subjected to ischemia followed by 120-min reperfusion. However, the anti-apoptotic effect induced by salidroside was inhibited by LY294002, which blocked the activation of Akt. These results suggested that intracoronary administration of salidroside at the onset of reperfusion could significantly reduce the IRI-induced apoptosis of cardiomyocytes, and this protective mechanism seemed to be mediated by the PI3K-Akt signaling pathway.

  18. Cyclosporin variably and inconsistently reduces infarct size in experimental models of reperfused myocardial infarction: a systematic review and meta-analysis.

    Science.gov (United States)

    Lim, W Y; Messow, C M; Berry, C

    2012-04-01

    Cyclosporin is an immunosuppressant that has recently been proposed as a treatment to prevent reperfusion injury in acute myocardial infarction (MI). We aimed to determine the overall efficacy of cyclosporin in experimental studies of acute reperfused MI. We conducted a systematic review and stratified meta-analysis of published studies describing the efficacy of cyclosporin in experimental models of acute reperfused MI. We included all in vivo publications of cyclosporin where infarct size was measured. A literature search identified 29 potential studies of which 20 fulfilled the eligibility criteria. In these studies (involving four species of animals), cyclosporin reduced myocardial infarct size by a standardized mean (95% confidence interval) difference of -1.60 (-2.17, -1.03) compared with controls. Cyclosporin failed to demonstrate a convincing benefit in studies involving pigs. Despite this observation, the overall efficacy of cyclosporin did not differ across species (P= 0.358). The dose of cyclosporin given did not affect final infarct size (P= 0.203). Funnel plots of these data suggested heterogeneity among the studies. Cyclosporin had variable effects on infarct size compared with placebo. Cyclosporin had no effect on myocardial infarct size in swine, raising a question over the potential cardioprotective effects of cyclosporin in man. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.

  19. Phellinus linteus Mycelium Alleviates Myocardial Ischemia-Reperfusion Injury through Autophagic Regulation

    Science.gov (United States)

    Su, Hsing-Hui; Chu, Ya-Chun; Liao, Jiuan-Miaw; Wang, Yi-Hsin; Jan, Ming-Shiou; Lin, Chia-Wei; Wu, Chiu-Yeh; Tseng, Chin-Yin; Yen, Jiin-Cherng; Huang, Shiang-Suo

    2017-01-01

    The incidence of myocardial ischemia-reperfusion (IR) injury is rapidly increasing around the world and this disease is a major contributor to global morbidity and mortality. It is known that regulation of programmed cell death including apoptosis and autophagy reduces the impact of myocardial IR injury. In this study, the cardioprotective effects and underlying mechanisms of Phellinus linteus (Berk. and Curt.) Teng, Hymenochaetaceae (PL), a type of medicinal mushroom, were examined in rats subjected to myocardial IR injury. The left main coronary artery of rats was ligated for 1 h and reperfused for 3 h. The arrhythmia levels were monitored during the entire process and the infarct size was evaluated after myocardial IR injury. Furthermore, the expression levels of proteins in apoptotic and autophagic pathways were observed. Pretreatment with PL mycelium (PLM) significantly reduced ventricular arrhythmia and mortality due to myocardial IR injury. PLM also significantly decreased myocardial infarct size and plasma lactate dehydrogenase level after myocardial IR injury. Moreover, PLM administration resulted in decreased caspase 3 and caspase 9 activation and increased Bcl-2/Bax ratio. Phosphorylation level of AMPK was elevated while mTOR level was reduced. Becline-1 and p62 levels decreased. These findings suggest that PLM is effective in protecting the myocardium against IR injury. The mechanism involves mediation through suppressed pro-apoptotic signaling and regulation of autophagic signaling, including stimulation of AMPK-dependent pathway and inhibition of beclin-1-dependent pathway, resulting in enhancement of protective autophagy and inhibition of excessive autophagy. PMID:28420993

  20. Cardioprotective Effect of the Aqueous Extract of Lavender Flower against Myocardial Ischemia/Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Dong Wang

    2014-01-01

    Full Text Available This study was conducted to evaluate the cardioprotective property of the aqueous extract of lavender flower (LFAE. The myocardial ischemia/reperfusion (I/R injury of rat was prepared by Langendorff retrograde perfusion technology. The heart was preperfused with K-H solution containing LFAE for 10 min before 20 minutes global ischemia, and then the reperfusion with K-H solution was conducted for 45 min. The left ventricular developed pressure (LVDP and the maximum up/downrate of left ventricular pressure (±dp/dtmax were recorded by physiological recorder as the myocardial function and the myocardial infarct size was detected by TTC staining. Lactate dehydrogenase (LDH and creatine kinase (CK activities in the effluent were measured to determine the myocardial injury degree. The superoxide anion dismutase (SOD and malondialdehyde (MDA in myocardial tissue were detected to determine the oxidative stress degree. The results showed that the pretreatment with LFAE significantly decreased the myocardial infarct size and also decreased the LDH, CK activities, and MDA level, while it increased the LVDP, ±dp/dtmax, SOD activities, and the coronary artery flow. Our findings indicated that LFAE could provide protection for heart against the I/R injury which may be related to the improvement of myocardial oxidative stress states.

  1. Reperfusion Therapies of Acute Ischemic Stroke: potentials and failures

    Directory of Open Access Journals (Sweden)

    Georgios eTsivgoulis

    2014-12-01

    Full Text Available Over the past twenty years clinical research has focused on the development of reperfusion therapies for acute ischemic stroke (AIS, which include the use of systemic intravenous thrombolytics (alteplase, desmoteplase or tenecteplase, the augmentation of systemic intravenous recanalization with ultrasound, the bridging of intravenous with intra-arterial thrombolysis, the use of multi-modal approaches to reperfusion including thrombectomy and thromboaspiration with different available retrievers. Clinical trials testing these acute reperfusion therapies provided novel insight regarding the comparative safety and efficacy, but also raised new questions and further uncertainty on the field. Intravenous alteplase (tPA remains the fastest and easiest way to initiate acute stroke reperfusion treatment, and should continue to be the first-line treatment for patients with AIS within 4.5 hours from onset. The use of tenecteplase instead of tPA and the augmentation of systemic thrombolysis with ultrasound are both novel therapeutical modalities that may emerge as significant options in AIS treatment. Endovascular treatments for AIS are rapidly evolving due to technological advances in catheter-based interventions and are currently emphasizing speed in order to result in timely restoration of perfusion of still-salvageable, infracted brain tissue, since delayed recanalization of proximal intracranial occlusions has not been associated with improved clinical outcomes. Comprehensive imaging protocols in AIS may enable better patient selection for endovascular interventions and for testing multi-modal combinatory strategies.

  2. Blockage of transient receptor potential vanilloid 4 alleviates myocardial ischemia/reperfusion injury in mice

    Science.gov (United States)

    Dong, Qian; Li, Jing; Wu, Qiong-feng; Zhao, Ning; Qian, Cheng; Ding, Dan; Wang, Bin-bin; Chen, Lei; Guo, Ke-Fang; Fu, Dehao; Han, Bing; Liao, Yu-Hua; Du, Yi-Mei

    2017-01-01

    Transient receptor potential vanilloid 4 (TRPV4) is a Ca2+-permeable nonselective cation channel and can be activated during ischemia/reperfusion (I/R). This study tested whether blockade of TRPV4 can alleviate myocardial I/R injury in mice. TRPV4 expression began to increase at 1 h, reached statistically at 4 h, and peaked at 24–72 h. Treatment with the selective TRPV4 antagonist HC-067047 or TRPV4 knockout markedly ameliorated myocardial I/R injury as demonstrated by reduced infarct size, decreased troponin T levels and improved cardiac function at 24 h after reperfusion. Importantly, the therapeutic window for HC-067047 lasts for at least 12 h following reperfusion. Furthermore, treatment with HC-067047 reduced apoptosis, as evidenced by the decrease in TUNEL-positive myocytes, Bax/Bcl-2 ratio, and caspase-3 activation. Meanwhile, treatment with HC-067047 attenuated the decrease in the activation of reperfusion injury salvage kinase (RISK) pathway (phosphorylation of Akt, ERK1/2, and GSK-3β), while the activation of survival activating factor enhancement (SAFE) pathway (phosphorylation of STAT3) remained unchanged. In addition, the anti-apoptotic effects of HC-067047 were abolished by the RISK pathway inhibitors. We conclude that blockade of TRPV4 reduces apoptosis via the activation of RISK pathway, and therefore might be a promising strategy to prevent myocardial I/R injury. PMID:28205608

  3. 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.

  4. Differential effects of heptanoate and hexanoate on myocardial citric acid cycle intermediates following ischemia-reperfusion.

    Science.gov (United States)

    Okere, Isidore C; McElfresh, Tracy A; Brunengraber, Daniel Z; Martini, Wenjun; Sterk, Joseph P; Huang, Hazel; Chandler, Margaret P; Brunengraber, Henri; Stanley, William C

    2006-01-01

    In the normal heart, there is loss of citric acid cycle (CAC) intermediates that is matched by the entry of intermediates from outside the cycle, a process termed anaplerosis. Previous in vitro studies suggest that supplementation with anaplerotic substrates improves cardiac function during myocardial ischemia and/or reperfusion. The present investigation assessed whether treatment with the anaplerotic medium-chain fatty acid heptanoate improves contractile function during ischemia and reperfusion. The left anterior descending coronary artery of anesthetized pigs was subjected to 60 min of 60% flow reduction and 30 min of reperfusion. Three treatment groups were studied: saline control, heptanoate (0.4 mM), or hexanoate as a negative control (0.4 mM). Treatment was initiated after 30 min of ischemia and continued through reperfusion. Myocardial CAC intermediate content was not affected by ischemia-reperfusion; however, treatment with heptanoate resulted in a more than twofold increase in fumarate and malate, with no change in citrate and succinate, while treatment with hexanoate did not increase fumarate or malate but increased succinate by 1.8-fold. There were no differences among groups in lactate exchange, glucose oxidation, oxygen consumption, and contractile power. In conclusion, despite a significant increase in the content of carbon-4 CAC intermediates, treatment with heptanoate did not result in improved mechanical function of the heart in this model of reversible ischemia-reperfusion. This suggests that reduced anaplerosis and CAC dysfunction do not play a major role in contractile and metabolic derangements observed with a 60% decrease in coronary flow followed by reperfusion.

  5. 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.

  6. Coronary flow velocity analysis during short term follow up after coronary reperfusion: use of transthoracic Doppler echocardiography to predict regional wall motion recovery in patients with acute myocardial infarction

    OpenAIRE

    Hozumi, T; Kanzaki, Y; Ueda, Y.; Yamamuro, A; Takagi, T; Akasaka, T; Homma, S; Yoshida, K.; Yoshikawa, J

    2003-01-01

    Background: A recent study using a Doppler guide wire showed that coronary flow velocity measurements immediately after coronary reperfusion were useful in predicting recovery of regional left ventricular function. The value of coronary flow velocity analyses during follow up after reperfusion has not been established in the clinical setting.

  7. Impact of active smoking on myocardial infarction severity in reperfused ST-segment elevation myocardial infarction patients: the smoker's paradox revisited.

    Science.gov (United States)

    Symons, Rolf; Masci, Pier Giorgio; Francone, Marco; Claus, Piet; Barison, Andrea; Carbone, Iacopo; Agati, Luciano; Galea, Nicola; Janssens, Stefan; Bogaert, Jan

    2016-09-21

    To investigate the influence of cardiovascular risk factors (CV-RFs) on infarct severity and post-infarction left ventricular (LV) remodelling in acutely reperfused ST-segment elevation myocardial infarction (STEMI) patients studied with cardiovascular magnetic resonance (CMR). Four-hundred seventy-one patients were included in the study. Baseline CMR was performed at 4 ± 1 days after STEMI to assess area-at-risk, infarct size (IS), myocardial salvage index (MSI), microvascular obstruction (MVO), intramyocardial haemorrhage (IMH), LV volumes, and function. Cardiovascular magnetic resonance was repeated 4 months after STEMI (n = 383) to assess adverse LV remodelling (increase of LV end-diastolic volume >20% between baseline and follow-up). Smoking was associated with IMH at baseline even after correction for other factors associated with ischaemia-reperfusion injury including MVO, IS, and MSI (OR: 2.17, 95% CI: 1.17-4.00, P = 0.01). Unexpectedly, smoking was an independent protective predictor against adverse LV remodelling (OR: 0.43, 95% CI: 0.24-0.77, P = 0.005), consistent with the 'smoker's paradox'. However, the presence of IMH at baseline abolished the paradoxical, beneficial effects of smoking with respect to IS, baseline LV function, and post-infarction LV remodelling. No association between other CV-RFs, infarct severity, or post-infarction LV remodelling was observed. In patients with reperfused STEMI, smoking is strongly and independently associated with IMH at baseline. Nonetheless, consistent with the 'smoker's paradox', smoking was an independent predictor of more favourable post-infarction LV remodelling. However, the paradoxical beneficial effects of smoking were lost in patients with IMH. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.

  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. 血栓抽吸联合替罗非班对急性ST段抬高型心肌梗死患者心肌再灌注及预后的影响研究%Influence of Thrombus Aspiration Combined With Tirofiban Therapy on Myocardial Reperfusion and Clinical prognosis of patients With Acute ST -elevation Myocardial Infarction

    Institute of Scientific and Technical Information of China (English)

    赵良平; 徐卫亭; 陈建昌; 肖飞; 邵春来; 李晖; 江建良; 罗小雨

    2015-01-01

    目的:评估血栓抽吸联合替罗非班对急性ST段抬高型心肌梗死( STEMI)患者早期经皮冠状动脉介入( PCI)术后心肌再灌注及预后的影响。方法连续选取2008年1月—2013年1月于苏州大学附属第二医院就诊的急性STEMI患者456例,采用随机数字表法分为:单纯PCI组(对照组)140例;血栓抽吸组168例;血栓抽吸+替罗非班组148例。比较各组PCI术后心肌梗死溶栓试验( TIMI)心肌再灌注( TMP)分级、校正的TIMI帧数( CTFC)、术后1个月和术后12个月主要不良心脏事件( MACE)发生情况。采用多因素Logistic回归分析急性STEMI患者术后1个月和术后12个月发生MACE的影响因素。结果3组患者梗死血管和病变血管支数比较,差异均无统计学意义( P>0.05);3组患者PCI术后TMP分级及药物洗脱支架使用率比较,差异均有统计学意义(P0. 05);the three groups were significantly different in TMP grading and the number of drug eluting stent(P<0. 05). The CTFCs of control group,thrombus aspiration group and thrombus aspiration + tirofiban group were(31. 5 ± 5. 8), (21. 8 ± 7. 2)and ( 20. 9 ± 6. 3 ) respectively, with significant differences among the three groups( F = 5. 176, P = 0. 006 );thrombus aspiration group and thrombus aspiration+ tirofiban group were lower than control group in CTFC(q=3. 225,3. 734;P<0. 001 ). Multivariate Logistic regression analysis showed that diabetes mellitus, serum creatinine level, left ventricular ejection fraction had regression relation with the MACE incidence of acute STEMI patients at 1 month after operation(P<0. 05);age,serum creatinine level, left ventricular ejection fraction and therapeutic method had regression relation with the MACE incidence of acute STEMI patients at 12 months after operation ( P <0. 05 ) . Conclusion The combined use of thrombus aspiration and tirofiban can effectively improve the myocardial reperfusion level of acute

  10. THE ROLE OF MYOCARDIAL ISCHEMIC POSTCONDITIONING AND TOLL-LIKE RECEPTORS IN MYOCARDIAL REPERFUSION INJURY%心肌缺血后适应和Toll样受体在心肌再灌注损伤中的作用

    Institute of Scientific and Technical Information of China (English)

    王妮妮; 王悦喜

    2014-01-01

    近年来随着急性心肌梗死发病率的不断增高,促进了溶栓、经皮穿刺冠状动脉介入治疗和冠状动脉旁路移植术( CABG)等再灌注疗法的广泛开展,由缺血/再灌注损伤( ischemia/reperfusion injury,IRI)引起的心脏损伤日益受到重视。因此,研究减轻心肌缺血/再灌注损伤安全、有效的方法对防治心脏疾病具有重大的价值和意义。近期国内外很多研究发现心肌缺血后适应(ischemic postconditioning,IPOC)及 Toll 样受体(Toll like receptor,TRL)在心肌缺血再灌注损伤中起重要作用,本文对此进行综述。%In recent years,the thrombolysis,percutaneous coronary intervention and coronary artery bypass grafting( CABG) and other reperfusion therapy are widely developing with incidence increasing of acute myocardial infarction. Heart damage induced by the ischemia/reperfusion injury ( ischemia/reperfusion injury,IRI) is increasingly concerned. Therefore,the study of safe and effective method in reducing myocardial ischemia/reperfusion injury has great value and significance in the prevention of heart disease. Recently many domestic and foreign researches found that ischemic postconditioning (IPOC)and toll-like receptors(Toll like receptor,TRL)play important role in myocardial ischemia-reperfusion injury.

  11. Selective cyclooxygenase-2 inhibition protects against myocardial damage in experimental acute ischemia

    Directory of Open Access Journals (Sweden)

    Alberto Carnieto Jr.

    2009-03-01

    Full Text Available BACKGROUND: Acute myocardial infarction is associated with tissue inflammation. Early coronary reperfusion clearly improves the outcome but may help propagate the inflammatory response and enhance tissue damage. Cyclooxygenase-2 is an enzyme that catalyzes the initial step in the formation of inflammatory prostaglandins from arachidonic acid. Cyclooxygenase-2 levels are increased when ischemic cardiac events occur. The overall function of COX-2 in the inflammatory process generated by myocardial ischemic damage has not yet been elucidated. GOAL: The objective of this study was to determine whether a selective cyclooxygenase-2 inhibitor (rofecoxib could alter the evolution of acute myocardial infarction after reperfusion. METHODS AND RESULTS: This study was performed with 48 mongrel dogs divided into two groups: controls and those treated with the drug. All animals were prepared for left anterior descending coronary artery occlusion. The dogs then underwent 180 minutes of coronary occlusion, followed by 30 minutes of reperfusion. Blood samples were collected from the venous sinus immediately before coronary occlusion and after 30 minutes of reperfusion for measurements of CPK-MB, CPK-MBm and troponin I. During the experiment we observed the mean blood pressure, heart rate and coronary flow. The coronary flow and heart rate did not change, but in the control group, there was blood pressure instability, in addition to maximal levels of CPK-MB post-infarction. The same results were observed for CPK-MBm and troponin I. CONCLUSION: In a canine model of myocardial ischemia-reperfusion, selective inhibition of Cyclooxygenase-2 with rofecoxib was not associated with early detrimental effects on the hemodynamic profile or the gross extent of infarction; in fact, it may be beneficial by limiting cell necrosis.

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

    Science.gov (United States)

    Gorressen, Simone; Stern, Manuel; van de Sandt, Annette M; Cortese-Krott, Miriam M; Ohlig, Jan; Rassaf, Tienush; Gödecke, Axel; Fischer, Jens W; Heusch, Gerd; Merx, Marc W; Kelm, Malte

    2015-01-01

    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; *pNOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.

  13. Molecular Characterization of Reactive Oxygen Species in Myocardial Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Tingyang Zhou

    2015-01-01

    Full Text Available Myocardial ischemia-reperfusion (I/R injury is experienced by individuals suffering from cardiovascular diseases such as coronary heart diseases and subsequently undergoing reperfusion treatments in order to manage the conditions. The occlusion of blood flow to the tissue, termed ischemia, can be especially detrimental to the heart due to its high energy demand. Several cellular alterations have been observed upon the onset of ischemia. The danger created by cardiac ischemia is somewhat paradoxical in that a return of blood to the tissue can result in further damage. Reactive oxygen species (ROS have been studied intensively to reveal their role in myocardial I/R injury. Under normal conditions, ROS function as a mediator in many cell signaling pathways. However, stressful environments significantly induce the generation of ROS which causes the level to exceed body’s antioxidant defense system. Such altered redox homeostasis is implicated in myocardial I/R injury. Despite the detrimental effects from ROS, low levels of ROS have been shown to exert a protective effect in the ischemic preconditioning. In this review, we will summarize the detrimental role of ROS in myocardial I/R injury, the protective mechanism induced by ROS, and potential treatments for ROS-related myocardial injury.

  14. 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.

  15. Effect of pre- and posttreatment of losartan in feline model of myocardial ischemic-reperfusion injury.

    Science.gov (United States)

    Kumari, R; Manchanda, S C; Maulik, S K

    2004-01-01

    This study investigated the differential effect of losartan, an AT1 receptor blocker, when administered in pre- and postischemic phases, on the biochemical, hemodynamic and oxidative stress associated with regional ischemic-reperfusion injury in cat. Losartan (5 microg/kg/min) or normal saline was administered intravenously in open chest barbiturate anesthetized cats, 15 min before and 10 min after the occlusion of the left anterior descending (LAD) coronary artery. The LAD was occluded for 15 min followed by 60 min reperfusion. In the saline treated group, there was significant depression of hemodynamic functions, i.e., mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP) and left ventricular (LV) peak (+/-) dP/dt, along with depletion of adenosine triphosphate (ATP) of the affected myocardium. Oxidative stress during reperfusion injury was evidenced by significant increase in plasma thiobarbituric acid reactive substances (TBARS) accompanied by significant reduction in myocardial superoxide dismutase (SOD) activities. In both treatment groups, losartan caused recovery of all the hemodynamic parameters and repletion of ATP along with no significant change in plasma TBARS and myocardial SOD activity. There was no effect on catalase activity. Results from the study suggest that the effects of pre- and posttreatment of losartan are comparable in functional recovery of the heart from ischemic-reperfusion injury. (c) 2004 Prous Science. All rights reserved.

  16. Acidic HEPES-KH Reperfusion Enhances Myocardial Protection in Immature Rabbits

    Institute of Scientific and Technical Information of China (English)

    孙忠东; 杨辰垣; 邢建洲; 陈涛; 董念国; 罗军

    2002-01-01

    Summary: To study the effects of different pH HEPES-KH reperfusate solution on immature myocardial protection, isolated perfused Langendorff model from immature rabbit hearts were developed formed. Control group (C) was perfused only with pH 7. 4 HEPES-KH solution for 90 min. Is chemia/reperfusion group (group I/R) was perfused with pH 7. 4 HEPES-KH solution before is chemia or after ischemia. Experimental group (group E), after ischemia, was perfused with pH 6.8,pH 7. 1 and pH7.4 HEPES-KH solutions for 5 min, 5 min, and 20 min, respectively. The left ven tricular function recovery, MWC, LDH and CK leakage, MDA, ATP content, and SOD activity were determined. Our results showed that the left ventricular function recovery, ATP content and SOD activity in group E were higher than those of group I/R (P<0. 05). MWC, MDA content,LDH and CK leakage in group E were lower than those of group I/R (P<0. 05). These findings suggested that pH paradox might be one of important mechanisms for immature myocardial ischemia reperfusion injury, and acidic perfusate, at the beginning of reperfusion, might attenuate pH paradox and ameliorate functional recovery in isolated perfused immature rabbit hearts.

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

    OpenAIRE

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

    2015-01-01

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

  18. [Characteristics of therapy of acute myocardial infarction in diabetes].

    Science.gov (United States)

    Motz, W; Kerner, W

    2012-05-01

    Therapy of acute myocardial infarction (STEMI and NSTEMI) in diabetics does not principally differ from that of non-diabetic patients. Due to the higher mortality in diabetics reperfusion measures, such as direct percutaneous coronary intervention (PCI), should be rapidly performed. An intensive drug treatment with thrombocyte aggregation inhibitors, angiotensin-converting enzyme (ACE) inhibitors and beta-receptor blocking agents must be carried out according to the current guidelines. An important factor is the high risk of renal failure due to the contrast dye administered during PCI in the presence of pre-existing diabetic kidney damage which should be limited to 100 ml if possible. Direct PCI should be limited to the infarcted vessel. After stabilization a comprehensive strategy to cure coronary artery disease, whether with PCI or coronary artery bypass graft (CABG) should be finalized. If severe coronary 3-vessel disease is present, CABG should be favored in diabetic patients. After surviving an acute myocardial infarction differentiated metabolic monitoring is mandatory.

  19. Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction.

    Science.gov (United States)

    de Couto, Geoffrey; Liu, Weixin; Tseliou, Eleni; Sun, Baiming; Makkar, Nupur; Kanazawa, Hideaki; Arditi, Moshe; Marbán, Eduardo

    2015-08-03

    Ischemic injury in the heart induces an inflammatory cascade that both repairs damage and exacerbates scar tissue formation. Cardiosphere-derived cells (CDCs) are a stem-like population that is derived ex vivo from cardiac biopsies; they confer both cardioprotection and regeneration in acute myocardial infarction (MI). While the regenerative effects of CDCs in chronic settings have been studied extensively, little is known about how CDCs confer the cardioprotective process known as cellular postconditioning. Here, we used an in vivo rat model of ischemia/reperfusion (IR) injury-induced MI and in vitro coculture assays to investigate how CDCs protect stressed cardiomyocytes. Compared with control animals, animals that received CDCs 20 minutes after IR had reduced infarct size when measured at 48 hours. CDCs modified the myocardial leukocyte population after ischemic injury. Specifically, introduction of CDCs reduced the number of CD68+ macrophages, and these CDCs secreted factors that polarized macrophages toward a distinctive cardioprotective phenotype that was not M1 or M2. Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection. Using both in vitro coculture assays and a rat model of adoptive transfer after IR, we determined that CDC-conditioned macrophages attenuated cardiomyocyte apoptosis and reduced infarct size, thereby recapitulating the beneficial effects of CDC therapy. Together, our data indicate that CDCs limit acute injury by polarizing an effector macrophage population within the heart.

  20. Infarct healing is a dynamic process following acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Pokorney Sean D

    2012-09-01

    Full Text Available Abstract Background The role of infarct size on left ventricular (LV remodeling in heart failure after an acute ST-segment elevation myocardial infarction (STEMI is well recognized. Infarct size, as determined by cardiovascular magnetic resonance (CMR, decreases over time. The amount, rate, and duration of infarct healing are unknown. Methods A total of 66 patients were prospectively enrolled after reperfusion for an acute STEMI. Patients underwent a CMR evaluation within 1 week, 4 months, and 14 months after STEMI. Results Mean infarct sizes for the 66 patients at baseline (acute necrosis, early follow-up (early scar, and late follow-up (late scar were 25 ± 17 g, 17 ± 12 g, and 15 ± 11 g, respectively. Patients were stratified in tertiles, based on infarct size, with the largest infarcts having the greatest absolute decrease in mass at early and late scar. The percent reduction of infarct mass was independent of initial infarct size. There was an 8 g or 32% decrease in infarct mass between acute necrosis and early scar (p  Conclusions Infarct healing is a continuous process after reperfusion for STEMI, with greatest reduction in infarct size in the first few months. The dynamic nature of infarct healing through the first year after STEMI indicates that decisions based on infarct size, and interventions to reduce infarct size, must take into consideration the time frame of measurement.

  1. Methylprednisolone improves microcirculation in streptozotocin-induced diabetic rats after myocardial ischemia/reperfusion

    Institute of Scientific and Technical Information of China (English)

    HU Zhi-cheng; CHEN Yun-dai; REN Yi-hong

    2011-01-01

    Background Methylprednisolone has been demonstrated to decrease inflammation, and it may protect organs from ischemia/reperfusion (I/R) injury. This study aimed to investigate the effects of methylprednisolone on diabetic myocardial I/R injury.Methods Forty adult male Sprague-Dawley (SD) rats were randomized into five groups (n=8 in each group) including a sham operation (sham) group, I/R group, diabetic sham operation (DMS) group, diabetic I/R (DM-I/R) group and methylprednisolone intervention (MP+DM-I/R) group. The diabetic model was produced by injection of streptozotocin (STZ). Body weight and blood glucose levels were determined after diabetes was established. Twelve weeks after induction of diabetes, a segmental I/R of the heart was induced by occluding the left anterior descending artery for one hour and then three hours of reperfusion in the I/R, DM-I/R and MP+DM-I/R groups. Blood pressure and electrocardiogram were continuously recorded during the procedure. IL-1β, IL-6 and TNF-α were measured at certain time points during the surgery. After reperfusion, a microcirculation scan was performed; myocardial biomarkers and tissue structure were utilized to evaluate the reperfusion damage. Intercellular adhesion molecule (ICAM)-1 and NF-κBp65 expression were quantified by immunohistological staining. Total Toil-like receptor 4 (TLR4) and nuclear NF-κBp65 protein were determined by Western blotting.Results Twelve weeks after diabetes was established, blood glucose levels were elevated and body weights were lower in diabetic rats. After reperfusion, infarction size was increased, myocardial biomarkers and inflammatory cytokines levels were elevated. Microcirculation perfusion was significantly reduced in the DM-I/R group compared with the I/R group, however it was improved in the MP+DM-I/R group. The expression of NF-κBp65 and ICAM-1 were increased in the DM-I/R group and decreased in the MP+DM-I/R group, Compared with the non-diabetic I/R group, TLR4 and NF

  2. "DETERMINANTS OF PREHOSPITAL DELAY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION"

    Directory of Open Access Journals (Sweden)

    M. Alidoosti

    2004-05-01

    Full Text Available Determination of pre-hospital delay time of patients with acute myocardial infarction and seeking ways of speeding up the time for reperfusion is an important factor to lower mortality in these patients. This is a cross-sectional study to determine pre-hospital delay time, its components, and related causes and conditions, obtained in 375 patients with prolonged chest pain referred to four hospitals of Tehran University of Medical Sciences. Means of transport to hospital, reasons of ambulance disuse, decision time by the patient and finally the entire time of pre-hospital delay were specified. Suspected factors related to delays of more than 2 and 6 h were scrutinized with chi-square test. Rate of ambulance utility (18.9% directly correlated with age of patients (P<0.05. Principal motives to disuse ambulance insuccession were unrememberance (33.7%, access to private vehicle (32.8% and supposition of sufficient speed of personal reference (18.9%. Pre-hospital delay time was 8.1 ± 9.1 h (mean ± SD in whole patients and 7.6 ± 9.1 h in those with acute myocardial infarction. Delays of more than 2 and 6 hoccurred in 67.5% and 33.6% of patients, respectively. Decision time constitute three fourth of whole pre-hospital delay and was correlated with female gender, older age, history of diabetes, lower level of literacy and nocturnal onset of symptoms. In conclusion, a significant number of patients with acute myocardial infarction have pre-hospital delay of more than 2 and even 6 h, when golden time for thrombolytic therapy has already been elapsed.

  3. 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

  4. 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

  5. Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats

    Directory of Open Access Journals (Sweden)

    Shiao Ding

    2016-01-01

    Full Text Available Objective. To investigate the protective effects of L-malate against myocardial ischemia/reperfusion (I/R injury in rats. Methods. Male Sprague-Dawley rats were randomly assigned to the following groups: sham (sham, an ischemia/reperfusion (I/R model group (model, an DMF pretreated group (DMF, and 5 L-malate pretreated groups (15, 60, 120, 240, or 480 mg/kg, gavage before inducing myocardial ischemia. Plasma LDH, cTn-I, TNF-α, hs-CRP, SOD, and GSH-PX were measured 3 h later I/R. Areas of myocardial infarction were measured; hemodynamic parameters during I/R were recorded. Hearts were harvested and Western blot was used to quantify Nrf2, Keap1, HO-1, and NQO-1 expression in the myocardium. Results. L-malate significantly reduced LDH and cTn-I release, reduced myocardial infarct size, inhibited expression of inflammatory cytokines, and partially preserved heart function, as well as increasing antioxidant activity after myocardial I/R injury. Western blot confirmed that L-malate reduced Kelch-like ECH-associated protein 1 in ischemic myocardial tissue, upregulated expression of Nrf2 and Nrf2 nuclear translocation, and increased expression of heme oxygenase-1 and NAD(PH:quinone oxidoreductase 1, which are major targets of Nrf2. Conclusions. L-malate may protect against myocardial I/R injury in rats and this may be associated with activation of the Nrf2/Keap1 antioxidant pathway.

  6. Inhibition of ALDH2 by O-GlcNAcylation contributes to the hyperglycemic exacerbation of myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    Liu, Baoshan; Wang, Jiali; Li, Minghua; Yuan, Qiuhuan; Xue, Mengyang; Xu, Feng; Chen, Yuguo

    2016-12-27

    Although hyperglycemia is causally related to adverse outcomes after myocardial ischemia/reperfusion (I/R), the underlying mechanisms are largely unknown. Here, we investigated whether excessive O-linked-N-acetylglucosamine (O-GlcNAc) modification of acetaldehyde dehydrogenase 2 (ALDH2), an important cardioprotective enzyme, was a mechanism for the hyperglycemic exacerbation of myocardial I/R injury. Both acute hyperglycemia (AHG) and diabetes (DM)-induced chronic hyperglycemia increased cardiac dysfunction, infarct size and apoptosis index compared with normal saline (NS)+I/R rats (PO-GlcNAc modification was increased whereas its activity was decreased in AHG+I/R and DM+I/R rats. High glucose (HG, 30mmol/L) markedly increased ALDH2 O-GlcNAc modification compared with Con group (5mmol/L) (PO-GlcNAc modification was increased by 62.9% in Con+PUGNAc group whereas it was decreased by 44.1% in Con+DON group compared with Con group (PO-GlcNAc modification and improved infarct size, apoptosis index and cardiac dysfunction induced by I/R combined with hyperglycemia. These findings demonstrate that ALDH2 O-GlcNAc modification is a key mechanism for the hyperglycemic exacerbation of myocardial I/R injury and Alda-1 has therapeutic potential for inducing cardioprotection.

  7. Relationship between nonsustained ventricular tachycardia after non-ST-elevation acute coronary syndrome and sudden cardiac death: observations from the metabolic efficiency with ranolazine for less ischemia in non-ST-elevation acute coronary syndrome-thrombolysis in myocardial infarction 36 (MERLIN-TIMI 36) randomized controlled trial.

    NARCIS (Netherlands)

    Scirica, B.M.; Braunwald, E.; Belardinelli, L.; Hedgepeth, C.M.; Spinar, J.; Wang, W.; Qin, J.; Karwatowska-Prokopczuk, E.; Verheugt, F.W.A.; Morrow, D.A.

    2010-01-01

    BACKGROUND: Most studies examining the relationship between ventricular tachycardia (VT) after acute coronary syndrome and sudden cardiac death (SCD) were performed before widespread use of reperfusion, revascularization, or contemporary medical therapy and were limited to ST-elevation myocardial in

  8. Quality indicators for acute myocardial infarction

    DEFF Research Database (Denmark)

    Schiele, Francois; Gale, Chris P; Bonnefoy, Eric

    2016-01-01

    infarction (AMI), but no such indicators exist in Europe. In this context, the European Society of Cardiology (ESC) Acute Cardiovascular Care Association (ACCA) has reflected on the measurement of quality of care in the context of AMI (ST segment elevation myocardial infarction (STEMI) and non-ST segment...... be estimated solely on the basis of patients' clinical outcomes. Thus, measuring the process of care through quality indicators (QIs) has become a widely used practice in this context. Other professional societies have published QIs for the evaluation of quality of care in the context of acute myocardial...... elevation myocardial infarction (NSTEMI)) and created a set of QIs, with a view to developing programmes to improve quality of care for the management of AMI across Europe. We present here the list of QIs defined by the ACCA, with explanations of the methodology used, scientific justification and reasons...

  9. Mechanism of Total Polyphenols Extracted from Toona sinensis Roem on Acute Inflammation during Myocardial Ischemia-reperfusion in Rats%基于炎症反应的香椿子总多酚抗大鼠心肌缺血再灌注损伤的机制研究

    Institute of Scientific and Technical Information of China (English)

    李红月; 陈超

    2012-01-01

    目的:观察香椿子总多酚对大鼠心肌缺血再灌注急性炎症的影响.方法:50只SD大鼠随机分成假手术组(冠脉下穿线不结扎+0.5%羧甲基纤维素钠)、模型组(冠脉结扎+0.5%羧甲基纤维素钠)、香椿子总多酚低剂量(XD,50 mg· kg-1+冠脉结扎)、中剂量(XZ,100 mg·kg-1+冠脉结扎)、高剂量(XG,200 mg· kg-1+冠脉结扎)组,各组均ig给药.采用左冠状动脉前降支结扎30 min再灌120 min的方法复制大鼠心肌缺血再灌注损伤模型.以ST抬高作为结扎成功的标志,以ST段逐渐回落、梗死性Q波出现作为再灌注成功的标志.再灌结束后行腹主动脉取血,分离血清,测定血清中白介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)含量.取左心室缺血区组织10 mg用RT-PCR测定核因子kB (NF-kB)p65 mRNA的表达水平,其余心肌组织做病理切片,并在光镜下观察左心室心肌组织的形态学变化.结果:模型组大鼠血清IL-6含量为(638.88±188.94) ng·L-1,XD,XZ,XG组与模型组相比,血清IL-6含量显著下降,分别为(491.58±142.59),(306.85±80.60),(246.11 ±71.64) ng·L-1.模型组大鼠血清TNF-α含量为(216.23 ±58.67) ng·L-1,XD,XZ,XG组大鼠血清TNF-α水平与之相比显著降低,分别为(148.24 -±36.30),(157.62 ±52.06),(144.10 ±36.64) ng·L-1.模型组大鼠心肌组织中NF-kBp65/β-actin为0.61 ±0.05,香椿子总多酚给药组大鼠NF-kB p65/β-actin与之相比显著降低,分别为0.53 ±0.08,0.45 ±0.13,0.38 ±0.11.香椿子总多酚组与模型组相比,大鼠心肌细胞的形态学损伤较轻.结论:香椿子总多酚能够减轻大鼠心肌缺血再灌注急性炎症,对其产生一定的保护作用.%Objective: To investigate effects of total polyphenols extracted from Toona sinensis Roem on acute inflammation in injury induced by myocardial ischemia-reperfusion in rats. Method: Fifty SD rats were randomly divided into 5 groups: sham operation group, model group and total polyphenols extracted from T

  10. N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy

    Science.gov (United States)

    Wang, Sheng; Yan, Fuxia; Wang, Tingting; He, Yi

    2017-01-01

    Background. Excessive autophagy is a major mechanism of myocardial ischemia reperfusion injury (I/RI) in diabetes with enhanced oxidative stress. Antioxidant N-acetylcysteine (NAC) reduces myocardial I/RI. It is unknown if inhibition of autophagy may represent a mechanism whereby NAC confers cardioprotection in diabetes. Methods and Results. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5 g/kg/day) for four weeks before being subjected to 30-minute coronary occlusion and 2-hour reperfusion. The results showed that cardiac levels of 15-F2t-Isoprostane were increased and that autophagy was evidenced as increases in ratio of LC3 II/I and protein P62 and AMPK and mTOR expressions were significantly increased in diabetic compared to nondiabetic rats, concomitant with increased postischemic myocardial infarct size and CK-MB release but decreased Akt and eNOS activation. Diabetes was also associated with increased postischemic apoptotic cell death manifested as increases in TUNEL positive cells, cleaved-caspase-3, and ratio of Bax/Bcl-2 protein expression. NAC significantly attenuated I/RI-induced increases in oxidative stress and cardiac apoptosis, prevented postischemic autophagy formation in diabetes, and reduced postischemic myocardial infarction (all p < 0.05). Conclusions. NAC confers cardioprotection against diabetic heart I/RI primarily through inhibiting excessive autophagy which might be a major mechanism why diabetic hearts are less tolerant to I/RI. PMID:28265179

  11. The protective effects of dexmedetomidine on liver injury-induced myocardial ischemia reperfusion.

    Science.gov (United States)

    Erer, D; Ozer, A; Arslan, M; Oktar, G L; Iriz, E; Elmas, C; Zor, M H; Tatar, T; Goktas, G

    2014-01-01

    The aim of this study was to evaluate the effect of dexmedetomidine (100 µg/kg-ip) on liver injury-induced myocardial ischemia and reperfusion (IR) in rats. Twenty-four Wistar Albino rats were separated into four groups. There were four experimental groups (Group C (Control; n = 6), Group IR (ischemia-reperfusion, n = 6), Group D (Dexmedetomidine; n = 6) that underwent left thoracotomy and received ip dexmedetomidine without IR administered via 100 µg/kg ip route 30 minutes before ligating the left coronary artery, and Group IR-D (IR-Dexmedetomidine; n = 6). A small plastic snare was threaded through the ligature and placed in contact with the heart. To produce IR, a branch of the left coronary artery was occluded for 30 min followed by two hours of reperfusion. However, after the above procedure, the coronary artery was not occluded or reperfused in the control rats. At the end of the study, liver tissue was obtained for histochemical and immunohistochemical determination.Some part of tissue samples were stained with Masson-trichrome for the evaluation of ultrastructural changes and inducible nitric oxide synthase (iNOS) expression was evaluated in other part of samples for immunohistochemical examination. Histopathological changes were detected in Group IR when compared with Group C. iNOS expression was found to be increased and stronger particularly in the vascular wall, perisinusoidal space and hepatocytes around vena centralis in this group compared to the control group. Perivascular oedema was detected to be decreased in Group IR-D compared to Group IR. It was also observed that the impairment in the radial arrangement of hepatocytes significantly recovered in Group IR-D. The immunoreactivity was found to be significantly decreased in the assessment of iNOS expression in the same group when compared with Group IR. Administration of dexmedetomidine ameliorates liver injury induced by myocardial ischemia and reperfusion (Fig. 8, Ref. 33).

  12. 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...

  13. Protective effects of emulsified isoflurane after myocardial ischemia-reperfusion injury and its mechanism in rabbits

    Institute of Scientific and Technical Information of China (English)

    RAO Yan; WANG Yan-lin; CHEN Yong-quan; ZHANG Wen-sheng; LIU Jin

    2009-01-01

    Objective: To evaluate the protective effects of 8% emulsified isoflurane after myocardial ischemia-reperfusion injury and its mechanism in rabbits.Methods: Twenty-four male adult New Zealand white rabbits were anesthetized with intravenous injection of 30 mg/kg pentobarbital followed by 5 mg·kg-1·h-1 infusion. All rabbits were subjected to 30 minutes of left anterior de-scending coronary artery (LAD) occlusion and 3 hours of subsequent reperfusion. Before LAD occlusion, the rabbits were randomly allocated into three groups for precondi-tioning treatment (eight for each group). The control group (C group) received intravenously 0.9% NaCl for 30 minutes. The emulsified isoflurane group (EI group) received 8% emulsified isoflurane intravenously till 0.64% end-tidal con-centration for 30 minutes that was followed by a 15-minute washout period. The Intralipid group (IN group) received 30% Intralipid for 30 minutes. The infarcted area, plasma malondialdehyde (MDA) content, superoxide dismutase activity (SOD) and nitrite concentration after 3-hour myo-cardial perfusion were recorded simultaneously.Results: For the myocardial ischemia-reperfusion in-jury animals, the infarcted size in the EI group was signifi-cantly reduced (91.9%±8%) as compared with control group (39%±6%,t=5.19, P<0.01). The plasma SOD activity and nitrite concentration in EI group were significantly higher than those in control group (t=2.82, t=8.46, P<0.05), but MDA content was lower in EI group than that in control group (t=2.56, P<0.05).Conclusions: The results indicate that emulsified isoflurane has a cardioprotection effect against ischemia-reperfusion injury. This beneficial effect of emulsified isoflurane is probably through NO release and consequently by increase in autioxidation of myocardium.

  14. Endurance exercise accelerates myocardial tissue oxygenation recovery and reduces ischemia reperfusion injury in mice.

    Directory of Open Access Journals (Sweden)

    Yuanjing Li

    Full Text Available Exercise training offers cardioprotection against ischemia and reperfusion (I/R injury. However, few essential signals have been identified to underscore the protection from injury. In the present study, we hypothesized that exercise-induced acceleration of myocardial tissue oxygenation recovery contributes to this protection. C57BL/6 mice (4 weeks old were trained on treadmills for 45 min/day at a treading rate of 15 m/min for 8 weeks. At the end of 8-week exercise training, mice underwent 30-min left anterior descending coronary artery occlusion followed by 60-min or 24-h reperfusion. Electron paramagnetic resonance oximetry was performed to measure myocardial tissue oxygenation. Western immunoblotting analyses, gene transfection, and myography were examined. The oximetry study demonstrated that exercise markedly shortened myocardial tissue oxygenation recovery time following reperfusion. Exercise training up-regulated Kir6.1 protein expression (a subunit of ATP-sensitive K(+channel on vascular smooth muscle cells, VSMC sarc-K(ATP and protected the heart from I/R injury. In vivo gene transfer of dominant negative Kir6.1AAA prolonged the recovery time and enlarged infarct size. In addition, transfection of Kir6.1AAA increased the stiffness and reduced the relaxation capacity in the vasculature. Together, our study demonstrated that exercise training up-regulated Kir6.1, improved tissue oxygenation recovery, and protected the heart against I/R injury. This exercise-induced cardioprotective mechanism may provide a potential therapeutic intervention targeting VSMC sarc-K(ATP channels and reperfusion recovery.

  15. 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...

  16. Endovascular reperfusion therapies for acute ischemic stroke: dissecting the evidence.

    Science.gov (United States)

    Tsivgoulis, Georgios; Safouris, Apostolos; Krogias, Christos; Arthur, Adam S; Alexandrov, Andrei V

    2016-05-01

    Ischemic stroke is a major cause of death and disability and intravenous thrombolysis has been the only approved acute reperfusion therapy (RT) for many years. Seven randomized-controlled clinical trials (RCTs) evaluating the safety and efficacy of endovascular therapy in patients with acute ischemic stroke (AIS) due to emergent large vessel occlusion (ELVO) have been recently published. These studies have changed the treatment paradigm by establishing mechanical thrombectomy (MT) as the most effective acute stroke therapy for improving functional outcome in anterior circulation ELVO with a NNT of 6. The present review will critically evaluate the results of these RCTs and of the existing meta-analyses investigating the safety and efficacy of endovascular therapy for AIS. Points of debate such as acute stroke imaging, posterior circulation stroke and general anesthesia will be addressed. We will also discuss health policies aiming to increase the availability of endovascular treatment for stroke patients.

  17. 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.

  18. Acute Myopericarditis Mimicking Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Seval İzdeş

    2011-08-01

    Full Text Available Acute coronary syndromes among young adults are relatively low when compared with older population in the intensive care unit. Electrocardiographic abnormalities mimicking acute coronary syndromes may be caused by non-coronary syndromes and the differential diagnosis requires a detailed evaluation. We are reporting a case of myopericarditis presenting with acute ST elevation and elevated cardiac enzymes simulating acute coronary syndrome. In this case report, the literature is reviewed to discuss the approach to distinguish an acute coronary syndrome from myopericarditis. (Journal of the Turkish Society Intensive Care 2011; 9:68-70

  19. Primary coronary angioplasty for acute myocardial infarction (the Primary Angioplasty Registry).

    Science.gov (United States)

    O'Neill, W W; Brodie, B R; Ivanhoe, R; Knopf, W; Taylor, G; O'Keefe, J; Grines, C L; Weintraub, R; Sickinger, B G; Berdan, L G

    1994-04-01

    During a 14-month period, 6 experienced centers prospectively enrolled 271 patients into a registry in which percutaneous transluminal coronary angioplasty was the primary treatment for acute myocardial infarction. Patients age > 18 years who presented with ST-segment elevation on the 12-lead electrocardiogram were enrolled if symptom duration was or = 2 units of blood occurred in 46 patients (18%); 14 of these transfusions were related to coronary artery bypass surgery. Primary angioplasty is associated with a high reperfusion rate, low in-hospital mortality and few recurrent myocardial ischemic events. These results point to the need for a large-scale trial comparing angioplasty with thrombolytic therapy in the setting of acute myocardial infarction.

  20. 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

  1. Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat.

    Science.gov (United States)

    Kumari, Rashmi; Maulik, Mohua; Manchanda, Subhash Chandra; Maulik, Subir Kumar

    2003-10-15

    The effect of icatibant (Hoe-140), a selective bradykinin receptor (B(2)) antagonist on myocardial ischemic-reperfusion injury was studied in open chest barbiturate anaesthetized cats. The left anterior descending coronary artery was occluded for 15 min, followed by 60 min of reperfusion. Saline or icatibant (200 microg/kg) was administered intravenously slowly over 2 min, 5 min before reperfusion. In the saline-treated group, myocardial ischemic-reperfusion injury was evidenced by depressed MAP, depressed peak positive and negative dP/dt and elevated left ventricular end-diastolic pressure and enhanced oxidative stress [elevated plasma thiobarbituric acid reactive substances (TBARS; a marker for lipid peroxidation), depressed myocardial GSH (reduced glutathione), superoxide dismutase (SOD), catalase] and depletion of adenosine triphosphate (ATP) along with rise in plasma creatine phosphokinase (CPK). Administration of icatibant resulted in complete hemodynamic recovery together with repletion of ATP and reduction in plasma TBARS without any significant change in myocardial SOD, catalase and GSH. The results of the present study suggest a protective role of icatibant in myocardial ischemic-reperfusion injury.

  2. Traditional Chinese Medicine Shuang Shen Ning Xin Attenuates Myocardial Ischemia/Reperfusion Injury by Preserving of Mitochondrial Function

    Directory of Open Access Journals (Sweden)

    Xueli Li

    2014-01-01

    Full Text Available To investigate the potential cardioprotective effects of Shuang Shen Ning Xin on myocardial ischemia/reperfusion injury. Wistar rats were treated with trimetazidine (10 mg/kg/day, ig, Shuang Shen Ning Xin (22.5, 45 mg/kg/day, ig, or saline for 5 consecutive days. Myocardial ischemia/reperfusion injury was induced by ligation of the left anterior descending coronary artery for 40 min and reperfusion for 120 min on the last day of administration. It is found that Shuang Shen Ning Xin pretreatment markedly decreased infarct size and serum LDH levels, and this observed protection was associated with reduced myocardial oxidative stress and cardiomyocyte apoptosis after myocardial ischemia/reperfusion injury. In addition, further studies on mitochondrial function showed that rats treated with Shuang Shen Ning Xin displayed decreased mitochondrial swelling and cytosolic cytochrome c levels, which were accompanied by a preservation of complex I activities and inhibition of mitochondrial permeability transition. In conclusion, the mitochondrial protective effect of Shuang Shen Ning Xin could be a new mechanism, by which Shuang Shen Ning Xin attenuates myocardial ischemia/reperfusion injury.

  3. Myocardial contrast echocardiography to assess perfusion in a mouse model of ischemia/reperfusion injury

    Science.gov (United States)

    Hossack, John A.; Li, Yinbo; Christensen, Jonathan P.; Yang, Zequan; French, Brent A.

    2004-04-01

    Noninvasive approaches for measuring anatomical and physiological changes resulting from myocardial ischemia / reperfusion injury in the mouse heart have significant value since the mouse provides a practical, low-cost model for modeling human heart disease. In this work, perfusion was assessed before, during and after an induced closed- chest, coronary ischemic event. Ultrasound contrast agent, similar to MP1950, in a saline suspension, was injected via cannulated carotid artery as a bolus and imaged using a Siemens Sequoia 512 scanner and a 15L8 intraoperative transducer operating in second harmonic imaging mode. Image sequences were transferred from the scanner to a PC for analysis. Regions of interest were defined in septal and anterior segments of the myocardium. During the ischemic event, when perfusion was diminished in the anterior segment, mean video intensity in the affected segment was reduced by one half. Furthermore, following reperfusion, hyperemia (enhanced blood flow) was observed in the anterior segment. Specifically, the mean video intensity in the affected segment was increased by approximately 50% over the original baseline level prior to ischemia. Following the approach of Kaul et al., [1], gamma variate curves were fitted to the time varying level of mean video intensity. This foundation suggests the possibility of quantifying myocardial blood flow in ischemic regions of a mouse heart using automated analysis of contrast image data sets. An improved approach to perfusion assessment using the destruction-reperfusion approach [2] is also presented.

  4. Cardioprotection by a novel recombinant serine protease inhibitor in myocardial ischemia and reperfusion injury.

    Science.gov (United States)

    Murohara, T; Guo, J P; Lefer, A M

    1995-09-01

    Polymorphonuclear neutrophils (PMN) play an important role in myocardial ischemia/reperfusion (MI/R) injury; however, the role of neutrophilic proteases is less understood. The effects of a novel serine protease inhibitor (serpin), LEX032, were investigated in a murine model of MI (20 min) and R (24 hr) injury in vivo. LEX032 is a recombinant human alpha 1-antichymotrypsin in which six amino acid residues were replaced around the active center with those of alpha-1 protease inhibitor. LEX032 has the ability to inhibit both neutrophil elastase and cathepsin G, two major neutral serine proteases in neutrophils, as well as superoxide generation. LEX032 (25 or 50 mg/kg) administered i.v. 1 min before reperfusion significantly attenuated myocardial necrotic injury evaluated by cardiac creatine kinase loss compared to MI/R rats receiving only vehicle (P LEX032 as compared with rats receiving vehicle (P LEX032 also moderately attenuated leukotriene B4-stimulated PMN adherence to rat superior mesenteric artery endothelium and markedly diminished superoxide radical release from LTB4-stimulated PMN in vitro. In a glycogen-induced rat peritonitis model, LEX032 (50 mg/kg) significantly attenuated PMN transmigration into the peritoneal cavity in vivo. In conclusion, the recombinant serine protease inhibitor, LEX032, appears to be an effective agent for attenuating MI/R injury by inhibiting neutrophil-accumulation into the ischemic-reperfused myocardium and by inactivating cytotoxic metabolites (proteases and superoxide radical) released from neutrophils.

  5. Reduction of myocardial ischemia reperfusion injury with regular consumption of grapes.

    Science.gov (United States)

    Cui, Jianhua; Cordis, Gerald A; Tosaki, Arpad; Maulik, Nilanjana; Das, Dipak K

    2002-05-01

    Recently several polyphenolic antioxidants derived from grape seeds and skins have been implicated in cardioprotection. This study was undertaken to determine if the grapes were equally cardioprotective. Sprague Dawley male rats were given (orally) standardized grape extract (SGE) for a period of three weeks. Time-matched control experiments were performed by feeding the animals 45 microg/100 of glucose plus 45 microg/100 g fructose per day for three weeks. After 30 days, rats were sacrificed, hearts excised and perfused via working-mode. Hearts were made ischemic for 30 min followed by two hours of reperfusion. At 100 mg/kg and at 200 mg/kg, SGE provided significant cardioprotection as evidenced by improved post-ischemic ventricular recovery and reduced amount of myocardial infarction. No cardioprotection was apparent when rats were given grape samples at a dose of 50 mg/100 g/day. In vitro studies demonstrated that the SGE could directly scavenge superoxide and hydroxyl radicals which are formed in the ischemic reperfused myocardium. The results demonstrate that the heats of the rats fed SGE reduced myocardial ischemia reperfusion injury by functioning as in vivo antioxidant.

  6. Aspergillus coronary embolization causing acute myocardial infarction.

    Science.gov (United States)

    Laszewski, M; Trigg, M; de Alarcon, P; Giller, R

    1988-05-01

    An increased frequency of disseminated aspergillosis has been observed in the last decade, mostly occurring in immunocompromised patients including the bone marrow transplant population. Cardiac involvement by Aspergillus remains rare. We report the clinical and postmortem findings of an unusual case of Aspergillus pancarditis in a 7-year-old bone marrow transplant patient with Aspergillus embolization to the coronary arteries leading to a massive acute myocardial infarction. This case suggests that myocardial injury secondary to disseminated aspergillosis should be included in the differential diagnosis of chest pain in the immunocompromised pediatric patient.

  7. 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

    This study assesses the effect of the superoxide anion scavenger superoxide dismutase on myocardial capillary permeability-surface area (PS) products for small hydrophilic molecules after ischemia and reperfusion. Open-chest dogs underwent a 20-minute occlusion of the left anterior descending...... the start of reperfusion. In 13 dogs, no scavenger treatment was given (nonprotected control group), whereas eight dogs were treated systemically with 15,000 units/kg superoxide dismutase during 1 hour, starting 20 minutes before ischemia. In the control group, three dogs developed reperfusion ventricular...... 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...

  8. 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.

  9. 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.)

  10. Stem cell mobilization by granulocyte colony-stimulating factor for myocardial recovery after acute myocardial infarction: a meta-analysis

    DEFF Research Database (Denmark)

    Zohlnhofer, D.; Dibra, A.; Koppara, T.;

    2008-01-01

    OBJECTIVES: The objective of this meta-analysis was to evaluate the effect of stem cell mobilization by granulocyte colony-stimulating factor (G-CSF) on myocardial regeneration on the basis of a synthesis of the data generated by randomized, controlled clinical trials of G-CSF after acute...... myocardial infarction (AMI). BACKGROUND: Experimental studies and early-phase clinical trials suggest that stem cell mobilization by G-CSF may have a positive impact on cardiac regeneration after AMI. The role of G-CSF in patients with AMI remains unclear considering the inconsistent results of several...... independently identified studies and abstracted data on sample size, baseline characteristics, and outcomes of interest. Eligible studies were randomized trials with stem cell mobilization by G-CSF after reperfused AMI that reported data regarding the change in left ventricular ejection fraction (LVEF...

  11. Myocardial ischemia, reperfusion, and infarction in chronically instrumented, intact, conscious, and unrestrained mice.

    Science.gov (United States)

    Lujan, Heidi L; Janbaih, Hussein; Feng, Han-Zhong; Jin, Jian-Ping; DiCarlo, Stephen E

    2012-06-15

    In the United States alone, the National Heart, Lung, and Blood Institute (NHLBI) has invested several hundred million dollars in pursuit of myocardial infarct-sparing therapies. However, due largely to methodological limitations, this investment has not produced any notable clinical application or cardioprotective therapy. Among the major methodological limitations is the reliance on animal models that do not mimic the clinical situation. In this context, the limited use of conscious animal models is of major concern. In fact, whenever possible, studies of cardiovascular physiology and pathophysiology should be conducted in conscious, complex models to avoid the complications associated with the use of anesthesia and surgical trauma. The mouse has significant advantages over other experimental models for the investigation of infarct-sparing therapies. The mouse is inexpensive, has a high throughput, and presents the ability of one to create genetically modified models. However, successful infarct-sparing therapies in anesthetized mice or isolated mouse hearts may not be successful in more complex models, including conscious mice. Accordingly, a conscious mouse model of myocardial ischemia and reperfusion has the potential to be of major importance for advancing the concepts and methods that drive the development of infarct-sparing therapies. Therefore, we describe, for the first time, the use of an intact, conscious, and unrestrained mouse model of myocardial ischemia-reperfusion and infarction. The conscious mouse model permits occlusion and reperfusion of the left anterior descending coronary artery in an intact, complex model free of the confounding influences of anesthetics and surgical trauma. This methodology may be adopted for advancing the concepts and ideas that drive cardiovascular research.

  12. 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.

  13. 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

  14. Secondary prevention with calcium antagonists after acute myocardial infarction

    DEFF Research Database (Denmark)

    Hansen, J F

    1992-01-01

    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...

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

    Institute of Scientific and Technical Information of China (English)

    WANG Shuo-ren

    2007-01-01

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

  16. Effect of reperfusion therapy for patients prognosis with complete atrioventricular block complicating acute myocardial infarction%再灌注治疗对急性心肌梗死合并Ⅲ度房室传导阻滞患者预后的影响

    Institute of Scientific and Technical Information of China (English)

    徐忠武; 李平

    2013-01-01

    Objective This study the different effect of reperfusion therapy for patients prognosis with complete atrioventricular block (CAVB) complicating acute myocardial infarction (AMI) comparatively.Methods 69 patients with CAVB complicating AMI from 2007 January to 2012 January were divided into control group,reperfusion group and intervention group,and compared the cardiogenic shock,arrhythmia,heart failure incidence and total mortality.The left ventricular ejection fraction (LVEF) and left ventricular end diastolic diameter (LVD) were measured by echocardiograma after 6 months for survivors of them.Results (1)The intervention group were significantly lower than those of the thrombolysis group and control group in cardiogenic shock,arrhythmia,heart failure incidence and total mortality after reperfusion therapy (P<0.05),and the thrombolysis group was significantly lower than that of the control group too (P<0.05).(2)The survivors of intervention group were significantly higher than that of the survivors of thrombolysis group and control group in the LVEF after 6 months(P<0.05),and were significantly lower in LVD(P<0.05).Conclusion Patients with CAVB complicating AMI have a significant poor prognosis for the higher cardiogenic shock,arrhythmia,heart failure incidence and total mortality.Coronary reperfusion therapy may contribute to improve the left ventricular function and prognosis,and the effect of primary percutaneous coronary intervention.is more outstanding than that of intravenous thrombolytic therapy.%目的 对比研究不同再灌注治疗对急性心肌梗死(AMI)合并Ⅲ度房室传导阻滞(Ⅲ.AVB)患者预后的影响.方法 2007年1月至2012年1月住院的AMI合并Ⅲ.AVB患者69例,分为对照组、溶栓组和介入组,比较三组患者心源性休克、恶性心律失常、心衰等发生率和总死亡率.于再灌注治疗后6个月对存活者行心脏超声检查,测定左室射血分数(LVEF)和左室舒张末期内径(LVD).结果

  17. Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion.

    Science.gov (United States)

    Lee, Hsin-Ling; Chen, Chwen-Lih; Yeh, Steve T; Zweier, Jay L; Chen, Yeong-Renn

    2012-04-01

    Mitochondrial electron transport chain (ETC) is the major source of reactive oxygen species during myocardial ischemia-reperfusion (I/R) injury. Ischemic defect and reperfusion-induced injury to ETC are critical in the disease pathogenesis of postischemic heart. The properties of ETC were investigated in an isolated heart model of global I/R. Rat hearts were subjected to ischemia for 30 min followed by reperfusion for 1 h. Studies of mitochondrial function indicated a biphasic modulation of electron transfer activity (ETA) and ETC protein expression during I/R. Analysis of ETAs in the isolated mitochondria indicated that complexes I, II, III, and IV activities were diminished after 30 min of ischemia but increased upon restoration of flow. Immunoblotting analysis and ultrastructural analysis with transmission electron microscopy further revealed marked downregulation of ETC in the ischemic heart and then upregulation of ETC upon reperfusion. No significant difference in the mRNA expression level of ETC was detected between ischemic and postischemic hearts. However, reperfusion-induced ETC biosynthesis in myocardium can be inhibited by cycloheximide, indicating the involvement of translational control. Immunoblotting analysis of tissue homogenates revealed a similar profile in peroxisome proliferator-activated receptor-γ coactivator-1α expression, suggesting its essential role as an upstream regulator in controlling ETC biosynthesis during I/R. Significant impairment caused by ischemic and postischemic injury was observed in the complexes I- III. Analysis of NADH ferricyanide reductase activity indicated that injury of flavoprotein subcomplex accounts for 50% decline of intact complex I activity from ischemic heart. Taken together, our findings provide a new insight into the molecular mechanism of I/R-induced mitochondrial dysfunction.

  18. Primary percutaneous coronary intervention as a national Danish reperfusion strategy of ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Sørensen, Jacob Thorsted; Steengaard, Carsten; Holmvang, Lene

    2013-01-01

    The use of primary percutaneous coronary intervention (PCI) as the preferred reperfusion strategy in ST-elevation myocardial infarction (STEMI) requires optimal systems-of-care and logistics in order to enable rapid treatment of all patients. In Denmark, this has been achieved through prehospital...... electrocardiogram diagnosis, field triage and dedicated PCI centres 24/7. Today, primary PCI is an option for all Danish patients with STEMI, regardless of the distance to a PCI centre. This has led to a decline in both mortality and morbidity....

  19. The effect of referral for cardiac rehabilitation on survival following acute myocardial infarction

    DEFF Research Database (Denmark)

    Lewinter, Christian; Bland, John M; Crouch, Simon

    2014-01-01

    BACKGROUND: International guidelines recommend referral for cardiac rehabilitation (CR) after acute myocardial infarction (AMI). However, the impact on long-term survival after CR referral has not been adjusted by time-variance. We compared the effects of CR referral after hospitalization for AMI......% CI, 0.66 to 0.96, p = 0.02 in 2003) when patients entered the model at three months after discharge and had a common exit at 90 months. Significant positive and negative predictors for CR referral were beta-blocker prescription (+), reperfusion (+) and age (-) in 1995, and reperfusion...... (+), revascularization (+), heart failure (HF) (+), antiplatelets (+), angiotensin-converting-enzyme inhibitor (ACE-I) (+), statins (+), diabetes (-), and the modified Global Registry of Acute Cardiac Events (GRACE) risk score (-) in 2003. CONCLUSIONS: CR referral was associated with improved survival in 2003...

  20. [Modulation of the beta-adrenergic system during acute myocardial infarction: rationale for a new clinical trial].

    Science.gov (United States)

    Ibáñez, Borja; Fuster, Valentín; Macaya, Carlos; Jiménez-Borreguero, Jesús; Iñiguez, Andrés; Fernández-Ortiz, Antonio; Sanz, Ginés; Sánchez-Brunete, Vicente

    2011-07-01

    Acute myocardial infarction is caused by sudden coronary artery occlusion. Persistent ischemia results in necrosis of the myocardial tissue supplied by the occluded vessel. It has recently been shown that the final size of the infarct is a major predictor of future clinical events, and is, therefore, used as a surrogate outcome in clinical trials. Moreover, it has become clear that the duration of ischemia in the main determinant of the success of myocardial salvage (i.e. of non-necrotic at-risk myocardium). In addition to minimizing the time between symptom onset and reperfusion, there is considerable interest in finding therapies that can further limit the size of the infarction (i.e. cardioprotective therapies) and they are the focus of numerous clinical studies. Oral β-blockade within the first few hours of an AMI is a class-IA indication in clinical practice guidelines. However, early intravenous β-blockade, even before coronary artery reperfusion, is not routinely recommended. Preclinical research has demonstrated that the selectiveβ1-blocker metoprolol is able to reduce the infarct size only when administered before coronary artery reperfusion, which indicates that its cardioprotective properties are secondary to its ability to reduce reperfusion injury. In addition, retrospective studies of AMI suggest that starting intravenous β-blockade early has clinical benefits (i.e. lower mortality and better recovery of left ventricular contractility) in patients without contraindications. Our general hypothesis is that early administration of metoprolol (i.e. intravenously before reperfusion) results in smaller infarcts than administering the drug orally after reperfusion. The Effect of METOprolol in CARDioproteCtioN during an acute myocardial InfarCtion (METOCARD-CNIC) trial will test this hypothesis in patients with ST-segment elevation AMI.

  1. Paracrine systems in the cardioprotective effect of angiotensin-converting enzyme inhibitors on myocardial ischemia/reperfusion injury in rats.

    Science.gov (United States)

    Liu, Y H; Yang, X P; Sharov, V G; Sigmon, D H; Sabbath, H N; Carretero, O A

    1996-01-01

    After transient episodes of ischemia, benefits of thrombolytic or angioplastic therapy may be limited by reperfusion injury. Angiotensin-converting enzyme inhibitors protect the heart against ischemia/reperfusion injury, an effect mediated by kinins. We examined whether the protective effect of the angiotensin-converting enzyme inhibitor ramiprilat on myocardial ischemia/reperfusion is due to kinin stimulation of prostaglandin and/or nitric oxide release. The left anterior descending coronary artery of Lewis inbred rats was occluded for 30 minutes, followed by 120 minutes of reperfusion. Immediately before reperfusion rats were treated with vehicle, ramiprilat, or the angiotensin II type 1 receptor antagonist losartan. We tested whether pretreatment with the kinin receptor antagonist Hoe 140, the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester, or the cyclooxygenase inhibitor indomethacin blocked the effect of ramiprilat on infarct size and reperfusion arrhythmias. In controls, infarct size as a percentage of the area at risk was 79 +/- 3%; ramiprilat reduced this to 49 +/- 4% (P < .001), but losartan had little effect (74 +/- 6%, P = NS). Pretreatment with Hoe 140, NG-nitro-L-arginine methyl ester, or indomethacin abolished the beneficial effect of ramiprilat. Compared with the 30-minute ischemia/120-minute reperfusion group, nonreperfused hearts with 30 minutes of ischemia had significantly smaller infarct size as a percentage of the area at risk, whereas in the 150-minute ischemia group it was significantly larger. This suggests that reperfusion caused a significant part of the myocardial injury, but it also suggests that compared with prolonged ischemia, reperfusion salvaged some of the myocardium. Ventricular arrhythmias mirrored the changes in infarct size. Thus, angiotensin-converting enzyme inhibitors protect the myocardium against ischemia/reperfusion injury and arrhythmias; these beneficial effects are mediated primarily by a kinin

  2. Clinical significance and treatment of reperfusion injury in acute myocardial infarction patients with hypoten-sion and cardiogenic shock%再灌注损伤在急性心肌梗死合并低血压及心源性休克中的临床意义和治疗对策

    Institute of Scientific and Technical Information of China (English)

    张科林; 郭战宏; 龙丽辉; 蔡天志; 刘佰学; 辛宏

    2016-01-01

    Objective To explore the clinical significance and treatment of reperfusion injury in acute myocar-dial infarction (AMI)with hypotension and cardiogenic shock.Methods One hundred and thirty -one AMI patients with hypotension and cardiogenic shock who were undergoing emergency PCI were collected.According to the occurring or worsening of hypotension and cardiogenic shock after reperfusion,45 patients were divided into treatment group,and the other 86 patients were divided into control group.To analyze the clinical manifestations of myocardial ischemia reper-fusion injury and the efficacy of emergency PCI supported by sequential therapy with optimized vasopressors and IABP in both groups.Results After reperfusion,45 patients (34.35% )were occurred or worsen of hypotension and cardiogen-ic shock as treatment group;86 patients (65.65%)as control group.There were 100 cases of reperfusion arrhythmia (76.34%)in both groups,including 43 cases of accelerated idioventricular rhythm,31 cases of bradyarrhythmia,23 ca-ses of premature ventricular contraction,and 3 cases of ventricular fibrillation.The fatality rate and cardiovascular event (such as left ventricular failure)rate were no statistically significant difference between the treatment group and the con-trol group.However,the number of patients that must use IABP of treatment group was significantly lower than control group (P <0.05).Conclusion Reperfusion injury is one of the leading causes of AMI with hypotension and cardiogen-ic shock.It can be treated with emergency PCI supported by sequential therapy with optimized vasopressors and IABP.%目的:探讨再灌注损伤在急性心肌梗死(AMI)合并低血压状态(简称低血压)及心源性休克(CS)中的临床意义和治疗对策。方法观察 AMI 合并低血压及 CS 行急诊经皮冠状动脉介入治疗(PCI)患者131例,术中再灌注后出现或加重低血压及 CS 为治疗组(45例),其他为对照组(86例),观察两

  3. Glycyrrhiza glabra protects from myocardial ischemia-reperfusion injury by improving hemodynamic, biochemical, histopathological and ventricular function.

    Science.gov (United States)

    Ojha, Shreesh; Golechha, Mahaveer; Kumari, Santosh; Bhatia, Jagriti; Arya, Dharamvir S

    2013-01-01

    Present study evaluated the cardioprotective effect of Glycyrrhiza glabra against ischemia-reperfusion injury (I-R) induced by ligation of left anterior descending coronary artery (LADCA) in rats. Ligation of LADCA for 45 min followed by 60 min of reperfusion has induced significant (pglabra significantly (pglabra also prevented GSH depletion and inhibited lipid peroxidation in heart. In addition to improving biochemical indices of myocardial function, G. glabra also significantly (pglabra. Taken together, results of the present study clearly suggest the cardioprotective potential of G. glabra against myocardial infarction by amelioration of oxidative stress and favorable modulation of cardiac function.

  4. Red propolis ameliorates ischemic-reperfusion acute kidney injury.

    Science.gov (United States)

    da Costa, Marcus Felipe Bezerra; Libório, Alexandre Braga; Teles, Flávio; Martins, Conceição da Silva; Soares, Pedro Marcos Gomes; Meneses, Gdayllon C; Rodrigues, Francisco Adelvane de Paulo; Leal, Luzia Kalyne Almeida Moreira; Miron, Diogo; Silva, Aline Holanda; Martins, Alice Maria Costa

    2015-08-15

    Acute kidney injury (AKI) remains a great problem in clinical practice. Renal ischemia/reperfusion (I/R) injury is a complex pathophysiological process. Propolis is a natural polyphenol-rich resinous substance collected by honeybees from a variety of plant sources that has anti-inflammatory and anti-oxidative properties. Red propolis (RP) protection in renal I/R injury was investigated. Male Wistar rats underwent unilateral nephrectomy and contralateral renal I/R (60 min). Rats were divided into four groups: (1) sham group, (2) RP group (sham-operated rats treated with RP), 3) IR group (rats submitted to ischemia) and (4) IR-RP (rats treated with RP before ischemia). At 48 h after reperfusion, renal function was assessed and kidneys were removed for analysis. I/R increased plasma levels of creatinine and reduced creatinine clearance (CrCl), and RP provided protection against this renal injury. Red propolis significantly improves oxidative stress parameters when compared with the IR group. Semiquantitative assessment of the histological lesions showed marked structural damage in I/R rats compared with the IR-RP rats. RP attenuates I/R-induced endothelial nitric oxide-synthase down regulation and increased heme-oxygenase expression in renal tissue. Red propolis protects kidney against acute ischemic renal failure and this protection is associated with reduced oxidative stress and eNOS and heme-oxygenase up regulation. Copyright © 2015 Elsevier GmbH. All rights reserved.

  5. Safety of reperfusion therapy with combination of tirofiban and half-dose reteplase in treating acute myocardial infarction%替罗非班联合瑞替普酶治疗急性心肌梗死安全性研究

    Institute of Scientific and Technical Information of China (English)

    卞秋武; 王乐; 王雪青; 张双月; 王庆胜; 林海龙; 谭强; 杨红梅; 王晓亮

    2013-01-01

    Objective:To investigate the safety of reperfusion therapy with combination of tirofiban and half-dose reteplase in the treatment of acute ST segment elevation myocardial infarction (STEMI).Methods:Totally 208 STEMI patients in our hospital were randomly assigned to the treatment of either half-dose reteplase combined with full-dose tirofiban or standard-dose reteplase alone.The incidence of death for various causes within 30 days,heart failure,cardiogenic shock,ventricular tachycardia or ventricular fibrillation,reinfarction,myocardial ischemia recurrence and hemorrhage between two groups were compared.Results:There was no difference in mortality between combined and reteplase alone groups,but in combined group the rates of recurrent myocardial infarction,recurrent ischemia,ventricular tachycardia or fibrillation,and severe pump failure were fewer.There was no difference in rates of mild,moderate and life-threatening bleedings between two groups.Conclusion:The safety profile of reperfusion therapy with combination of tirofiban and half-dose reteplase for STEMI is similar to that of standard-dose reteplase.%目的:探讨替罗非班联合半量瑞替普酶溶栓用于急性ST段抬高性心肌梗死治疗的安全性.方法:入选我院急性ST段抬高性心肌梗死患者208例,年龄27~75岁,随机分为联合溶栓组及瑞替普酶组.比较两组30 d内各种原因导致的死亡、心力衰竭或肺水肿、室性心动过速或心室颤动、非致死性再梗死、心肌缺血复发等临床事件发生率以及轻度出血、中度出血、严重出血及脑出血事件发生率.结果:两组患者死亡、心源性休克、心室颤动、Ⅱ ~ Ⅲ度房室传导阻滞、补救性PCI事件发生率无差异,联合溶栓组非致死性心肌再梗死发生率、心肌缺血、室性心动过速、心力衰竭及肺水肿发生率明显低于瑞替普酶组.两组轻度出血、中度出血、严重或威胁生命的出血及总出血发生率无差

  6. 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

    (STEMI) treated with primary percutaneous coronary intervention (pPCI). Methods and results A total of 172 patients with STEMI and Thrombolysis in Myocardial Infarction flow 0/1 were randomly assigned to exenatide or placebo (saline) intravenously. Study treatment was commenced 15 min before intervention...... the infarct size and the AAR for both treatment groups and an analysis of covariance showed that datapoints in the exenatide group lay significantly lower than for the placebo group (P= 0.011). There was a trend towards smaller absolute infarct size in the exenatide group (13 ± 9 vs. 17 ± 14 g; P= 0.......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....

  7. The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited

    Directory of Open Access Journals (Sweden)

    Gino A. Kurian

    2016-01-01

    Full Text Available Oxidative and reductive stress are dual dynamic phases experienced by the cells undergoing adaptation towards endogenous or exogenous noxious stimulus. The former arises due to the imbalance between the reactive oxygen species production and antioxidant defenses, while the latter is due to the aberrant increase in the reducing equivalents. Mitochondrial malfunction is the common denominator arising from the aberrant functioning of the rheostat that maintains the homeostasis between oxidative and reductive stress. Recent experimental evidences suggest that the maladaptation during oxidative stress could play a pivotal role in the pathophysiology of major cardiovascular diseases such as myocardial infraction, atherosclerosis, and diabetic cardiovascular complications. In this review we have discussed the role of oxidative and reductive stress pathways in the pathogenesis of myocardial ischemia/reperfusion injury and diabetic cardiomyopathy (DCM. Furthermore, we have provided impetus for the development of subcellular organelle targeted antioxidant drug therapy for thwarting the deterioration of the failing myocardium in the aforementioned cardiovascular conditions.

  8. Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats

    Directory of Open Access Journals (Sweden)

    Rui Xia

    2011-01-01

    Full Text Available Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P<0.05. Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P<0.05. L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.

  9. Ginkgolide B Reduces the Degradation of Membrane Phospholipids to Prevent Ischemia/Reperfusion Myocardial Injury in Rats.

    Science.gov (United States)

    Pei, Hong-Xia; Hua, Rong; Guan, Cha-Xiang; Fang, Xiang

    2015-01-01

    Platelet-activating factor (PAF), a bioactive phospholipid, plays an important role in the integrity of the cellular membrane structure, and is involved in the pathogenesis of myocardial ischemia/reperfusion (IR) injuries. In this study, we tested the hypothesis that blockage of PAF receptor by BN 52021 (Ginkgolide B) can prevent IR-induced degradation of the myocardial membrane phospholipid, and deterioration of the cardiac function. Rat hearts in situ were subjected to 5 min ischemia and followed by 10 min reperfusion. Cardiac performances during periods of ischemia and reperfusion were monitored, and the amount of membrane phospholipids was analyzed. Myocardial total phospholipids, phosphatidylcholine, and phosphatidylethanolamine were decreased significantly in ischemia-reperfusion rat hearts compared with those of sham-operated rat hearts. Degradation of the membrane phospholipid was accompanied by the deterioration of cardiac functions and increase in serum lactate dehydrogenase (LDH) activity. BN 52021 (15 mg/kg), given by intravenous infusion 10 min prior to the left anterior descending coronary artery occlusion, reduced IR-related degradation of the myocardial phospholipids, the activity of serum LDH, and was concomitant with improvement of cardiac function. Furthermore, we demonstrated that the production of PAF was increased and BN 52021 decreased cellular damage in cultured anoxic cardiomyocytes. These results indicated that PAF antagonist BN 52021 has a protective effect against IR-induced myocardial dysfunction and degradation of the membrane phospholipids.

  10. Effect of loading-dose ticagrelor on coronary blood flow, left ventricular remodeling and myocardial enzyme spectrum in patients with acute myocardial infarction after interventional therapy

    Institute of Scientific and Technical Information of China (English)

    Xiao-Rui Xie; Pu Yang

    2016-01-01

    Objective:To study the effect of loading-dose ticagrelor on coronary blood flow, left ventricular remodeling and myocardial enzyme spectrum in patients with acute myocardial infarction after interventional therapy.Methods: A total of 86 patients with acute myocardial infarction who received emergency PCI in our hospital between May 2013 and May 2016 were selected and randomly divided into two groups, ticagrelor group received perioperative ticagrelor therapy and clopidogrel group received perioperative clopidogrel therapy. After PCI, coronary blood flow reperfusion was evaluated, serum myocardial remodeling indexes and myocardial enzymes were determined, and cardiac color Doppler ultrasonography was conducted to determine the cardiac function indexes.Results:TIMI grading and TMPG grading of ticagrelor group after PCI were significantly higher than those of clopidogrel group; serum MMP9, BNP, CITP, PICP, PIIINP, CK, CK-MB, cTnI and cTnT content of ticagrelor group 24h after operation were significantly lower than those of clopidogrel group; LVEDD, LVSED and LVMI of ticagrelor group 2 weeks after operation were significantly lower than those of clopidogrel group while LVEF was significantly higher than that of clopidogrel group.Conclusion:Peri-PCI loading-dose ticagrelor can improve coronary blood perfusion and reduce ventricular remodeling and myocardial injury in patients with acute myocardial infarction.

  11. Effects of KR-32570, a new sodium hydrogen exchanger inhibitor, on myocardial infarction and arrhythmias induced by ischemia and reperfusion.

    Science.gov (United States)

    Lee, Byung Ho; Yi, Kyu Yang; Lee, Sunkyung; Lee, Sunghou; Yoo, Sung-eun

    2005-10-31

    The present study was performed to evaluate the cardioprotective effects of [5-(2-methoxy-5-chloro-5-phenyl)furan-2-ylcarbonyl]guanidine (KR-32570) in rat and dog models of coronary artery occlusion and reperfusion. In addition, we sought to clarify the efficacy of KR-32570 on reperfusion-induced fatal ventricular arrhythmia. In anesthetized rats subjected to 45-min coronary occlusion and 90-min reperfusion, KR-32570 (i.v. bolus) dose-dependently reduced myocardial infarct size from 58.0% to 50.7%, 35.3%, 33.5% and 27.0% for 0.03, 0.1, 0.3 and 1.0 mg/kg, respectively (PKR-32570 (3 mg/kg, i.v. bolus) markedly decreased infarct size from 28.9% in vehicle-treated group to 8.0% (PKR-32570 dose-dependently decreased the incidence of premature ventricular contraction, ventricular tachycardia or ventricular fibrillation induced by ischemia and reperfusion in rats. Similar results were obtained in dogs with reperfusion-induced arrhythmia. In separate experiments to assess the effects of timing of treatment, KR-32570 given 10 min before or at reperfusion in rat models also significantly reduced the myocardial infarct size (40.9% and 46.1%, respectively) compared with vehicle-treated group. In all studies, KR-32570 caused no significant changes in any hemodynamic profiles. Taken together, these results indicate that KR-32570 significantly reduced the myocardial infarction and incidence of arrhythmias induced by ischemia and reperfusion in rats and dogs, without affecting hemodynamic profiles. Thus, it could be potentially useful in the prevention and treatment of myocardial injuries and lethal ventricular arrhythmias.

  12. 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 ...

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

    DEFF Research Database (Denmark)

    Hamshere, Stephen; Jones, Daniel A; 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...

  14. 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...... (W) were predictive with respect to mortality, heart failure, and angina pectoris requiring drug treatment. Exercise tests following acute myocardial infarction could not predict the chances of returning to work....

  15. Acute myocarditis triggering coronary spasm and mimicking acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Andreas; Kumar; Rodrigo; Bagur; Patrick; Béliveau; Jean-Michel; Potvin; Pierre; Levesque; Nancy; Fillion; Benoit; Tremblay; éric; Larose; Valérie; Gaudreault

    2014-01-01

    A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause.

  16. Acute myocarditis triggering coronary spasm and mimicking acute myocardial infarction.

    Science.gov (United States)

    Kumar, Andreas; Bagur, Rodrigo; Béliveau, Patrick; Potvin, Jean-Michel; Levesque, Pierre; Fillion, Nancy; Tremblay, Benoit; Larose, Eric; Gaudreault, Valérie

    2014-09-26

    A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause.

  17. 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

    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...... 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...... following pPCI in patients with AMI. MATERIAL AND METHODS: The IMPACT trial is a multicentre, randomised, double-blinded, placebo-controlled study. We wish to include 2 × 20 patients with ST-elevation myocardial infarctions undergoing pPCI within six hours from symptom onset. The primary end...

  18. 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

    Objective: Despite its high prevalence among patients suffering myocardial infarction, the significance of left ventricle hypertrophy for infarct size is not known. We asked whether infarct size might be increased by this condition, and whether any such increase might be associated with an increa......Objective: Despite its high prevalence among patients suffering myocardial infarction, the significance of left ventricle hypertrophy for infarct size is not known. We asked whether infarct size might be increased by this condition, and whether any such increase might be associated...... with an increased mitochondrial damage following coronary occlusion.  Methods: Occlusion of the left descending artery in isolated, perfused hearts of SHR-SP (spontaneously hypertensive rat stroke-prone) (left ventricular hypertrophy) or Wistar-Kyoto (WKY) (control) rats was used, followed by reperfusion.......  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...

  19. Effect of transplantation of BMP-2-induced bone marrow mesenchymal stem cells on myocardial infarction of rats after reperfusion

    Directory of Open Access Journals (Sweden)

    Zhong-cheng MIAO

    2014-10-01

    Full Text Available Objective To observe whether the bone morphogenetic protein-2 (BMP-2 could induce bone marrow mesenchymal stem cells (BMSCs to differentiate into cardiomyocyte-like cells, and investigate its effect on cardiac function in rats. Methods IBMSCs were isolated, cultured, amplified and identified in vitro. The expression of specific cardiac proteins was identified after pre-induction of BMP-2, and BMSCs were marked in vitro by DAPI. In order to reproduce the reperfusion after acute myocardial infarction (AMI model, the left anterior descending (LAD coronary artery was interrupted for 100min and then freed in SD rat. The rats with successful manipulation were randomly assigned into 3 groups, i.e. control group: the culture medium was injected with micro syringe at 4 points around infarcted zone; stem cell group: non-induced BMSCs were injected with the same amount and at the same sites as in control group; and pre-induction group: induced BMSCs were injected with the same amount and at the same sites as in control group. The surviving state of transplanted cells in myocardial tissue was observed with fluorescence microscopy at 4 hours, 4 days and 4 weeks postoperatively. Cardiac function was evaluated by employing color Doppler echocardiography, and the morphology of rat myocardial tissue was observed at 4 weeks after operation by HE and Masson staining, and the therapeutic effect was compared among 3 groups. Results After the BMP-2 pre-induction, changes in morphology were found in a part of BMSCs, and the specific cardiomyocyte protein connexin 43 (Cx43 and cardiac troponin T (cTnT were expressed. Fluorescence microscopy revealed that DAPI-labeled BMSCs survived in myocardial infarction in pre-induction group and stem cell group 4 hours, 4 days and 4 weeks postoperatively. Compared with the control group, the left ventricular ejection fraction (LVEF and left ventricular fractional shortening (FS significantly increased in stem cell group and

  20. 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.

  1. System delay and timing of intervention in acute myocardial infarction (from the Danish Acute Myocardial Infarction-2 [DANAMI-2] trial)

    DEFF Research Database (Denmark)

    Nielsen, Peter Haubjerg; Terkelsen, Christian Juhl; Nielsen, Torsten Toftegård;

    2011-01-01

    The interval from the first alert of the healthcare system to the initiation of reperfusion therapy (system delay) is associated with mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention (pPCI). The importance of system dela...

  2. Amphetamine Abuse Related Acute Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Archana Sinha

    2016-01-01

    Full Text Available Amphetamine abuse is a global problem. The cardiotoxic manifestations like acute myocardial infarction (AMI, heart failure, or arrhythmia related to misuse of amphetamine and its synthetic derivatives have been documented but are rather rare. Amphetamine-related AMI is even rarer. We report two cases of men who came to emergency department (ED with chest pain, palpitation, or seizure and were subsequently found to have myocardial infarction associated with the use of amphetamines. It is crucial that, with increase in amphetamine abuse, clinicians are aware of this potentially dire complication. Patients with low to intermediate risk for coronary artery disease with atypical presentation may benefit from obtaining detailed substance abuse history and urine drug screen if deemed necessary.

  3. Protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury in rats

    Institute of Scientific and Technical Information of China (English)

    Fang-Jiang Li; Tao Hsu; Hui-Xian Li; Jin-Zheng Shi; Mei-Ling Du; Xiao-Yuan Wang; Wen-Ting Zhang

    2014-01-01

    Objective:To investigate the protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury(I-RI) in rats.Methods:A total of60SD rats were randomly divided into control group, model group, lithium chloride intervention group and L-arginine methyl ester+ lithium chloride intervention group with15 in each.TheI-RI model was established in model group, the lithium chloride intervention group andL-arginine methyl ester+ lithium chloride intervention group by method of seaming along left anterior descending coronary artery myocardial, control group was only opened the chest without seaming,ST-elevation within2 min was regarded as modeling success.Model group did not adopted any intervention, lithium chloride intervention group was treated with lithium chloride injection 15 mg/kg by jugular venipuncture preoperatively,L-arginine methyl ester+ lithium chloride intervention group was treated with intraperitoneal injection of30 mg•kg-1•d-1L-arginine methyl ester7 d before the test, and intravenous catheter of15 mg/kg lithium chloride preoperatively. The hydroxybutyric acid dehydrogenase(HBDH), creatine kinase isoenzyme(CK-MB), superoxide dismutase(SOD), malondialdehyde(MDA) level and nitric oxide synthase(NOS) activites were tested.Each large area of myocardial ischemia tissue was extracted for determination of the MDA content,SOD activity in tissue and serum, and morphological changes of myocardial tissue.Results:SOD activity was highest in lithium chloride intervention group, followed by L-arginine methyl ester+ lithium chloride intervention group, control group and model group (P0.05);HBDH andCK-MB of plasma were highest in model group, followed byL-arginine methyl ester+ lithium chloride intervention group, lithium chloride intervention group and control group(P<0.05).A significantly lighter myocardial damage was observed microscopically in lithium chloride intervention group than that inL-arginine methyl ester+ lithium

  4. Cardioprotective Effects of Salvianolic Acid A on Myocardial Ischemia-Reperfusion Injury In Vivo and In Vitro

    Directory of Open Access Journals (Sweden)

    Huaying Fan

    2012-01-01

    Full Text Available Salvianolic acid A (SAA, one of the major active components of Danshen that is a traditional Chinese medicine, has been reported to possess protective effect in cardiac diseases and antioxidative activity. This study aims to investigate the cardioprotection of SAA in vivo and in vitro using the model of myocardial ischemia-reperfusion in rat and hydrogen peroxide (H2O2-induced H9c2 rat cardiomyoblasts apoptosis. It was found that SAA significantly limited infarct size of ischemic myocardium when given immediately prior to reperfusion. SAA also significantly suppressed cellular injury and apoptotic cell death. Additionally, the results of western blot and phospho-specific antibody microarray analysis showed that SAA could up-regulate Bcl-2 expression and increase the phosphorylation of proteins such as Akt, p42/p44 extracellular signal-related kinases (Erk1/2, and their related effectors. The phosphorylation of those points was related to suppress apoptosis. In summary, SAA possesses marked protective effect on myocardial ischemia-reperfusion injury, which is related to its ability to reduce myocardial cell apoptosis and damage induced by oxidative stress. The protection is achieved via up-regulation of Bcl-2 expression and affecting protein phosphorylation. These findings indicate that SAA may be of value in cardioprotection during myocardial ischemia-reperfusion injury, which provide pharmacological evidence for clinical application.

  5. Cardioprotective Effects of Salvianolic Acid A on Myocardial Ischemia-Reperfusion Injury In Vivo and In Vitro

    Science.gov (United States)

    Fan, Huaying; Yang, Liu; Fu, Fenghua; Xu, Hui; Meng, Qinggang; Zhu, Haibo; Teng, Lirong; Yang, Mingyan; Zhang, Leiming; Zhang, Ziliang; Liu, Ke

    2012-01-01

    Salvianolic acid A (SAA), one of the major active components of Danshen that is a traditional Chinese medicine, has been reported to possess protective effect in cardiac diseases and antioxidative activity. This study aims to investigate the cardioprotection of SAA in vivo and in vitro using the model of myocardial ischemia-reperfusion in rat and hydrogen peroxide (H2O2)-induced H9c2 rat cardiomyoblasts apoptosis. It was found that SAA significantly limited infarct size of ischemic myocardium when given immediately prior to reperfusion. SAA also significantly suppressed cellular injury and apoptotic cell death. Additionally, the results of western blot and phospho-specific antibody microarray analysis showed that SAA could up-regulate Bcl-2 expression and increase the phosphorylation of proteins such as Akt, p42/p44 extracellular signal-related kinases (Erk1/2), and their related effectors. The phosphorylation of those points was related to suppress apoptosis. In summary, SAA possesses marked protective effect on myocardial ischemia-reperfusion injury, which is related to its ability to reduce myocardial cell apoptosis and damage induced by oxidative stress. The protection is achieved via up-regulation of Bcl-2 expression and affecting protein phosphorylation. These findings indicate that SAA may be of value in cardioprotection during myocardial ischemia-reperfusion injury, which provide pharmacological evidence for clinical application. PMID:21789047

  6. 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 a

  7. 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

  8. 替罗非班对未行早期再灌注治疗急性ST段抬高型心肌梗死患者的疗效%The effect and safety of tirofiban on acute ST segment elevation myocardial infarction patients receiving no early reperfusion therapy

    Institute of Scientific and Technical Information of China (English)

    张大鹏; 王乐丰; 王红石; 徐立; 李惟铭; 倪祝华; 夏昆; 刘宇; 杨新春

    2016-01-01

    Objective To study the efficacy and safety of tirofiban on acute ST segment elevation myocardial infarction (STEMI) in patients who do not receive early reperfusion therapy.Methods A total of 153 STEMI patients without early reperfusion therapy were randomly distributed into tirofiban group (therapeutic group,n =78) and non-tirofiban group (control group,n =75).Coronary angiography was performed on the 5th and 10th day after treatment,and percutaneous coronary intervention (PCI) was conducted when necessary.The differences of initial patency of the infarct related artery (IRA),bleeding complication and clinic events within 30 days between these two groups were compared.Results Tirofiban did not increase the percentage of patients with initial patency of IRA (60.3% vs 64.0%,P =0.63).The percentage of patients with thrombolysis in myocardial infarction (TIMI) 3 after PCI was 100.0% in tirofiban group and 97.1% in the control group (P =0.09).However,application of tirofiban significantly decreased poor myocardial perfusion rate after PCI (1.4% vs 8.8%,P =0.04).No significant differences were observed in major adverse cardiovascular events (MACE) (3.8% vs 2.7%,P =0.68) between therapeutic and control group.The same is true for mild (5/78 vs 4/75 cases,P =0.78) and severe hemorrhage (2/78 vs 1/75 cases,P =0.58),and severe thrombocytopenia (2/78 vs 0/75 cases,P =0.10) between these two groups within 30 days.Conclusions Tirofiban did not increase initial patency in STEMI patients without early reperfusion therapy.However,it can improve myocardial perfusion after PCI.%目的 探讨对于未行早期再灌注治疗的急性ST段抬高型心肌梗死(STEMI)患者应用替罗非班的有效性和安全性.方法 选择153例未行早期再灌注治疗的STEMI患者,随机分为替罗非班组(治疗组,78例)与非替罗非班组(对照组,75例),在发病第5~10日行冠状动脉造影检查,必要时进行经皮冠状动脉介

  9. 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 AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

  10. A quantitative analysis of the benefits of pre-hospital infarct angioplasty triage on outcome in patients undergoing primary angioplasty for acute myocardial infarction

    NARCIS (Netherlands)

    van 't Hof, AWJ; van de Wetering, H; Ernst, N; Hollak, F; de Pooter, F; Suryapranata, H; Hoorntje, JCA; Gosselink, M; Zijlstra, F; de Boer, MJ; Dambrink, Jan Hendrik Everwijn

    2005-01-01

    Primary coronary angioplasty has been shown to be a very effective reperfusion modality in patients with acute myocardial infarction (MI). However, the time from diagnosis to therapy is often very long, often due to interhospital transfer of the patient. This study evaluates the effect of improving

  11. MCT1 and MCT4 Expression During Myocardial Ischemic-Reperfusion Injury in the Isolated Rat Heart

    Directory of Open Access Journals (Sweden)

    Yi Zhu

    2013-09-01

    Full Text Available Background/Aims: Myocardium ischemia-reperfusion (I/R injury can be caused by imbalances in cellular metabolism. Lactate, transported by monocarboxylate transporters (MCTs, has been implicated as a mechanism in this process. The present study was designed to investigate the expression and functional role of MCTs in rat hearts during ischemia and reperfusion. Methods: Langendorff-perfused rat hearts were subjected to 20 minutes stabilization, 30 minutes of global ischemia and 60 minutes reperfusion. Hearts were collected serially for detecting expression changes in MCT1, MCT4 during myocardial I/R injury and lactate concentration was measured. Post-ischemic left ventricular function and infract size were determined at end-point, followed by the pretreatment of D-lactate, a competitive inhibitor of MCTs. Results: MCT4 was significantly increased following global ischemia and MCT1 expression was increased during the early stages of reperfusion in isolated rat hearts, while the expression of the ancillary protein CD147 was increased during I/R injury. We determined increases in AMPK phosphorylation status, which was significantly elevated following ischemia and early reperfusion. Blocking monocarboxylate transport by competitive inhibition with D-lactate caused decreased left ventricular performance and increased infarct size. Conclusion: Increased MCT4 expression facilitates lactate extrusion during the ischemic period, while increased MCT1 may facilitate lactate transport into and out of cells simultaneously during early reperfusion, with increases in AMPK phosphorylation status during the myocardial I/R period. Lactate transport by MCTs has a profound protective effect during myocardial ischemia reperfusion injury.

  12. Diverse Effects of L-arginine on Cardiac Function of Rats Subjected to Myocardial Ischemia and Reperfusion in vivo

    Institute of Scientific and Technical Information of China (English)

    Xiaoliang WANG; Feng LIANG; Xiangying JIAO; Lei LIU; Xiaojie BAI; Meixia LI; Jianmin ZHI; Huirong LIU

    2007-01-01

    In vivo administration of L-arginine at different time points during the course of myocardial ischemia and reperfusion (MI/R) has been shown to differentially regulate postischemic apoptosis.Cardiac function is one of the most important indexes used to judge the degree of myocardial injury.The present study attempted to determine whether in vivo administration of L-arginine at different stages of MI/R has a diverse influence on cardiac function of ischemic reperfused hearts and,if So,to investigate the mechanisms involved.Male adult rats were subjected to 30 min myocardial ischemia followed by 5 h reperfusion.An intravenous L-arginine bolus was given either 10 min before and 50 min after reperfusion (early treatment) or 3 h and 4 h after reperfusion (late treatment).Early treatment with L-arginine markedly increased the left ventricular systolic pressure (LVSP) and dP/dtmax,and decreased myocardial nitrotyrosine content.In strict contrast,late treatment with L-arginine resulted in a significant decrease in LVSP and dP/dtmx from 4 h to 5h after reperfusion,and increase in toxic peroxynitrite formation as measured by nitrotyrosine.These results suggest that the administration of L-arginine at different time points during the course of MI/R leads to diverse effects on cardiac dysfunction.Early supplementation decreased the nitrative stress and improved left ventricular function.However,late treatment with L-arginine increased the formation of peroxynitrite and aggravated cardiac functional injury.

  13. Retrospective Analysis of Thrombolysis Therapy for 64 Cases of Acute Myocardial Infarction with Elevated ST Segment

    Institute of Scientific and Technical Information of China (English)

    傅晓霞; 肖文剑; 吕健; 吴乐文; 杨帆

    2009-01-01

    Objective:To explore the cardiac protective effect of integrative therapy in acute myocardial infarction(AMI) with elevated ST segment after reperfusion.Methods:Sixty-four AMI patients who having received decimalization by thrombolysis were assigned to two groups by retrospective analysis,36 patients in the treated group and 28 in the control group.Both were treated by intravenous administering of urokinase for thrombolysis,and to the treated group,intravenous dripping of Xueshuantong Injection(血栓通注射液,XS...

  14. Evaluation of Early Reperfusion Criteria in Acute Ischemic Stroke

    DEFF Research Database (Denmark)

    Ozenne, Brice; Cho, Tae-Hee; Mikkelsen, Irene Klaerke;

    2015-01-01

    BACKGROUND AND PURPOSE: Though still debated, early reperfusion is increasingly used as a biomarker for clinical outcome. However, the lack of a standard definition hinders the assessment of reperfusion therapies and study comparisons. The objective was to determine the optimal early reperfusion ...

  15. Protective effects of pinacidil hyperpolarizing cardioplegia on myocardial ischemia reperfusion injury by mitochondrial KATP channels

    Institute of Scientific and Technical Information of China (English)

    YU Tian; FU Xiao-yun; LIU Xing-kui; YU Zhi-hao

    2011-01-01

    Background Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels (KATP) were the end effectors of cardio-protection.But whether mitochondrial KATP plays an important role in hyperpolarizing cardioplegia is not apparent.The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil (a nonselective KATP opener) on ischemia/reperfusion injury in rat hearts,especially the role of mitochondrial KATP in pinacidil hyperpolarizing cardioplegia.Methods Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37℃before equilibration.Cardiac arrest was then induced in different treatments:there was no arrest and ischemia in the normal group,the control group were arrested by clamping the aorta,depolarizing caidioplegia (St.Thomas solution containing 16 mmol/L KCI) and hyperpolarizing cardioplegia groups used St.Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCI to induce cardiac arrest in group hyperkalemic and group pinacidil,in group hyperkalemic + 5-hydroxydecanote (5HD) and Pinacidil + 5HD,5HD (0.1 mmol/L) was added to the above two solutions to block mitochondria KATP channels.Global ischemia was then administrated for 40 minutes at 37℃,followed by 30 minutes of reperfusion.At the end of equilibration and reperfusion,hemodynamics,ultrastructure,and mitochondrial function were measured.Results In the control group,ischemia/reperfusion decreased the left ventricular developed pressure,heart rate,coronary flow,mitochondrial membrane potential,impaired mitochondrial respiratory function,increased reactive oxygen species and left ventricular end diastolic pressure.Damage to myocardial ultrastructure was also evident.Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions.5HD partially blocked the

  16. Factors Influencing Pre-hospital Patient Delay in Patients with Acute Myocardial Infarction

    Institute of Scientific and Technical Information of China (English)

    La Xie; Su-Fang Huang∗; You-Zhen Hu

    2015-01-01

    Acute myocardial infarction ( AMI) is a dangerous disease with a high mortality rate. For AMI patients, the outcome of the patients depends on time to beginning of effective treatment in addition to other factors such as severity of disease and involved vessels etc. The key is whether reperfusion therapy is started early enough after the onset of symptoms, and the benefit of reperfu-sion therapy depends on the time, too. The delay of AMI treatment is divided into pre-hospital de-lay and in-hospital delay. In-hospital delay, Door-to-Balloon Time, has been well controlled. Pre-hospital delay, accounting for 75% of the total delay time, is the most important factor affect-ing AMI treatment. Patient delay ( PD) time for AMI patients is summarised in this study.

  17. 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...

  18. Protective Effects of Elaeagnus angustifolia Leaf Extract against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

    Directory of Open Access Journals (Sweden)

    Binsheng Wang

    2014-01-01

    Full Text Available The purpose of this study is to clarify the cardioprotective property of the aqueous extract of Elaeagnus angustifolia L. leaf (EA against myocardial ischemia/reperfusion injury in isolated rat heart. The myocardial ischemia/reperfusion (I/R injury model of isolated rat heart was set up by the use of improved Langendorff retrograde perfusion technology. Compared with the ischemia/reperfusion (I/R group, the aqueous extract of Elaeagnus angustifolia L. leaf (0.5 mg/mL, 1.0 mg/mL pretreatment markedly improved the coronary flow (CF and raised left ventricular developed pressure (LVDP and maximum rise/down velocity (±dp/dtmax. The infarct size of the EA-treated hearts was smaller than that of I/R group. After treatment with EA, the superoxide dismutase (SOD activity increased; malondialdehyde (MDA and protein carbonyl content reduced more obviously (P<0.01 than that of I/R injury myocardial tissue. Conclusion. Results from the present study showed that the aqueous extract of Elaeagnus angustifolia L. leaf has obvious protective effects on myocardial I/R injury, which may be related to the improvement of myocardial oxidative stress states.

  19. Ethyl pyruvate reduces myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats.

    Science.gov (United States)

    Hu, Xiaorong; Cui, Bo; Zhou, Xiaoya; Xu, Changwu; Lu, Zhibing; Jiang, Hong

    2012-01-01

    High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Ethyl pyruvate (EP), a potent reactive oxygen species scavenger, has been reported to inhibit myocardial apoptosis and reduce myocardial I/R injury. The aim of this study was to investigate the mechanism by which EP reduces myocardial I/R injury in rats. Anesthetized male rats were once treated with EP (50 mg/kg, i.p.) before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that pretreatment of EP (50 mg/kg) could significantly reduce the infarct size and the levels of LDH and CK after 4 h reperfusion (all PR. The present study suggested that ethyl pyruvate could attenuate myocardial I/R injury by inhibiting HMGB1 expression.

  20. Effects of N-n-butyl Haloperidol Iodide on Myocardial Ischemia/Reperfusion Injury and Egr-1 Expression in Rat

    Institute of Scientific and Technical Information of China (English)

    Yan-Mei ZHANG; Gang-Gang SHI; Zhao TANG; Jin-Hong ZHENG; Wei-Qiu LI; Fu-Xiao GUO; Qiang-Yong JIA

    2006-01-01

    We have previously shown that N-n-butyl haloperidol iodide (F2) derived from haloperidol reduces ischemia/reperfusion-induced myocardial injury by blocking intracellular Ca2+ overload. This study tested the hypothesis that cardio-protection with F2 is associated with an attenuation in the expression of early growth response gene 1 (Egr-1). In an in vivo rat model of 60 min coronary occlusion followed by 180 min of reperfusion, treatment with F2 significantly reduced myocardial injury evidenced by the reduction in release of plasma creatine kinase, myocardial creatine kinase isoenzyme and lactate dehydrogenase. In cultured neonatal rat cardiomyocytes of hypoxia for 3 h and reoxygenation for 1 h, F2 treatment attenuated necrotic and apoptotic cell death, as demonstrated by electron microscopy. Concomitant with cardio-protection by F2, the increased expression levels of Egr-1 mRNA and proteinwere significantly reduced in myocardial tissue and cultured cardiomyocytes as detected by reverse transcription-polymerase chain reaction, immunohistochemistry and immunocytochemistry. In conclusion, these results suggest that the protective effect of F2 on ischemia/reperfusion- or hypoxia/reoxygenation-induced myocardial injury might be partly mediated by downregulating Egr-1 expression.

  1. 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.

  2. 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....

  3. 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....

  4. Nanog expression in heart tissues induced by acute myocardial infarction.

    Science.gov (United States)

    Luo, Huanhuan; Li, Qiong; Pramanik, Jogen; Luo, Jiankai; Guo, Zhikun

    2014-10-01

    Nanog is a potential stem cell marker and is considered a regeneration factor during tissue repair. In the present study, we investigated expression patterns of nanog in the rat heart after acute myocardial infarction by semi-quantitative RT-PCR, immunohistochemistry and Western blot analyses. Our results show that nanog at both mRNA and protein levels is positively expressed in myocardial cells, fibroblasts and small round cells in different myocardial zones at different stages after myocardial infarction, showing a spatio-temporal and dynamic change. After myocardial infarction, the nanog expression in fibroblasts and small round cells in the infarcted zone (IZ) is much stronger than that in the margin zone (MZ) and remote infarcted zone (RIZ). From day 7 after myocardial infarction, the fibroblasts and small cells strongly expressed nanog protein in the IZ, and a few myocardial cells in the MZ and the RIZ and the numbers of nanog-positive fibroblasts and small cells reached the highest peak at 21 days after myocardial infarction, but in this period the number of nanog-positive myocardial cells decreased gradually. At 28 days after myocardial infarction, the numbers of all nanog-positive cells decreased into a low level. Therefore, our data suggest that all myocardial cells, fibroblasts and small round cells are involved in myocardial reconstruction after cardiac infarction. The nanog-positive myocardial cells may respond to early myocardial repair, and the nanog-positive fibroblasts and small round cells are the main source for myocardial reconstruction after cardiac infarction.

  5. 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

  6. Cardioprotective effects of Guanxinshutong (GXST) against myocardial ischemia/reperfusion injury in rats

    Institute of Scientific and Technical Information of China (English)

    Zhuo Liang; Li-Feng Liu; Tian-Ming Yao; Yu Huo; Ya-Ling Han

    2012-01-01

    Background The protective effects against reperfusion injury of cardioprotective drugs have recently been evaluated and found to be inadequate. Guanxinshutong (GXST), a combination of the traditional herb and Mongolian medicine, is effective and safe in treating angina pectoris in clinical trials. We assess the cardioprotective effects of GXST against myocardial ischemia and reperfusion (MI/R) injury in rats and explore its possible mechanism. Methods Forty-five male Sprague Dawley rats were randomized into three groups: non-MI/R group (Sham, n = 15), MI/R group treated with vehicle (Control, n = 15) and MI/R group treated with GXST (Drug, n = 15). MI/R was induced by ligation of the left anterior descending coronary artery (LAD) for 30 minutes, followed by 2/24 hour reperfusion in the Control and Drug groups. In the Sham group, the LAD was exposed without occlusion. GXST powder (in the Drug group) or saline (in the Control and Sham groups) were administered via direct gastric gavage from 7 day prior to surgery. Blood samples were collected from the carotid artery (10 rats each group) after 2 hours of reperfusion, to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) using enzyme-linked immunosorbent assays. The animals were then sacrificed and the hearts were harvested for histopathology and western blot analysis. Infarct size was measured in the remaining five rats in each group after 24 hours reperfusion. Results GXST significantly decreased levels of TNF-α, IL-1β, IL-6, ICAM-1, apoptosis index (AI) and infarct size. GXST also obviously inhibited nuclear factor kappa B (NF-κB) activity when compared with the Control group (all P < 0.05). Conclusions GXST is effective in protecting the myocardium against MI/R injury in rats. Its possible cardioprotective mechanism involves inhibition of the inflammatory response and apoptosis following MI/R injury.

  7. Systemic inflammatory response following acute myocardial infarction.

    Science.gov (United States)

    Fang, Lu; Moore, Xiao-Lei; Dart, Anthony M; Wang, Le-Min

    2015-05-01

    Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.

  8. Systemic inflammatory response following acute myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    Lu FANG; Xiao-Lei Moore; Anthony M Dart; Le-Min WANG

    2015-01-01

    Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial in-farction, and heart failure) in patients with AMI.

  9. Low dose metoprolol in acute myocardial infarction.

    Science.gov (United States)

    Kumar, K P; Krishnaswami, S; Prasad, N K; Rath, P C; Jose, J

    1989-01-01

    A study of the effects of low dose Metoprolol was undertaken in 37 patients with acute myocardial infarction. These patients were randomly divided into three groups depending on the dose of the drug per kg body weight. Group I, consisting of 18 patients, received 0.36 to 0.65 mg per kg per day, Group II (10 patients) received 0.66 to 0.99 mg/kg/day, and Group III (9 patients) 1 to 1.81 mg/kg/day. To assess the degree of beta blockade achieved, the parameters that were evaluated were the fall in blood pressure and heart rate. There was a fall in systolic blood pressure which ranged from 7 to 17%, and fall in heart rate of 6.6 to 12.8% in the 3 groups over the 48-hour study period. These observations were compared with the results obtained from the Goteberg Metoprolol trial and Metoprolol in acute myocardial infarction (MIAMI) trials wherein 200 mg of Metoprolol per day were used. Our preliminary observations suggest that Indian patients may not need such a high dose, and Metoprolol at 50-100 mg per day would probably be sufficient to get the desired effect.

  10. Influence of ulinastatin on myocardial enzyme spectrum, inflammatory state and reperfusion injury of patients with extracorporeal circulation heart operation

    Institute of Scientific and Technical Information of China (English)

    Ming-Bin Deng; Ju-Yi Wan; Yi-Bing Fang

    2016-01-01

    Objective:To study the influence of ulinastatin on the myocardial enzymes, the inflammatory state and the reperfusion injury of patients with cardiopulmonary bypass.Methods:A total of 60 patients with extracorporeal circulation heart operation in our hospital from September 2012 to August 2015 were taken as research objects. 60 patients were randomly divided into two groups: observation group (conventional surgery group with ulinastatin, 30 cases) and control group (conventional surgery group, 30 cases), and then detected and compared the related indicators of serum cardiac enzymes, inflammatory state and ischemia-reperfusion injury of two test groups at 12 h, 24 h, 72 h after operation.Results:The serum myocardial zymogram of the observation group at 12 h, 24 h and 72 h after the operation were all lower than those of the control group. Meanwhile, the inflammatory indexes and the reperfusion injury indexes of the observation group were also better than those of the control group. The test result of two groups had significant differences.Conclusions: Ulinastatin can effectively improve the myocardial enzyme spectrum and the inflammatory state of patients with extracorporeal circulation heart operation. Besides, ulinastatin is also plays active role in the prevention of reperfusion injury.

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

    Science.gov (United States)

    Jeddi, Sajad; Khalifi, Saeedeh; Ghanbari, Mahboubeh; Bageripour, Fatemeh; Ghasemi, Asghar

    2016-01-01

    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. PMID:27849257

  12. 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.

  13. Combination of electrocardiographic and angiographic markers of reperfusion in the prediction of infarct size in patients with ST segment elevation myocardial infarction undergoing successful primary angioplasty

    NARCIS (Netherlands)

    De Luca, Giuseppe; Suryapranata, Harry; de Boer, Menko-Jan; Ottervanger, Jan Paul; Hoorntje, Jan C. A.; Gosselink, A. T. Marcel; Dambrink, Jan-Henk; Ernst, Nicolette; van't Hof, Arnoud W. J.

    2007-01-01

    Background: Optimal epicardial recanalization does not guarantee optimal myocardial perfusion. The aim of the current study was to evaluate angiographic and electrocardiographic markers of reperfusion in the prediction of infarct size in patients with STEMI undergoing successful primary angioplasty.

  14. Protective effect of dietary n-3 polyunsaturated fatty acids on myocardial resistance to ischemia-reperfusion injury in rats.

    Science.gov (United States)

    Zeghichi-Hamri, Sabrina; de Lorgeril, Michel; Salen, Patricia; Chibane, Mohamed; de Leiris, Joël; Boucher, François; Laporte, François

    2010-12-01

    Dietary n-3 polyunsaturated fatty acids (PUFA) reduce coronary heart disease (CHD) complications, such as chronic arrhythmia and sudden cardiac death. Improved myocardial resistance to ischemia-reperfusion injury results in smaller myocardial infarction, which is a major factor in the occurrence of CHD complications. We hypothesized that a specific dietary fatty acid profile (low in saturated and n-6 PUFA but high in plant and marine n-3 PUFA) may improve myocardial resistance to ischemia-reperfusion injury and reduce infarct size. To test this assumption, we used a well-defined rat model of myocardial infarction. Based on our results, in comparison to a diet that is high in either saturated or n-6 PUFA but poor in plant and marine n-3 PUFA, a diet that is low in saturated fats and n-6 PUFA but rich in plant and marine n-3 PUFA results in smaller myocardial infarct size (P fatty acid composition of plasma, erythrocyte cell membranes, and the phospholipids of myocardial mitochondria. The results show a great accumulation of n-3 PUFA and a parallel decrease in arachidonic acid, the main n-6 PUFA, in plasma, cell membranes, and cardiac mitochondria (P < .0001). We conclude that improved myocardial resistance to ischemia-reperfusion may be one of the critical factors explaining the protective effects of dietary n-3 PUFA against CHD complications in humans. In addition to increasing n-3 PUFA intake, an optimal dietary pattern aimed at reducing cardiovascular mortality should include a reduction of the intake of both saturated and n-6 PUFA.

  15. B beta(15-42) (FX06) reduces pulmonary, myocardial, liver, and small intestine damage in a pig model of hemorrhagic shock and reperfusion

    NARCIS (Netherlands)

    Roesner, Jan P.; Petzelbauer, Peter; Koch, Alexander; Tran, Nguyen; Iber, Thomas; Vagts, Dierk A.; Scheeren, Thomas W. L.; Vollmar, Brigitte; Noeldge-Schomburg, Gabriele E. F.; Zacharowski, Kai

    2009-01-01

    Objective:  The fibrin-derived peptide B beta(15-42) (also called FX06) has been shown to reduce myocardial infarct size following ischemia/reperfusion. Hemorrhagic shock (HS) followed by volume resuscitation represents a similar scenario, whereby a whole organism is vulnerable to reperfusion injury

  16. 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.

  17. 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.

  18. Research on Traditional Chinese Medicine in Treaof the present myocardial ischemia-reperfusion injury%中医药对心肌缺血再灌注损伤的研究现状

    Institute of Scientific and Technical Information of China (English)

    赵珏; 吴少俊; 王卫星

    2014-01-01

    Acute coronary syndrome was coronary heart disease in acute onset , clinical types of acute myocardial ischemic injury .In recent years, with thrombolytic therapy and percutaneous coronary intervention technology the establishment and promotion of artery bypass surgery and other methods significantly reduced the myocardial cell death due to ischemia and the ischemia myocardium after restoring blood flow myocardial ischemia-reperfusion injury in a cause for concern .This article analyzed injury mechanism and clinical research mainly from medical intervention to myocardial ischemia reperfusion .%急性冠脉综合征是冠心病中急性发病的临床类型,造成心肌急性缺血性损伤。近年来,随着溶栓疗法、经皮冠状动脉介入技术( Percutaneous coronary intervention ,PCI)、动脉搭桥术等方法的建立和推广,明显的减少了心肌由于缺血导致的细胞坏死,但缺血心肌恢复血流后,出现的心肌缺血再灌注损伤已成关注重点。本文主要从中医药对心肌缺血再灌注损伤干预机制及相关的临床研究进行阐述。

  19. 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....

  20. Combined postconditioning with ischemia and α7nAChR agonist produces an enhanced protection against rat myocardial ischemia reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    XIONG Jun; YUAN Yu-jing; XUE Fu-shan; WANG Qiang; LI Shan; LIAO Xu; LIU Jian-hua; CHEN Yi; LI Rui-ping

    2012-01-01

    Background Inflammation is one of important mechanisms for myocardial ischemia reperfusion injury (IRI).Ischemia postconditioning (IPOC) can protect the heart against IRI by inhibiting inflammation,but its cardioprotection is weaker than that of ischemia preconditioning.Recently,the α7 subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist has shown anti-infiammatory effects in many diseases related to inflammation.This randomized controlled experiment was designed to evaluate whether combined postconditioning with IPOC and the α7nAChR agonist could produce an enhanced cardioprotection in a rat in vivo model of acute myocardial IRI.Methods Fifty Sprague-Dawley rats were randomly divided into five equal groups:sham group,control group,IPOC group,α7nAChR agonist postconditioning group (APOC group) and combined postconditioning with IPOC and α7nAChR agonist group (combined group).Hemodynamic parameters were recorded during the periods of ischemia and reperfusion.Serum concentrations of troponin I (Tnl),tumor necrosis factor α (TNF-α) and high-mobility group box 1 (HMGB-1) at 180 minutes after reperfusion were assayed in all groups.At the end of the experiment,the infarct size was assessed from excised hearts by Evans blue and triphenyl tetrazolium chloride staining.Results As compared to the sham group,the infarct size in the other four groups was significantly increased,serum levels of Tnl,TNF-α and HMGB1 in the control group and TNF-α,HMGB1 in the IPOC group were significantly increased.The infarct size and serum concentrations of TNF-α,HMGB1 and Tnl in the IPOC,APOC and combined groups were significantly lower than those in the control group.As compared to the IPOC group,the infarct size in the combined group was significantly decreased,serum concentrations of Tnl,TNF-α and HMGB1 in the APOC and combined groups were significantly reduced.Although the infarct size was significantly smaller in the combined group than in the APOC group

  1. Hyperintense Acute Reperfusion Marker on FLAIR in Posterior Circulation Infarction.

    Directory of Open Access Journals (Sweden)

    Alex Förster

    Full Text Available In the present study, we aimed to investigate the frequency of blood brain barrier injury in posterior circulation infarction as demonstrated by the hyperintense acute reperfusion marker (HARM on fluid attenuated inversion recovery images (FLAIR.From a MRI report database we identified patients with posterior circulation infarction who underwent MRI, including perfusion-weighted images (PWI, within 12 hours after onset and follow-up MRI within 24 hours and analyzed diffusion-weighted images (DWI, PWI, FLAIR, and MR angiography (MRA. On FLAIR images, the presence of HARM was noted by using pre-specified criteria (focal enhancement in the subarachnoid space and/or the ventricles.Overall 16 patients (median age of patients 68.5 (IQR 55.5-82.75 years with posterior circulation infarction were included. Of these, 13 (81.3% demonstrated PCA occlusion, and 3 (18.7% patients BA occlusion on MRA. Initial DWI demonstrated ischemic lesions in the thalamus (68.8%, splenium (18.8%, hippocampus (75%, occipital lobe (81.3%, mesencephalon (18.8%, pons (18.8%, and cerebellum (50%. On follow-up MRA recanalization was noted in 10 (62.5% patients. On follow-up FLAIR images, HARM was observed in 8 (50% patients. In all of these, HARM was detected remote from the acute ischemic lesion. HARM was more frequently observed in patients with vessel recanalization (p = 0.04, minor infarction growth (p = 0.01, and smaller ischemic lesions on follow-up DWI (p = 0.05.HARM is a frequent finding in posterior circulation infarction and associated with vessel recanalization, minor infarction growth as well as smaller infarction volumes in the course. Neuroradiologists should be cognizant of the fact that HARM may be present on short interval follow-up FLAIR images in patients with acute ischemic infarction who initially underwent MRI and received intravenous gadolinium-based contrast agents.

  2. Double coronary artery thrombosis presenting as acute extensive anterior ST-segment elevation myocardial infarction

    Directory of Open Access Journals (Sweden)

    Ching-Wei Lee

    2013-07-01

    Full Text Available Simultaneous thrombosis of more than one coronary artery is an uncommon angiographic finding in acute ST-segment elevation myocardial infarction (STEMI, and usually leads to cardiogenic shock or even sudden cardiac death. We reported a 56-year-old man presenting with persistent chest tightness and ST-segment elevation over precordial leads in electrocardiography (ECG. Emergent coronary angiogram showed total occlusion of both the proximal right coronary artery (RCA and the proximal left anterior descending artery (LAD. We performed thrombus aspiration and stenting over the LAD with thrombolysis in myocardial infarction (TIMI III flow to the distal LAD. However, diminishing collateral flow to the distal RCA complicated with complete atrioventricular block (CAVB and cardiogenic shock developed thereafter. Because distal embolization of the collateral circulation from the LAD to the distal RCA was suspected, thrombus aspiration and stenting over the proximal RCA were performed. After reperfusion of the RCA, the patient's hemodynamic status stabilized and he recovered uneventfully.

  3. Capsaicin, arterial hypertensive crisis and acute myocardial infarction associated with high levels of thyroid stimulating hormone.

    Science.gov (United States)

    Patanè, Salvatore; Marte, Filippo; Di Bella, Gianluca; Cerrito, Marco; Coglitore, Sebastiano

    2009-05-01

    Chili peppers are rich in capsaicin. The potent vasodilator calcitonin gene-related peptide (CGRP) is stored in a population of C-fiber afferents that are sensitive to capsaicin. CGRP and peptides released from cardiac C fibers have a beneficial effect in myocardial ischemia and reperfusion. It has been reported that capsaicin pretreatment deplete cardiac C-fiber peptide stores. Furthermore, it has also been reported that capsaicin-treated pigs significantly increase mean arterial blood pressure compared with controls and that the decrease in CGRP synthesis and release contributes to the elevated blood pressure. It has also been reported that sub-clinical hypothyroidism is associated with a significant risk of coronary heart disease (CHD). We present a case of arterial hypertensive crisis and acute myocardial infarction in a 59-year-old Italian man with high levels of thyroid stimulating hormone and with an abundant ingestion of peppers and of chili peppers which occurred the day before.

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

    Science.gov (United States)

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

    2016-09-01

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

  5. 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.

  6. Intracoronary thallium-201 scintigraphy after thrombolytic therapy for acute myocardial infarction compared with 10 and 100 day intravenous thallium-201 scintigraphy

    Energy Technology Data Exchange (ETDEWEB)

    Heller, G.V.; Parker, J.A.; Silverman, K.J.; Royal, H.D.; Kolodny, G.M.; Paulin, S.; Braunwald, E.; Markis, J.E.

    1987-02-01

    Thallium-201 imaging has been utilized to estimate myocardial salvage after thrombolytic therapy for acute myocardial infarction. However, results from recent animal studies have suggested that as a result of reactive hyperemia and delayed necrosis, thallium-201 imaging may overestimate myocardial salvage. To determine whether early overestimation of salvage occurs in humans, intracoronary thallium-201 scans 1 hour after thrombolytic therapy were compared with intravenous thallium-201 scans obtained approximately 10 and 100 days after myocardial infarction in 29 patients. In 10 patients with angiographic evidence of coronary reperfusion, immediate improvement in thallium defects and no interim clinical events, there was no change in imaging in the follow-up studies. Of nine patients with coronary reperfusion but no initial improvement of perfusion defects, none showed worsening of defects in the follow-up images. Six of these patients demonstrated subsequent improvement at either 10 or 100 days after infarction. Seven of 10 patients with neither early evidence of reperfusion nor improvement in perfusion defects had improvement of infarct-related perfusion defects, and none showed worsening. In conclusion, serial scanning at 10 and 100 days after infarction in patients with no subsequent clinical events showed no worsening of the perfusion image compared with images obtained in acute studies. Therefore, there is no evidence that thallium-201 imaging performed early in patients with acute myocardial infarction overestimates improvement.

  7. Acute myocardial infarction in the obstetric patient.

    Science.gov (United States)

    Firoz, Tabassum; Magee, Laura A

    2012-06-01

    Acute myocardial infraction (AMI) in the obstetric patient is a rare event, although the incidence is rising due to advancing maternal age and pre-existing cardiac risk factors and medical co-morbidities. While atherosclerotic disease is the leading cause of AMI, coronary artery dissection is an important consideration in pregnancy and in the postpartum period. The physiological changes of pregnancy as well as pregnancy-specific risk factors can predispose the obstetric patient to AMI. Diagnosis of AMI can be challenging as symptoms may be atypical. Furthermore, diagnostic tests must be interpreted in the context of pregnancy. While the overall management of the obstetric patient with AMI is similar to that outside of pregnancy, drug therapy requires modification as some medications may be contraindicated in pregnancy and breastfeeding. There is limited information about prognosis and risk stratification but it is anticipated that future studies will address this issue.

  8. Reactive thrombocytosis leading to acute myocardial infarction.

    Science.gov (United States)

    Aundhakar, Swati C; Mahajan, Sanket K; Mane, Makarand B; Lakhotiya, Akshay N

    2013-10-01

    Thrombocytosis is defined as platelet count of > 600000. An elevated platelet count may be primarily (essential) or secondary (reactive). Acute myocardial infarction and other vaso-occlusive phenomenon are seen in less than 5% of the patients of reactive thrombocytosis. Here we report such a case. A 49 yr old lady presented with chest pain and had isolated right ventricular infarction that progressed to anteroseptal wall STEMI. Her platelet count was 11 lac; the triggering factor in this case was reactive thrombocytosis secondary to lower respiratory tract infection and iron-deficiency anaemia confirmed after investigations. The clinical diagnosis was confirmed through IL6 levels. The patient was managed aggressively in ICCU, she had an uneventful recovery and was discharged with a normal platelet count.

  9. Copeptin Testing in Acute Myocardial Infarction: Ready for Routine Use?

    Directory of Open Access Journals (Sweden)

    Sebastian Johannes Reinstadler

    2015-01-01

    Full Text Available Suspected acute myocardial infarction is one of the leading causes of admission to emergency departments. In the last decade, biomarkers revolutionized the management of patients with suspected acute coronary syndromes. Besides their pivotal assistance in timely diagnosis, biomarkers provide additional information for risk stratification. Cardiac troponins I and T are the most sensitive and specific markers of acute myocardial injury. Nonetheless, in order to overcome the remaining limitations of these markers, novel candidate biomarkers sensitive to early stage of disease are being extensively investigated. Among them, copeptin, a stable peptide derived from the precursor of vasopressin, emerged as a promising biomarker for the evaluation of suspected acute myocardial infarction. In this review, we summarize the currently available evidence for the usefulness of copeptin in the diagnosis and risk stratification of patients with suspected acute myocardial infarction in comparison with routine biomarkers.

  10. The nuclear melatonin receptor RORα is a novel endogenous defender against myocardial ischemia/reperfusion injury.

    Science.gov (United States)

    He, Ben; Zhao, Yichao; Xu, Longwei; Gao, Lingchen; Su, Yuanyuan; Lin, Nan; Pu, Jun

    2016-04-01

    Circadian rhythm disruption or decrease in levels of circadian hormones such as melatonin increases ischemic heart disease risk. The nuclear melatonin receptors RORs are pivotally involved in circadian rhythm regulation and melatonin effects mediation. However, the functional roles of RORs in the heart have never been investigated and were therefore the subject of this study on myocardial ischemia/reperfusion (MI/R) injury pathogenesis. RORα and RORγ subtypes were detected in the adult mouse heart, and RORα but not RORγ was downregulated after MI/R. To determine the pathological consequence of MI/R-induced reduction of RORα, we subjected RORα-deficient staggerer mice and wild-type (WT) littermates to MI/R injury, resulting in significantly increased myocardial infarct size, myocardial apoptosis and exacerbated contractile dysfunction in the former. Mechanistically, RORα deficiency promoted MI/R-induced endoplasmic reticulum stress, mitochondrial impairments, and autophagy dysfunction. Moreover, RORα deficiency augmented MI/R-induced oxidative/nitrative stress. Given the emerging evidence of RORα as an essential melatonin effects mediator, we further investigated the RORα roles in melatonin-exerted cardioprotection, in particular against MI/R injury, which was significantly attenuated in RORα-deficient mice, but negligibly affected by cardiac-specific silencing of RORγ. Finally, to determine cell type-specific effects of RORα, we generated mice with cardiomyocyte-specific RORα overexpression and they were less vulnerable to MI/R injury. In summary, our study provides the first direct evidence that the nuclear melatonin receptor RORα is a novel endogenous protective receptor against MI/R injury and an important mediator of melatonin-exerted cardioprotection; melatonin-RORα axis signaling thus appears important in protection against ischemic heart injury.

  11. Treatment with the C5a receptor antagonist ADC-1004 reduces myocardial infarction in a porcine ischemia-reperfusion model

    Directory of Open Access Journals (Sweden)

    Arheden Håkan

    2010-09-01

    Full Text Available Abstract Background Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model. Methods In anesthetized pigs (42-53 kg, a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8 or saline (9 mg/ml, n = 8. Area at risk (AAR was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis. Results ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007. Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23. The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data. Conclusions ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.

  12. 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...... of routine practice for patients with acute myocardial infarction....... 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...

  13. 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

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

    Directory of Open Access Journals (Sweden)

    Krishnamoorthy Karthikeyan K

    2006-09-01

    Full Text Available Abstract 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.

  15. Effect of Shenfu injection on nuclear factor-kB during myocardial ischemia/reperfusion injury in rats

    Institute of Scientific and Technical Information of China (English)

    ZHANG Ben-jing; WANA Yan-lin; WANG Cheng-yao; KE Jian-juan

    2005-01-01

    Objective: To investigate effects of Shenfu injection on the concentrations of plasma tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), activity of Nuclear Factor kappa B (NF-κB) and heart tissue ultrastructure during myocardial ischemia/reperfusion (I/R) injury in rats and its potential mechanism.Methods: Myocardial ischemia/reperfusion (I/R) was produced by ligation and release of the left anterior descending coronary artery. Ischemia lasted for 30 min and reperfusion for 60 min. Twenty-four healthy male SD rats weighing 230-280 g were randomly divided into three groups (n=8, each): Group I (Sham-operation group); Group II (I/R group); Group III (Shenfu group), in which Shenfu injection (10 ml/kg) was intraperitoneally injected 30 min before ischemia in animals with I/R. The plasma concentrations of IL-6 and TNF-α were measured by ELISA, and the heart was harvested for determination of NF-κB levels by Ecl-western blot analysis. Electron microscopy was used to study its ultrastructure.Results: After reperfusion, NF-κB binding activity in myocardial nuclei and the plasma concentrations of IL-6 and TNF-α were significantly increased in Group II, compared with Group I (P<0.01), and they were markedly reduced in Group III, compared with Group II (P<0.01). In addition, electron microscopic examination showed more serious injury of the myocardium ultrastructure in Group II, while in Group III the myocardial ultrastructure was similar to normal state.Conclusions: Shenfu injection inhibits NF-κB activity in I/R myocardium and leads to down-regulation of proinflammatory cytokine expression, which might be one of the molecular mechanisms of Shenfu injection in cardioprotection.

  16. 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...

  17. Achyranthes bidentata Polypeptides Reduces Oxidative Stress and Exerts Protective Effects against Myocardial Ischemic/Reperfusion Injury in Rats

    Directory of Open Access Journals (Sweden)

    Haifeng Zhang

    2013-09-01

    Full Text Available Achyranthes bidentata, a Chinese medicinal herb, is reported to be neuroprotective. However, its role in cardioprotection remains largely unknown. Our present study aimed to investigate the effects of Achyranthes bidentata polypeptides (ABPP preconditioning on myocardial ischemia/reperfusion (MI/R injury and to test the possible mechanisms. Rats were treated with ABPP (10 mg/kg/d, i.p. or saline once daily for one week. Afterward, all the animals were subjected to 30 min of myocardial ischemia followed by 4 h of reperfusion. ABPP preconditioning for one week significantly improved cardiac function following MI/R. Meanwhile, ABPP reduced infarct size, plasma creatine kinase (CK/lactate dehydrogenase (LDH activities and myocardial apoptosis at the end of reperfusion in rat hearts. Moreover, ABPP preconditioning significantly inhibited superoxide generation, gp91phox expression, malonaldialdehyde formation and enhanced superoxide dismutase activity in I/R hearts. Furthermore, ABPP treatment inhibited PTEN expression and increased Akt phosphorylation in I/R rat heart. PI3K inhibitor wortmannin blocked Akt activation, and abolished ABPP-stimulated anti-oxidant effect and cardioprotection. Our study demonstrated for the first time that ABPP reduces oxidative stress and exerts cardioprotection against MI/R injury in rats. Inhibition of PTEN and activation of Akt may contribute to the anti-oxidant capacity and cardioprotection of ABPP.

  18. Acute posteroinferior wall myocardial infarction secondary to football chest trauma.

    Science.gov (United States)

    Espinosa, R; Badui, E; Castaño, R; Madrid, R

    1985-12-01

    Myocardial infarction secondary to nonpenetrating chest trauma is rare. We present the case of a sportsman who developed an acute transmural posteroinferior wall myocardial infarction due to chest trauma by a football. The angiographic study revealed total obstruction of the proximal right coronary artery.

  19. Effects of phytoestrogen genistein on myocardial ischemia/reperfusion injury and apoptosis in rabbits

    Institute of Scientific and Technical Information of China (English)

    En-sheng JI; Hua YUE; Yu-ming WU; Rui-rong HE

    2004-01-01

    AIM: To study the effect of genistein (GST) on rabbit heart ischemia/reperfusion (I/R) injury. METHODS: Rabbit heart I/R injury was induced by occluding the left anterior descending coronary artery for 45 min and reperfusing for 180 min. GST (1.0 mg/kg) was intravenously injected 5 min before heart ischemia. Hemodynamic data, infarct size, and cardiomyocytic apoptosis were measured. The pathologic changes of I/R myocardium were observed.RESULTS: During the I/R, heart rate, mean arterial blood pressure, myocardial oxygen consumption, left ventricular (LV) -dp/dtmax and +dp/dtmax were decreased progressively. The infarct size was occupied 60.23 %±3.97 % (%of area at risk) in vehicle +I/R group while GST reduced the infarct size to 39.62 %±4.30 % (P<0.01). DNA ladder patter in myocardium was revealed by agarose gel electrophoresis in vehicle +I/R group while was not found in GST+I/R group. Apoptotic cardiomyocytes were sparse within ischemic myocardium at risk in GST+I/R group as compared with that in vehicle +I/R group (TUNEL stain). Apoptosis rate in ischemic myocardium from vehicle +I/R and GST+I/R groups detected by flow cytometry were 15.33 %±1.31% and 3.88 %±0.33 %,respectively. Fas and Bax protein expressions in ischemic myocardium of vehicle +I/R group were higher than that in GST+I/R group (P<0.01). Bcl-2/Bax ratio in vehicle +I/R group was lower than that in nonischemic myocardium (P<0.01), while in GST+I/R group, the Bcl-2/Bax ratio was higher than that in vehicle +I/R group (P<0.01).CONCLUSION: GST reduced infarct size and apoptosis of myocytes in I/R rabbit heart.

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

    NARCIS (Netherlands)

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

    2006-01-01

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

  1. Lipoprotein lipase gene variants: Association with acute myocardial ...

    African Journals Online (AJOL)

    Lipoprotein lipase gene variants: Association with acute myocardial infarction and lipid profiles. ... Therefore, genes involved in lipid and lipoprotein metabolism pathways such as lipoprotein lipase (LPL), are proper candidates ... Article Metrics.

  2. Pretreatment with low doses of acenocoumarol inhibits the development of acute ischemia/reperfusion-induced pancreatitis.

    Science.gov (United States)

    Warzecha, Z; Sendur, P; Ceranowicz, P; Dembinski, M; Cieszkowski, J; Kusnierz-Cabala, B; Tomaszewska, R; Dembinski, A

    2015-10-01

    Coagulative disorders are known to occur in acute pancreatitis and are related to the severity of this disease. Various experimental and clinical studies have shown protective and therapeutic effect of heparin in acute pancreatitis. Aim of the present study was to determine the influence of acenocoumarol, a vitamin K antagonist, on the development of acute pancreatitis. Studies were performed on male Wistar rats weighing 250 - 270 g. Acenocoumarol at the dose of 50, 100 or 150 μg/kg/dose or vehicle were administered once a day for 7 days before induction of acute pancreatitis. Acute pancreatitis was induced in rats by pancreatic ischemia followed by reperfusion. The severity of acute pancreatitis was assessed after 5-h reperfusion. Pretreatment with acenocoumarol given at the dose of 50 or 100 μg/kg/dose reduced morphological signs of acute pancreatitis. These effects were accompanied with a decrease in the pancreatitis-evoked increase in serum activity of lipase and serum concentration of pro-inflammatory interleukin-1β. Moreover, the pancreatitis-evoked reductions in pancreatic DNA synthesis and pancreatic blood flow were partially reversed by pretreatment with acenocoumarol given at the dose of 50 and 100 μg/kg/dose. Administration of acenocoumarol at the dose of 150 μg/kg/dose did not exhibit any protective effect against ischemia/reperfusion-induced pancreatitis. We concluded that pretreatment with low doses of acenocoumarol reduces the severity of ischemia/reperfusion-induced acute pancreatitis.

  3. Oxygen therapy for acute myocardial infarction.

    Science.gov (United States)

    Cabello, Juan B; Burls, Amanda; Emparanza, José I; Bayliss, Susan E; Quinn, Tom

    2016-12-19

    Oxygen (O2) is widely used in people with acute myocardial infarction (AMI). Previous systematic reviews concluded that there was insufficient evidence to know whether oxygen reduced, increased or had no effect on heart ischaemia or infarct size. Our first Cochrane review in 2010 also concluded there was insufficient evidence to know whether oxygen should be used. Since 2010, the lack of evidence to support this widely used intervention has attracted considerable attention, prompting further trials of oxygen therapy in myocardial infarction patients. It is thus important to update this Cochrane review. To assess the effects of routine use of inhaled oxygen for acute myocardial infarction (AMI). We searched the following bibliographic databases on 6 June 2015: the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE (OVID), Embase (OVID), CINAHL (EBSCO) and Web of Science (Thomson Reuters). LILACS (Latin American and Caribbean Health Sciences Literature) was last searched in September 2016. We also contacted experts to identify eligible studies. We applied no language restrictions. Randomised controlled trials in people with suspected or proven AMI (ST-segment elevation myocardial infarction (STEMI) or non-STEMI) within 24 hours after onset, in which the intervention was inhaled oxygen (at normal pressure) compared to air, regardless of co-therapies provided to participants in both arms of the trial. Two authors independently reviewed the titles and abstracts of identified studies to see if they met the inclusion criteria and independently undertook the data extraction. We assessed the quality of studies and the risk of bias according to guidance in the Cochrane Handbook for Systematic Reviews of Interventions. The primary outcome was death. The measure of effect used was the risk ratio (RR) with a 95% confidence interval (CI). We used the GRADE approach to evaluate the quality of the evidence and the GRADE profiler (GRADEpro) to

  4. Comparison of hospital mortality during ST-segment elevation myocardial infarction in the era of reperfusion therapy in women versus men and in older versus younger patients.

    Science.gov (United States)

    Juliard, Jean-Michel; Golmard, Jean Louis; Himbert, Dominique; Feldman, Laurent J; Delorme, Laurent; Ducrocq, Gregory; Descoutures, Fleur; Sorbets, Emmanuel; Garbarz, Eric; Boudvillain, Olivier; Aubry, Pierre; Vahanian, Alec; Steg, Philippe Gabriel

    2013-06-15

    There is intense interest in examining hospital mortality in relation to gender in ST-segment elevation myocardial infarction. The aim of the present study was to determine whether gender influences outcomes in men and women treated with the same patency-oriented reperfusion strategy. The influence of gender on hospital mortality was tested using multivariate analysis and local regression. The influence of age was tested as a continuous and as a categorical variable. In the overall population of 2,600 consecutive patients, gender was not correlated with hospital mortality except in the subgroup of women aged ≥65 years. The risk for death increased linearly in logit scale for men. Up to the age of 65 years, the risk also increased linearly in women but thereafter increased faster than in men. Testing age as a categorical variable, hospital mortality was higher in women than in men aged ≥75 years but was similar between the genders in the younger age categories. In conclusion, despite following an equal patency-oriented management strategy in men and women with ST-segment elevation myocardial infarctions, the risk for hospital death increased linearly with age but with an interaction between age and gender such that older women had an independent increase in hospital mortality. Longer time to presentation and worse baseline characteristics probably contributed to determine a high-risk subset but reinforce the need to apply, as recommended in the international guidelines in the management of patients with ST-segment elevation myocardial infarctions, the same strategy of acute reperfusion in men and women.

  5. 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

  6. 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

  7. 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

  8. Experimental Approaches to Acute Myocardial Infarction

    NARCIS (Netherlands)

    D.B. Uitterdijk (André)

    2015-01-01

    markdownabstractAbstract This thesis is dedicated to i) novel methods and optimization studies to improve the diagnosis of myocardial ischemia and myocardial infarction as well as fundamental studies that precede novel therapies for myocardial infarction. In part ii) 2 novel, adjunctive therapies f

  9. Experimental Approaches to Acute Myocardial Infarction

    NARCIS (Netherlands)

    D.B. Uitterdijk (André)

    2015-01-01

    markdownabstractAbstract This thesis is dedicated to i) novel methods and optimization studies to improve the diagnosis of myocardial ischemia and myocardial infarction as well as fundamental studies that precede novel therapies for myocardial infarction. In part ii) 2 novel, adjunctive therapies

  10. Sleep impairment and prognosis of acute myocardial infarction

    DEFF Research Database (Denmark)

    Clark, Alice; Lange, Theis; Hallqvist, Johan

    2014-01-01

    fatality and subsequent cardiovascular events following first-time acute myocardial infarction (AMI). DESIGN: Prospective cohort study. SETTING: The Stockholm Heart Epidemiology Program, Sweden. PARTICIPANTS: There were 2,246 first-time AMI cases. MEASUREMENTS AND RESULTS: SLEEP IMPAIRMENT WAS ASSESSED...... assessment that could benefit secondary cardiovascular prevention. CITATION: Clark A, Lange T, Hallqvist J, Jennum P, Rod NH. Sleep impairment and prognosis of acute myocardial infarction: a prospective cohort study. SLEEP 2014;37(5):851-858....

  11. Rapid initial reduction of hyperenhanced myocardium after reperfused first myocardial infarction suggests recovery of the peri-infarction zone: one-year follow-up by MRI.

    Science.gov (United States)

    Engblom, Henrik; Hedström, Erik; Heiberg, Einar; Wagner, Galen S; Pahlm, Olle; Arheden, Håkan

    2009-01-01

    The time course and magnitude of infarct involution, functional recovery, and normalization of infarct-related electrocardiographic (ECG) changes after acute myocardial infarction (MI) are not completely known in humans. We sought to explore these processes early after MI and during infarct-healing using cardiac MRI. Twenty-two patients with reperfused first-time MI were examined by MRI and ECG at 1, 7, 42, 182, and 365 days after infarction. Global left ventricular function and regional wall thickening were assessed by cine MRI, and injured myocardium was depicted by delayed contrast-enhanced MRI. Infarct size by ECG was estimated by QRS scoring. The reduction of hyperenhanced myocardium occurred predominantly during the first week after infarction (64% of the 1-year reduction). Furthermore, during the first week the amount of nonhyperenhanced myocardium increased significantly (Pinfarction. Also, the time course and magnitude for reduction of hyperenhanced myocardium were associated with normalization of infarct-related ECG changes.

  12. Activated Notch1 reduces myocardial ischemia reperfusion injury in vitro during ischemic postconditioning by crosstalk with the RISK signaling pathway

    Institute of Scientific and Technical Information of China (English)

    ZHOU Xue-liang; WAN Li; LIU Ji-chun

    2013-01-01

    Background Ischemic postconditioning (IPost),able to significantly attenuate myocardial ischemia reperfusion injury,is dependent on RISK signaling.Studies have shown that Notch signaling repairs damaged myocardium,and this study aimed to investigate the effect of Notch signaling in myocardial IPost.Methods We used H9c2 cells to establish the myocardial IPost and Hypoxia/Reoxygenation (H/R) model in vitro,which were randomly divided into control,H/R,IPost,Hepatocyte growth factor (HGF)+IPost and DAPT+IPost,N1ICD+IPost,miRNA+lPost,and Mock treatment groups.The myocardial cell viability was assessed by MTT,the cell apoptosis was detected using Annexin V/PI double staining and flow cytometry analyses.The expression of N1ICD,Hes1,PTEN Phospho-Akt/Akt,Phospho-GSK-3β/GSK-3β were detected by Western blotting.Finally,we assessed the changes in Ψm using the potential-sensitive dye JC-1 and measured using flow cytometry analyses.Results The Notch1 signaling is activated by HGF and ectopic expression of N1ICD during myocardial IPost,which increased myocardial cell viability,prevented cardiomyocyte apoptosis,and reduced loss of the mitochondrial membrane potential.However,myocardial ischemia reperfusion injury was increased in IPost when Notch1 signaling was inhibited using DAPT or with knockdown by Notch1-miRNA.Western blotting found that PTEN was down-regulated by Hes1 when Notch1 was activated,which consequently promoted Akt and GSK-3β phosphorylation.Conclusions Notch1 crosstalk with RISK signaling may be dependent on PTEN,which plays a cardioprotective role during IPost.This mechanism could provide a promising therapeutic target for the treatment of ischemic heart disease.

  13. An unusual cause of mismanagement in an acute myocardial infarction case: pseudothrombocytopenia.

    Science.gov (United States)

    Kocum, Tolga H; Katircibasi, Tuna M; Sezgin, Alpay T; Atalay, Hakan

    2008-07-01

    Thrombocytopenia determined by an automated counter may represent a benign, incidental finding in an asymptomatic patient or a potentially life-threatening disorder. Even if the low platelet count actually is a benign condition itself, in some conditions, any delay resulting from this condition consequently may be seriously hazardous. Low platelet count may alter the decision of heparin administration, which is an essential part of management during acute coronary syndromes. EDTA-dependent pseudothrombocytopenia (PTCP) is reported to have a prevalence of 0.1% in a general hospital; however, it is also reported that around 15% of the patients referred for a specialized center for isolated thrombocytopenia are actually cases of PTCP. In this report, we describe a patient with PTCP who could not receive reperfusion therapy during acute myocardial infarction because of the low platelet counts reported by an automated counter.

  14. Acute Carbon Monoxide Poisoning Resulting in ST Elevation Myocardial Infarction: A Rare Case Report

    Directory of Open Access Journals (Sweden)

    Po-Chao Hsu

    2010-05-01

    Full Text Available Acute carbon monoxide (CO poisoning with cardiac complications is well documented in the literature. However, ST segment elevation is a rare presentation, and most of these cases with ST elevation have revealed non-occlusive or normal coronary arteries. We report a case of CO poisoning complicated with ST elevation myocardial infarction. Emergency coronary angiography revealed total occlusion of the left anterior descending artery and primary percutaneous coronary intervention was performed. This report of a rare case should remind physicians that cardiovascular investigations, including electrocardiography, must be performed in cases with CO poisoning because mortality might increase if reperfusion therapy or appropriate medical treatments are not performed in patients with acute coronary artery occlusion.

  15. Comparison of the veracity of real-time perfusion, harmonic angio, and ultraharmonic myocardial contrast imaging modes in evaluation of acute myocardial infarction area

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    Background Innovative advancements in ultrasound instrumentation present a number of imaging modalities for myocardial contrast echocardiography (MCE) in ischemic syndromes. How well they compare to each other in diagnostic accuracy in the detection of acute myocardial infarction is unclear. The purpose of this study was to assess the relative accuracy of 3 different imaging modes of MCE, low mechanical index (MI) real-time perfusion imaging (RTPI), triggered harmonic angio mode (HA), and ultraharmonic imaging mode (UH) in the detection of acute experimental myocardial infarction within the time frame suitable for potential reperfusion. Methods MCE was performed in 10 open-chest dogs using RTPI, triggered HA and triggered UH modes at baseline and one hour after occlusion of left anterior descending coronary artery. Presence or absence of perfusion defects, and the perfusion defect size when present, were analyzed and compared with the infarct size delineated by triphenyltetrazolium chloride(TTC)staining. Results The infarct area was (15.8±2.4)% by TTC staining; Perfusion defect area by MCE was similar to anatomic infarct area in all the three MCE approaches: (16.1±2.7)% by RTPI mode, (15.5±2.9)% by HA mode, and (15.5±3.0)% by UH mode. The sensitivity, specificity and overall diagnostic accuracy in the detection of myocardial infarction were 100%, 88%, and 94% for RTPI mode, 88%, 100%, and 94 % for HA mode, and 100%, 75%, and 88% for UH mode. Conclusion All modes of MCE, RTPI, triggered HA mode and triggered UH mode have excellent diagnostic accuracy in the immediate hour of acute coronary occlusion within the optimal time frame suitable for reperfusion therapy.

  16. Carvedilol versus metoprolol in the acute phase of myocardial infarction:.

    Science.gov (United States)

    Bonnemeier, Hendrik; Ortak, Jasmin; Tölg, Ralph; Witt, Maren; Schmidt, Jörg; Wiegand, Uwe K H; Bode, Frank; Schunkert, Heribert; Richardt, Gert

    2005-01-01

    Beta-adrenergic blockers provide significant cardioprotection during acute ischemia and reperfusion. To further explore the effects of additional alpha-1-adrenoceptor blockade on autonomic modulation in acute myocardial infarction (AMI), carvedilol was compared with metoprolol in the setting of primary percutaneous coronary interventions (PCI). In a prospective study, 100 consecutive patients (61.1 +/- 11 years; 23 females) undergoing primary PCI for AMI were randomly assigned to metoprolol 200 mg/day vs carvedilol 25 mg/day. The first oral dose of study drug was administered upon hospital admission, and a 24-hour ambulatory electrocardiogram was recorded. A total of 40 recordings of patients assigned to metoprolol and 39 of patients assigned to carvedilol were eligible for analysis of heart rate turbulence. Turbulence onset (TO), turbulence slope (TS), and turbulence timing were measured after ventricular premature beats (VPBs). The mean value of the 10 preceding RR intervals (mean RR) before VPBs was also measured. There were no significant differences in mean age, gender distributions, TIMI perfusion grades, left ventricular ejection fraction, site and size of infarction, duration of ischemia, and mean 24-hour heart rate between the two groups. Though the mean RR were not significantly different (metoprolol 863.1 +/- 157 ms; carvedilol 839.6 +/- 151 ms), there was a trend toward lower values of TO in the carvedilol group (-0.015 +/- 0.016 vs -0.012 +/- 0.023%; P = NS) and significantly higher values for TS in the metoprolol group (6.96 +/- 5.8 vs 5.6 +/- 4.22; P metoprolol 5.8 +/- 2.4 vs carvedilol 6.1 +/- 2.1). In patients undergoing direct PCI for AMI, treatment with carvedilol, in contrast to metoprolol, was associated with a higher early acceleration and a lower deceleration of heart rate after VPBs, indicating differing effects on baroreceptor response due to additional alpha-1-adrenoceptor blockade. These data offer new insights into effects of a broader

  17. Acute myocardial infarction and renal failure following naphtha ingestion.

    Science.gov (United States)

    Roberge, R J; Crippen, D R; Jayadevappa, D; Kosek, T L

    2001-10-01

    We present a case of a non-Q wave myocardial infarction and acute renal failure following an ingestion of naphtha, a petroleum distillate composed primarily of hydrocarbons. The patient's renal, metabolic, and cardiac status improved over several days with aggressive volume replacement and bicarbonate therapy. Acute cardiotoxic effects of hydrocarbon exposure generally manifest as dysrhythmias, secondary to myocardial sensitization to circulating catecholamines, or, possibly, coronary vasospasm. Ischemia from associated hypotension or direct myocardial toxicity are other potential causes of naphtha-related cardiac injury.

  18. The role and modulation of autophagy in experimental models of myocardial ischemia-reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Carol Chen-Scarabelli; Richard Knight; Pratik R Agrawal; Louis Saravolatz; Cadigia Abuniat; Gabriele Scarabelli; Anastasis Stephanou; Leena Loomba; Jagat Narula; Tiziano M Scarabelli

    2014-01-01

    A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cyto-plasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated cata-bolic cellular‘housekeeping’ process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protec-tive mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the va-riability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic ma-nipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.

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

    Science.gov (United States)

    2013-01-01

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

  20. Targeting reperfusion injury in the era of primary percutaneous coronary intervention

    DEFF Research Database (Denmark)

    Lønborg, Jacob Thomsen

    2015-01-01

    Introduction of reperfusion therapy by primary percutaneous coronary intervention (PCI) has resulted in improved outcomes for patients presenting with ST-segment elevation myocardial infarction. Despite the obvious advantages of primary PCI, acute restoration of blood flow paradoxically also...

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

    Science.gov (United States)

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

    2015-01-01

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

  2. Autophagy protects cardiomyocytes from the myocardial ischaemia-reperfusion injury through the clearance of CLP36

    Science.gov (United States)

    Li, Shiguo; Liu, Chao; Gu, Lei; Wang, Lina; Shang, Yongliang; Liu, Qiong; Wan, Junyi; Shi, Jian; Wang, Fang; Xu, Zhiliang; Ji, Guangju

    2016-01-01

    Cardiovascular disease (CVD) is the leading cause of the death worldwide. An increasing number of studies have found that autophagy is involved in the progression or prevention of CVD. However, the precise mechanism of autophagy in CVD, especially the myocardial ischaemia-reperfusion injury (MI/R injury), is unclear and controversial. Here, we show that the cardiomyocyte-specific disruption of autophagy by conditional knockout of Atg7 leads to severe contractile dysfunction, myofibrillar disarray and vacuolar cardiomyocytes. A negative cytoskeleton organization regulator, CLP36, was found to be accumulated in Atg7-deficient cardiomyocytes. The cardiomyocyte-specific knockout of Atg7 aggravates the MI/R injury with cardiac hypertrophy, contractile dysfunction, myofibrillar disarray and severe cardiac fibrosis, most probably due to CLP36 accumulation in cardiomyocytes. Altogether, this work reveals autophagy may protect cardiomyocytes from the MI/R injury through the clearance of CLP36, and these findings define a novel relationship between autophagy and the regulation of stress fibre in heart. PMID:27512143

  3. Intermedin protects against myocardial ischemia-reperfusion injury in hyperlipidemia rats.

    Science.gov (United States)

    Yang, S M; Liu, J; Li, C X

    2014-10-20

    Hyperlipidemia is a well-established risk factor for the development of coronary atherosclerosis, while intermedin (IMD) has been identified as a novel calcitonin/calcitonin gene-related peptide family member involved in cardiovascular protection. However, whether IMD protects against hyperlipidemia-associated myocardial ischemia/reperfusion (MI/R) injury is unknown. We established a hyperlipidemia model using Sprague-Dawley rats, and created a MI/R condition by ligating the cardiac left circumflex artery. The possible pathophysiological role of IMD and its physiological function in MI/R was further studied. The level of IMD significantly decreased in hyperlipidemia rats (P hyperlipidemia rats compared to the sham-operated rats (P hyperlipidemia rats (P hyperlipidemia-associated MI/R injury. Additional IMD could protect cardiac myocytes against MI/R injury via reduction of apoptosis and inflammation in the hyperlipidemia rat model, and thus, it may play a potential role as a novel therapeutic target for cardiac ischemic injury in hyperlipidemic patients.

  4. 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.

  5. Is acute reperfusion therapy safe in acute ischemic stroke patients who harbor unruptured intracranial aneurysm?

    Science.gov (United States)

    Mowla, Ashkan; Singh, Karanbir; Mehla, Sandhya; Ahmed, Mohammad K; Shirani, Peyman; Kamal, Haris; Krishna, Chandan; Sawyer, Robert N; Ching, Marilou; Siddiqui, Adnan H; Levy, Elad I; Snyder, Kenneth V; Crumlish, Annemarie; Hopkins, L N

    2015-10-01

    Intracranial aneurysms are currently considered as contraindication for intravenous thrombolysis in acute ischemic stroke, very likely due to a possible increase in the risk of bleeding from aneurysm rupture; however, there is limited data available on whether intravenous thrombolysis is safe for acute ischemic stroke patients with pre-existing intracranial aneurysms. To find out the safety of intravenous thrombolysis in acute ischemic stroke patients who harbor unruptured intracranial aneurysms. We retrospectively reviewed the medical records and cerebrovascular images of all the patients treated with intravenous thrombolysis for acute ischemic stroke in our center from the beginning of 2006 till the end of April 2014. Those with unruptured intracranial aneurysm present on cerebrovascular images prior to acute reperfusion therapy were identified. Post-thrombolysis brain imaging was reviewed to evaluate for any intraparenchymal or subarachnoid hemorrhage related or unrelated to the aneurysm. A total of 637 patients received intravenous thrombolysis for acute ischemic stroke in our center during an 8·3-year period. Thirty-three (5·2%) were found to have at least one intracranial aneurysms. Twenty-three (70%) of those received only intravenous thrombolysis, and 10 patients received combination of intravenous and intra-arterial thrombolysis. The size of the largest aneurysm was 10 mm in maximum diameter (range: 2-10 mm). The mean size of aneurysms was 4·8 mm. No symptomatic intracranial hemorrhage occurred among the 23 patients receiving only intravenous thrombolysis. Out of those who received a combination of intravenous and intra-arterial thrombolysis, one developed symptomatic intracranial hemorrhage in the location of acute infarct, distant to the aneurysm location. Our findings suggest that neither intravenous thrombolysis nor combination of intravenous and intra-arterial thrombolysis increases the risk of aneurysmal hemorrhage in acute ischemic stroke

  6. Effects of dual endothelin receptor blockade on sympathetic activation and arrhythmogenesis during acute myocardial infarction in rats.

    Science.gov (United States)

    Kolettis, Theofilos M; Baltogiannis, Giannis G; Tsalikakis, Dimitrios G; Tzallas, Alexandros T; Agelaki, Maria G; Fotopoulos, Andreas; Fotiadis, Dimitrios I; Kyriakides, Zenon S

    2008-02-02

    The effects of dual (ETA and ETB) endothelin receptor blockade on ventricular arrhythmogenesis during acute myocardial infarction are not well defined. We randomly allocated Wistar rats to bosentan (100 mg/kg daily, n=24), a dual endothelin receptor antagonist, or vehicle (n=23). After 7 days of treatment, myocardial infarction was induced by permanent coronary ligation. Ventricular tachyarrhythmias were evaluated for 24 h following ligation, using a miniature telemetry electrocardiogram recorder. Action potential duration was measured from monophasic epicardial recordings and sympathetic activation was assessed by heart rate variability and catecholamine serum level measurements. Compared to controls (1012+/-185 s), bosentan (59+/-24 s) markedly decreased (PDual endothelin-1 receptor blockade decreases ventricular tachyarrhythmias during myocardial infarction without reperfusion, by preventing repolarization inhomogeneity. Diverse treatment effects on sympathetic activation may ameliorate the antiarrhythmic action.

  7. Protective effects of Ping-Lv-Mixture (PLM), a medicinal formula on arrhythmias induced by myocardial ischemia-reperfusion.

    Science.gov (United States)

    An, Wei; Yang, Jing

    2006-11-03

    Ping-Lv-Mixture (PLM) is a Chinese medicinal formula. The present study aimed to determine the effects of PLM on myocardial ischemia-reperfusion (MI/R) induced arrhythmias in rats. Arrhythmia model was established by occlusion of the left arterial descending coronary artery and thereafter reperfusion. A lead II electrocardiogram was monitored throughout the experiment. The results showed that pretreatment of PLM to MI/R rats significantly reduced the incidence and duration of ventricular tachycardia and ventricular fibrillation. On induction of MI/R, the activities of creatine kinase and lactate dehydrogenase were increased in vehicle group. PLM (0.04-1.00 g/kg) administration prevented the increase of these enzymes. Moreover, a significant increase of myocardium superoxide dismutase and decrease of malondialdehyde contents were observed in rats of PLM groups. On the other hand, the expressions of platelet activating factor (PAF) receptor mRNA was down-regulated in a dose-dependent manner in the PLM-treated groups by RT-PCR. Thus, it can be concluded that pretreatment with PLM inhibited lipid peroxidation in rats through suppressing the expression of PAF receptor, which may contribute to its preventive effect on myocardial ischemia-reperfusion induced arrhythmias.

  8. Protection of rutaecarpine against myocardial ischemia—reperfusion injury in rats:possible involvement of vanilloid receptors

    Institute of Scientific and Technical Information of China (English)

    HuCP; LiNS

    2002-01-01

    Previous investigations have shown that calcitonin gen-related peptide(CGRP) protects against myocardial ischemia-reperfusion injury and that rutaecarpine activates vanilloid receptors to evoke CGRP release.In the present study,SD rats were pretreated with rutaecarpine 10min before the experiment,and then the left main coronary artery was subjected to 60min occlusion followed by 3h reperfusion.Pretreatment with rutaecarpine(100 or 300μg·kg-1,iv) significantly reduced infarce size and creatine kinase release concomitantly with a significant increase in plasma concentrations of CGPR.These effects of rutaecarpine were completely abolished by pretreatment with capsazepine(38mg·kg-1,ic),a competitive vanilloid receptor antagonist or capsaicin (50mg·kg-1,sc),which selectively depletes transmitters in capsaicin-sensitive sensory nerves.These results suggest that the kprotection of rutaecarpine against myocardial ischemia-reperfusion injury is due to stimulation of endogenous CGRP release via activating vanilloid receptors in rats.

  9. 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.

  10. 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.

  11. 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...

  12. Time course of metabolic findings in coronary occlusion and reperfusion and their role for assessing myocardial salvage

    Energy Technology Data Exchange (ETDEWEB)

    Schwaiger, M.

    1986-08-01

    The techniques currently used to assess myocardial infarction are limited in their ability to determine the amount of viable myocardium after a temporary ischemic event. Blood flow and segmental function may not necessarily demonstrate salvage, whereas metabolic parameters will determine cell survival. In a dog open chest model, short occlusion times of 20 min and subsequent reperfusion using C-11 palmitate as an index of fatty acid metabolism showed depresssion of fatty acid oxidation, which recovered after 3 hours of reperfusion, indicating the partial reversibility of the ischemic condition. In more extensive studies, using positron emission tomography (PET) and, as an indicator of glucose metabolism, fluoro-F-18-deoxyglucose (FDG); N-13 ammonia in addition to C-11 palmitate for the determination of blood flow; and ultrasonic crystals to measure shortening in the reperfused and control territories, the duration of occlusion was 3h. Metabolic studies were repeated 24 h, 1 week, and 4 weeks after the ischemic injury. Reperfused viable myocardium exhibited residual glucose metabolism with FDG, whereas fatty acid oxidation remained impaired for a longer period. Gradual metabolic recovery during a 4-week period was associated with the prolonged recovery of regional function, whereas a lack of residual metabolic activity indicated that little change in function was likely to occur. Increased FDG uptake and impaired C-11 palmitate turnover are characteristic of reversibly injured tissue. Therefore, PET studies may offer a unique potential for the evaluation of therapeutic measures such as thrombolysis and early revascularization.

  13. Chronic Losartan Treatment Up-Regulates AT1R and Increases the Heart Vulnerability to Acute Onset of Ischemia and Reperfusion Injury in Male Rats.

    Science.gov (United States)

    Song, Minwoo A; Dasgupta, Chiranjib; Zhang, Lubo

    2015-01-01

    Inhibition of angiotensin II type 1 receptor (AT1R) is an important therapy in the management of hypertension, particularly in the immediate post-myocardial infarction period. Yet, the role of AT1R in the acute onset of myocardial ischemia and reperfusion injury still remains controversial. Thus, the present study determined the effects of chronic losartan treatment on heart ischemia and reperfusion injury in rats. Losartan (10 mg/kg/day) was administered to six-month-old male rats via an osmotic pump for 14 days and hearts were then isolated and were subjected to ischemia and reperfusion injury in a Langendorff preparation. Losartan significantly decreased mean arterial blood pressure. However, heart weight, left ventricle to body weight ratio and baseline cardiac function were not significantly altered by the losartan treatment. Of interest, chronic in vivo losartan treatment significantly increased ischemia-induced myocardial injury and decreased post-ischemic recovery of left ventricular function. This was associated with significant increases in AT1R and PKCδ expression in the left ventricle. In contrast, AT2R and PKCε were not altered. Furthermore, losartan treatment significantly increased microRNA (miR)-1, -15b, -92a, -133a, -133b, -210, and -499 expression but decreased miR-21 in the left ventricle. Of importance, addition of losartan to isolated heart preparations blocked the effect of increased ischemic-injury induced by in vivo chronic losartan treatment. The results demonstrate that chronic losartan treatment up-regulates AT1R/PKCδ and alters miR expression patterns in the heart, leading to increased cardiac vulnerability to ischemia and reperfusion injury.

  14. Twenty-four-hour Tl-201 delayed scan underestimates myocardial viability in patients with acute myocardial infarction after percutaneous transluminal coronary angioplasty

    Energy Technology Data Exchange (ETDEWEB)

    Mochizuki, Teruhito; Sugawara, Yoshifumi; Kikuchi, Takanori; Ikezoe, Junpei [Ehime Univ., Matsuyama (Japan). School of Medicine; Murase, Kenya; Higashino, Hiroshi; Miyagawa, Masao

    2001-04-01

    Myocardial viability in area at risk of acute myocardial infarction (AMI) after reperfusion therapy may be underestimated by the 24-hour images due to reverse redistribution (r-RD). Subjects were 37 AMI patients in whom Tc-99m pyrophosphate (PYP)/Tl-201 dual-isotope SPECT was positive. The 24-hour delayed scan was performed with only a Tl window. One month later, follow up rest Tl SPECT was performed to evaluate myocardial viability. In early (at PYP/Tl-201 dual-isotope SPECT), 24-hour, and one month follow up Tl studies, Tl uptake in the area of AMI was scored into four grades: 3 as normal to 0 as severely reduced. The scores were evaluated. Among the 37 AMI lesions, there were 16 r-RD, 3 RD, 16 fixed defect (FD) and 2 normal (positive PYP and normal Tl). Mean Tl scores were early; 1.4{+-}1.1, 24-hr; 0.9{+-}0.9 and one month; 1.3{+-}1.1. The 24-hour Tl score was lower than the early and one month Tl scores (p<0.01). Reverse redistribution is frequently observed in an area at risk where PYP SPECT was positive. Nuclear medicine physicians should be aware of the existence of frequent r-RD in Tl scan to avoid the underestimation of myocardial viability in the acute phase after PTCA. (author)

  15. Temporal changes in biomarkers and their relationships to reperfusion and to clinical outcomes among patients with ST segment elevation myocardial infarction.

    Science.gov (United States)

    van Diepen, Sean; Alemayehu, Wendimagegn G; Zheng, Yinggan; Theroux, Pierre; Newby, L Kristin; Mahaffey, Kenneth W; Granger, Christopher B; Armstrong, Paul W

    2016-10-01

    Coronary plaque rupture mediating acute ST segment elevation myocardial infarction (STEMI) is associated with a systemic inflammatory response. Whether early temporal changes in inflammatory biomarkers are associated with angiographic and electrocardiographic markers of reperfusion and subsequent clinical outcomes is unclear. In the APEX-AMI biomarker substudy, 376 patients with STEMI had inflammatory biomarkers measured at the time of hospital presentation and 24 h later. The primary outcome was the 90-day composite of death, shock, or heart failure. Secondary reperfusion outcomes were (1) worst least residual ST segment elevation (ST-E: <1 mm, 1 to <2 mm, ≥2 mm) and (2) post-percutaneous coronary intervention (PCI) TIMI flow grade (0/1/2 vs 3) and TIMI myocardial perfusion grade (TMPG 0/1 vs 2/3). The 90-day incidence of death, shock or heart failure was 21.3 % in this cohort. Electrocardiographic reperfusion (worst residual ST-E <1 mm, 1 to <2 mm, ≥2 mm) was associated with differences in 24 h change in N-terminal proB-type natriuretic peptide (NT-proBNP) (1192.8, 1332.5, 1859.0 ng/mL; p = 0.043) and the pro-inflammatory cytokines Interleukin (IL)-6 (14.0, 13.6, 22.1 pg/mL; p = 0.016), IL-12 (-0.5, -0.9, -0.1 pg/mL; p = 0.013), and tumor necrosis factor α (TNFα) (1.0, 0.6, 3.6 pg/mL; p = 0.023). Angiographic reperfusion (TMPG 0/1 vs 2/3) was associated with changes in median NT-proBNP (2649.3, 1382.7 ng/mL; p = 0.002) and IL-6 (28.7, 15.1; p = 0.040). After adjustment for baseline covariates, the 24 h change in the pro-inflammatory cytokine TNFα [hazard ratio (HR) 0.49; 95 % CI 0.26-0.95; p = 0.035] and the anti-inflammatory cytokine IL 10 (HR 1.41; 95 % CI 1.06-1.87; p = 0.018) were independently associated with the primary composite outcome. Successful coronary reperfusion was associated with less systemic inflammatory response and greater temporal inflammatory changes were independently associated with higher 90-day

  16. Comparative analysis of different cyclosporine A doses on protection after myocardial ischemia/reperfusion injury in rat

    Institute of Scientific and Technical Information of China (English)

    Kang Huang; Shi-Juan Lu; Jiang-Hua Zhong; Qun Xiang; Liu Wang; Miao Wu

    2014-01-01

    Objective:To investigate the protective effect of different cyclosporinA(CsA) doses on myocardial ischemia/reperfusion injury in rat models.Methods:A rat model of myocardial ischemia/reperfusion injury was established in vivoand the rats were randomly divided into four groups: placebo(PBS;T1), low-dose(CsA dose:1.0 mg/kg;T2), medium-dose(CsA dose:2.5 mg/kg;T3), and high-dose(CsA dose:5.0 mg/kg;T4) groups.Heart function indexes were monitored at different time points, the extent of myocardial infarction was assessed byEvans Blue-TTC staining, and creatine kinase MB mass and cardiac troponinI values were measured by biochemical assays.Results:Compared with theT1 andT2 groups, both the creatine kinase MB mass and cardiac troponinI were significantly lower in theT3 andT4 groups(P<0.05).The mean arterial pressure(MAP) and left ventricular systolic pressure(LVSP) decreased sequentially in each group, with the extending reperfusion time.Significant decreases inLVSP andMAP were observed in theT3 andT4 groups as compared to theT1 andT2 group(P<0.05), and theT2 group showed a significantly lowerLVSP andMAP decline than theT1 group(P<0.05).Compared with theT1 group, the rats from theT2,T3, andT4 groups suffered from a significantly lower extent of myocardial infarction(P<0.05).Also, the animals in theT3 andT4 groups had a significantly smaller extent of myocardial infarction than those in theT2 group(P<0.05).Conclusions:Various CsA doses exert different degrees of protection against ischemia/reperfusion injury, and this protective effect peaks at approximately2.5 mg/kg in rat models.

  17. 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.

  18. Earlier reperfusion in patients with ST-elevation Myocardial infarction by use of helicopter

    Directory of Open Access Journals (Sweden)

    Knudsen Lars

    2012-10-01

    Full Text Available Abstract Background In patients with ST-elevation myocardial infarction (STEMI reperfusion therapy should be initiated as soon as possible. This study evaluated whether use of a helicopter for transportation of patients is associated with earlier initiation of reperfusion therapy. Material and methods A prospective study was conducted, including patients with STEMI and symptom duration less than 12 hours, who had primary percutaneous coronary intervention (PPCI performed at Aarhus University Hospital in Skejby. Patients with a health care system delay (time from emergency call to first coronary intervention of more than 360 minutes were excluded. The study period ran from 1.1.2011 until 31.12.2011. A Western Denmark Helicopter Emergency Medical Service (HEMS project was initiated 1.6.2011 for transportation of patients with time-critical illnesses, including STEMI. Results The study population comprised 398 patients, of whom 376 were transported by ambulance Emergency Medical Service (EMS and 22 by HEMS. Field-triage directly to the PCI-center was used in 338 of patients. The median system delay was 94 minutes among those field-triaged, and 168 minutes among those initially admitted to a local hospital. Patients transported by EMS and field-triaged were stratified into four groups according to transport distance from the scene of event to the PCI-center: ≤25 km., 26–50 km., 51–75 km. and > 75 km. For these groups, the median system delay was 78, 89, 99, and 141 minutes. Among patients transported by HEMS and field-triaged the estimated median transport distance by ground transportation was 115 km, and the observed system delay was 107 minutes. Based on second order polynomial regression, it was estimated that patients with a transport distance of >60 km to the PCI-center may benefit from helicopter transportation, and that transportation by helicopter is associated with a system delay of less than 120 minutes even at a transport

  19. The impaired activity of sensory afferent nerves in diabetes mellitus of rats in acute myocardial ischemia and reperfusion%糖尿病诱发大鼠神经退化及其对心肌缺血-再灌注神经反应性病理改变的影响

    Institute of Scientific and Technical Information of China (English)

    刘超杰; 李兔平; 郭政

    2015-01-01

    Objective The aim of the study was to investigate the diabetic neuro-degeneration and its changes in neuroreaction to myocardial ischemia and reperfusion,by evaluation of the altera-tion of noxious thermal threshold and expression of substance P (SP),calcitonin gene related peptide (CGRP)in dorsal root ganglia in upper thoracic segments (T1-5 )in diabetic rats.Methods Thirty two male Sprague-Dawley rats,weighing 180-200g,were randomly divided into control group (group C)and diabetic group (group DM),1 6 rats in each group.rats in DM group were fed with high sug-ar-fat diet for 14 weeks and were given streptozotocin (STZ,35 mg/mg,i.p.)at the end of the 4 th week,to set up diabetes experimental model.The animals in control group were fed with standard la-boratory diet.Tail flick latency to thermal stimulation was measured weekly.At the end of 10 weeks after administration of STZ,diabetic rats (and rats in control group)were further divided into myo-cardial ischemia-reperfusion group (group IR)and sham operation group (group Sham).The left an-terior descending branch of coronary artery was occluded for 30 min followed by reperfusion for 120 min,establishing myocardial ischemia-reperfusion.The histological immunofluorescence assay and Enzyme-linked immunosorbent assay (ELISA)were carried out to evaluate the changes of the expres-sions of CGRP and SP in the dorsal root ganglia.Results The tail flick latency was significantly in-creased in group DM,compared to the group C (P < 0.01).The immunoreactive materials for CGRP and SP in the sensory neurons in dorsal root ganglia of upper thoracic segments (T1-5 )were markedly declined in group DM (P <0.01 or P < 0.05).Furthermore,levels of SP and CGRP were signifi-cantly lower in the DRG of the group IR after myocardial ischemia-reperfusion,compared to that in the group sham (P <0.01).Conclusion Diabetes causes sensory denervation and obvious reduction of expression of SP and CGRP in the sensory neuron innervating heart during

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

    DEFF Research Database (Denmark)

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

    2009-01-01

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

  1. Expression of Bcl-2 and NF-κB in brain tissue after acute renal ischemia-reperfusion in rats

    Institute of Scientific and Technical Information of China (English)

    Na Zhang; Gen-Yang Cheng; Xian-Zhi Liu; Feng-Jiang Zhang

    2014-01-01

    Objective:To investigate the effect of acute renal ischemia reperfusion on brain tissue. Methods:Fourty eight rats were randomly divided into four groups(n=12): sham operation group,30 min ischemia60 min reperfusion group,60 min ischemia60 min reperfusion group, and 120 min ischemia60 min reperfusion group.The brain tissues were taken after the experiment. TUNEL assay was used to detect the brain cell apoptosis, and western blot was used to detect the expression of apoptosis-related proteins and inflammatory factors.Results:Renal ischemia-reperfusion induced apoptosis of brain tissues, and the apoptosis increased with prolongation of ischemia time.The detection at the molecular level showed decreasedBcl-2 expression, increasedBax expression, upregulated expression ofNF-κB and its downstream factor COX-2/PGE2.Conclusions:Acute renal ischemia-reperfusion can cause brain tissue damage, manifested as induced brain tissues apoptosis and inflammation activation.

  2. Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling.

    Science.gov (United States)

    Erikson, John M; Valente, Anthony J; Mummidi, Srinivas; Kandikattu, Hemanth Kumar; DeMarco, Vincent G; Bender, Shawn B; Fay, William P; Siebenlist, Ulrich; Chandrasekar, Bysani

    2017-02-10

    Re-establishing blood supply is the primary goal for reducing myocardial injury in subjects with ischemic heart disease. Paradoxically, reperfusion results in nitroxidative stress and a marked inflammatory response in the heart. TRAF3IP2 (TRAF3 Interacting Protein 2; previously known as CIKS or Act1) is an oxidative stress-responsive cytoplasmic adapter molecule that is an upstream regulator of both IκB kinase (IKK) and c-Jun N-terminal kinase (JNK), and an important mediator of autoimmune and inflammatory responses. Here we investigated the role of TRAF3IP2 in ischemia/reperfusion (I/R)-induced nitroxidative stress, inflammation, myocardial dysfunction, injury, and adverse remodeling. Our data show that I/R up-regulates TRAF3IP2 expression in the heart, and its gene deletion, in a conditional cardiomyocyte-specific manner, significantly attenuates I/R-induced nitroxidative stress, IKK/NF-κB and JNK/AP-1 activation, inflammatory cytokine, chemokine, and adhesion molecule expression, immune cell infiltration, myocardial injury, and contractile dysfunction. Furthermore, Traf3ip2 gene deletion blunts adverse remodeling 12 weeks post-I/R, as evidenced by reduced hypertrophy, fibrosis, and contractile dysfunction. Supporting the genetic approach, an interventional approach using ultrasound-targeted microbubble destruction-mediated delivery of phosphorothioated TRAF3IP2 antisense oligonucleotides into the LV in a clinically relevant time frame significantly inhibits TRAF3IP2 expression and myocardial injury in wild type mice post-I/R. Furthermore, ameliorating myocardial damage by targeting TRAF3IP2 appears to be more effective to inhibiting its downstream signaling intermediates NF-κB and JNK. Therefore, TRAF3IP2 could be a potential therapeutic target in ischemic heart disease.

  3. 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.)

  4. Strophanthus hispidus attenuates the Ischemia-Reperfusion induced myocardial Infarction and reduces mean arterial pressure in renal artery occlusion

    Directory of Open Access Journals (Sweden)

    Rohit Gundamaraju

    2014-01-01

    Full Text Available Background: The myocardium is generally injured in the case of reperfusion injury and arterial damage is caused by hypertension. In reference to these statements, the present study was focused. Cardiac glycosides were said to have protective effects against myocardial infarction and hypertension. Strophanthus hispidus was thus incorporated in the study. Objective: The prime objective of the study was to investigate the protective effects of Strophanthus hispidus against ischemia-reperfusion myocardial Infarction and renal artery occluded hypertension in rats. Materials and Methods: The animal model adopted was surgically-induced myocardial ischemia, performed by means of left anterior descending coronary artery occlusion (LAD for 30 min followed by reperfusion for another 4 h. Infarct size was assessed by using the staining agent TTC (2,3,5-triphenyl tetrazolium chloride. Hypertension was induced by clamping the renal artery with renal bulldog clamp for 4 h. Results: The study was fruitful by the effect of Strophanthus hispidus on infarction size, which got reduced to 27.2 ± 0.5and 20.0 ± 0.2 by 500 mg/Kg and 1000 mg/Kg ethanolic extracts which was remarkably significant when compared with that of the control group 52.8 ± 4.6. The plant extract did reduce heart rate at various time intervals. There was also a protective effect in the case of mean arterial blood pressure were the 500 mg/Kg and 1000 mg/Kg of the plant extract did reduce the hypertension after 60 minutes was 60.0 ± 4.80 and 50.50 ± 6.80. Conclusion: The results suggest that 500 mg/Kg and 100 mg/Kg ethanolic extract of Strophanthus hispidus was found to possess significant cardiac protective and anti-hypertensive activity.

  5. Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury

    Indian Academy of Sciences (India)

    Chang-Kui Gao; Hui Liu; Cheng-Ji Cui; Zhao-Guang Liang; Hong Yao; Ye Tian

    2016-03-01

    This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detected by TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, the hypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane potential were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax and cytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed by luciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increased significantly in I/R group (both < 0.05). Compared to H/R + negative control (NC) group, rate of cardiomyocyte apoptosis increased in H/R + miR-195 mimic group while decreased in H/R + miR-195 inhibitor group (both < 0.05). MiR-195 knockdown alleviated the loss of mitochondrial membrane potential ( < 0.05). MiR-195 overexpression decreased Bcl-2 mRNA and protein expression, increased BaxmRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all < 0.05). While, downregulated MiR-195 increased Bcl-2 mRNA and protein expression, decreased Bax mRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all < 0.05). Our study identified that miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promote cardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway.

  6. Redox activation of Ref-1 potentiates cell survival following myocardial ischemia reperfusion injury.

    Science.gov (United States)

    Gurusamy, Narasimman; Malik, Gautam; Gorbunov, Nikolai V; Das, Dipak K

    2007-08-01

    A recent study showed that cardiac adaptation could potentiate translocation of thioredoxin-1 (Trx-1) into the nucleus, which then interacted with Ref-1, resulting in a survival signal. Here, we present evidence that such adaptation also causes nuclear translocation of Ref-1, which is almost completely inhibited when the hearts were pretreated with antisense Ref-1 that also abolished the cardioprotective adaptive response. Significant amounts of NFkappaB and Nrf2 were found to be associated with Ref-1 when the nuclear extract obtained from the left ventricle was immunoprecipitated with Ref-1. Such Ref-1-NFkappaB and Ref-1-Nrf2 interactions were significantly inhibited with antisense Ref-1. However, immunoprecipitation of nuclear extract with NFkappaB showed that the association of Trx-1 with NFkappaB is increased in the adapted heart, which was again significantly blocked by antisense Ref-1. Nrf2 was also associated with NFkappaB; however, such association appeared to be independent of Ref-1. In contrast, myocardial adaptation to ischemia inhibited the ischemia reperfusion-induced loss of Nrf2 from the nucleus, which was inhibited by antisense Ref-1. The nuclear translocation and activation of Ref-1 appeared to generate a survival signal as evidenced by the increased phosphorylation of Akt that was inhibited with antisense Ref-1. Finally, confocal microscopy confirmed the results of immunoblotting, clearly showing the nuclear translocation of Ref-1 and nuclear 3D colocalization of Ref-1 with NFkappaB in the adapted heart and its inhibition with antisense Ref-1. Our results show that PC potentiates a survival signal through the phosphorylation of Akt by causing nuclear translocation and activation of Ref-1, where significant interaction among NFkappaB and Ref-1, Trx-1, and Nrf2 appears to regulate Ref-1-induced survival signal.

  7. 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...

  8. 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

  9. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    Science.gov (United States)

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Vesey, Alex T; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L; Fletcher, Alison M; van Beek, Edwin J R; Rudd, James H F; Fox, Keith A A; Dweck, Marc R; Newby, David E

    2015-01-01

    Background Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans. Methods and Results Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non–ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI. Conclusions The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI. Clinical Trial Registration URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254. PMID:26316523

  10. Severe Hyperthyroidism Presenting with Acute ST Segment Elevation Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Dayan Zhou

    2015-01-01

    Full Text Available Introduction. Acute myocardial infarction is life-threatening. A cardiac troponin rise accompanied by typical symptoms, ST elevation or depression is diagnostic of acute myocardial infarction. Here, we report an unusual case of a female who was admitted with chest pain. However, she did not present with a typical profile of an acute myocardial infarction patient. Case Presentation. A 66-year-old Han nationality female presented with chest pain. The electrocardiogram (ECG revealed arched ST segment elevations and troponin was elevated. However, the coronary angiography showed a normal coronary arterial system. Thyroid function tests showed that this patient had severe hyperthyroidism. Conclusion. Our case highlights the possibility that hyperthyroidism may cause a large area of myocardium injury and ECG ST segment elevation. We suggest routine thyroid function testing in patients with chest pain.

  11. Aortoenteric Fistula Assocaited with Acute Myocardial Infarcation

    OpenAIRE

    Fingerote, Robert J.; Alan BR Thomson

    1990-01-01

    A 64-year-old male with a prior abdominal aortic graft for lower limb ischemia presented with melena and myocardial infarction. Despite aggressive investigation, an aortoenteric fistula was not diagnosed until after massive gastrointestinal hemorrhage. The patient's myocardial infarction may have heen precipitated by hypotension induced by hemorrhage through the aortoenteric fistula. Patients with prior abdominal aortic graft surgery presenting with gastrointestinal bleeding, abdominal pain o...

  12. Regularity of hypoxia inducible factor 1 alpha expression in acute myocardial ischaemia in rats

    Institute of Scientific and Technical Information of China (English)

    LI Zhi-gang; WANG Jiang-feng; CHENG Jian-ding; LIU Yan-wei; XING Hao-wei; WANG Yong; CHEN Yu-chuan

    2007-01-01

    @@ Acute myocardial ischaemia is a common acute disease and a common cause of sudden death. However, it is difficult to diagnose in patients who died within 6 hours after the onset of myocardial ischaemia.

  13. 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.

  14. Risk profile in women with acute myocardial infarction.

    Science.gov (United States)

    Târlea, Mihaela; Deleanu, D; Bucşa, A; Zarma, L; Croitoru, M; Platon, P; Ginghină, Carmen

    2009-01-01

    The studies in the literature of the past years have noticed the particular characteristics of the ischemic heart disease in women, who seem to be lacking early diagnosis and invasive treatment of coronary heart disease. They especially emphasize that the evolution, complications and mortality in myocardial infarction in women are more severe. The evaluation of clinical, investigational and therapeutic aspects in a lot of women with acute myocardial infarction (AMI) versus a lot of men with the same pathology, hospitalised in the same period. 78 women hospitalised in the Emergency Institute of Cardiovascular Diseases between 1st January 1999 and 30th October 2001 with acute myocardial infarction. 109 men hospitalised in the Emergency Institute of Cardiovascular Diseases with acute myocardial infarction in the same period. acute myocardial infarction, coronary angiography +/=left ventriculography. The lot of study and the witness lot were divided into 3 subgroups based on the severity of coronary lesions: Group I: left main stenoses, Group II: stenoses >60% on the other epicardial coronary vessels, Group III: stenoses <60% on the other epicardial coronary vessels. The risk factors, clinical data, cardiac performance indices and medical and invasive treatment were compared between the two groups. The women hospitalised with AMI were older than men, had more diabetes and hypertension as main risk factors than men, with the exception of smoking, had more frequent heart failure and diastolic dysfunction of left ventricle. The favorite invasive treatment in women was the angioplasty with application of stent and in men--coronary bypass.

  15. PROCOAGULANT EFFECTS OF THROMBOLYTIC THERAPY IN ACUTE MYOCARDIAL INFARCTION

    Institute of Scientific and Technical Information of China (English)

    王燕妮; 刘茜茜; 祝家庆; 袁祖贻; 马西

    2002-01-01

    Objective.To examine the procoagulant effects of thrombolytic agent on hemostasis and study the role of hemostatic markers as predictors of clinical outcomes.Methods.In the present study,eighteen patients with acute myocardial infarction(AMI) received 1.5 or 2.0 million U nonspecific urokinase(UK),or 70~80 mg fibrin specific recombinant tissue plasminogen activator(rt PA)and did not use heparin until 8 hours after intravenous injection of the above agents.Eight patients with AMI and without thrombolytic therapy were enrolled as controls.Coagulant and thrombolytic activity markers included thrombin antithrombin Ⅲ complex (TAT),D dimer,fibrinogen (Fg),FMPV/Amax.All markers were determined before,immediately,1,2,4 and 8 hours after the administration of thrombolytic agents respectively. Results.Molecular marker of thrombin generation- - TAT showed an activated coagulant state immediately after thrombolytic therapy.Level of TAT showed no significant changes between every two observed phases in controls.However,level of TAT increased significantly from 4.95± 1.75μ g/L ( 4.63± 1.37μ g/L) to 14.71± 3.31μ g/L ( 14.25± 2.53μ g/L) before and immediately after administration of thrombolytic agents UK(or rt PA).There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P< 0.05).Patients achieving clinical reperfusion had lower TAT level than those failing in thrombolytic therapy,and higher FMPV/Amax level than controls.D dimer,a surrogate of thrombolytic activity increased markedly and Fg significantly declined after thrombolytic therapy(P< 0.05). Conclusions.Thrombin generation occurred in plasma in response to excess fibrinolysis induced by thrombolytic therapy.Both urokinase and rt PA had procoagulant action.This transient activation of the coagulant system might contribute to early reocclusion.These data provided the theoretical support for simultaneous administration of anticoagulant therapy with thrombolytic

  16. 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...... in this retrospective study by comparison of the use of analgesics during admission for a first acute myocardial infarction with the occurrence of silent ischemia at exertion tests four weeks after discharge from hospital. The study did not show a lower use of analgesics in patients with silent ischemia, but this may...

  17. Acute anteroseptal myocardial infarction in a patient with dextrocardia.

    Science.gov (United States)

    Alzand, Becker S N; Dennert, Robert; Kalkman, Robert; Gorgels, Anton P M

    2009-01-01

    Dextrocardia with situs inversus is an uncommon congenital condition in which the major visceral organs are reversed. The clinical diagnosis and electrocardiographic localization of myocardial infarctions in these patients remain a great challenge. We report a case of a 64-year-old man known with dextrocardia and situs inversus totalis presenting with acute chest pain irradiating to the right arm. The admission and reversed "normalized" electrocardiogram are presented, allowing for correct diagnosis of an acute anteroseptal myocardial infarction. The present case emphasizes the importance of performing a reversed electrocardiogram in patients with dextrocardia.

  18. ST-elevation acute myocardial infarction in pregnancy: 2016 update.

    Science.gov (United States)

    Ismail, Sahar; Wong, Cynthia; Rajan, Priya; Vidovich, Mladen I

    2017-02-13

    Acute myocardial infarction (AMI) during pregnancy or the early postpartum period is rare, but can be devastating for both the mother and the fetus. There have been major advances in the diagnosis and treatment of acute coronary syndromes in the general population, but there is little consensus on the approach to diagnosis and treatment of pregnant women. This article reviews the literature relating to the pathophysiology of AMI in pregnant patients and the challenges in diagnosis and treatment of ST-elevation myocardial infarction (STEMI) in this unique population. From a cardiologist, maternal-fetal medicine specialist, and anesthesiologist's perspective, we provide recommendations for the diagnosis and management of STEMI occurring during pregnancy.

  19. Effect of monoamine nervous transmitter and neuropeptide Y in the aged rats with myocardial injury after brain ischemia-reperfusion

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    AIM: To study the mechanism of myocardial injury after brain ischemia-reperfusion in aged rats from the changes in Dopamine (DA), Noradrenalin (NE), Epinephrine(E) and Neuropeptide Y(NPY).METHODS: Young (5 months) and aged (20 months or more) rats were divided into model groups and normal control groups, respectively. We observed the following items in rats with 60 minute reperfusion after 30 minute brain ischemia: the pathological changed of myocardium, the activities of lactic dehydrrogenase(LDH), creatine phosphokinase(CPK), the contents of NE, DA, E, NPY. RESULTS:The CPK and LDH activities in the young model rats were higher than those in the young control rats was higher than that in the young control rats (P<0.05). The serum CPK activity in the aged control rats was higher than that in the young control rats (P<0.05). The myocardial CPK activity was higher in the aged model rats compared with the young molel rats (P<0.05) and was higher in aged control rats compared with the young control rats (P<0.01). The myocardial LDH activity was lower in the aged control rats than that in the young control rats (P<0.05) and aged model rats (P<0.01). The serum NE level, the level of NE and DA in the hypothalamus were higher obviously than those in the young control rats. The serum NE contents in the two model groups (young and aged) were higher respectively than the two control rats (young and aged). The following items’ contents were higher in the aged model rats than in the young model rats: serum NE, serum E, hypothalamus NE. The hypothalamus NE and E content was lower in the aged model rats than in te aged control rats. NPY level in the brain tissue was lower in the aged control rats than that in the young control rats and aged model rats (P<0.05).CONCLUSION: The myocardial injury after brain ischemia-reperfusion was concerned with the enhanced excitability of sympathetic-adrenal system, espectially in the aged rats. However, the change in myocardial

  20. 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...

  1. 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.

  2. Protective effects of sitagliptin on myocardial injury and cardiac function in an ischemia/reperfusion rat model.

    Science.gov (United States)

    Chang, Guanglei; Zhang, Peng; Ye, Lin; Lu, Kai; Wang, Ying; Duan, Qin; Zheng, Aihua; Qin, Shu; Zhang, Dongying

    2013-10-15

    The purpose of this study is to investigate the effects and the underlying mechanisms of sitagliptin pretreatment on myocardial injury and cardiac function in myocardial ischemia/reperfusion (I/R) rat model. The rat model of myocardial I/R was constructed by coronary occlusion. Rats were pretreated with sitagliptin (300 mg/kg/day) for 2 weeks, and then subjected to 30 min ischemia and 2h reperfusion. The release of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), cardiac function and cardiomyocyte apoptosis were evaluated. The levels of malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in heart and glucagon-like peptide-1 (GLP-1) level in plasma were measured. Western blot analysis was performed to detect the target proteins of sitagliptin. Our results showed that sitagliptin pretreatment decreased LDH and CK-MB release, and MDA level in I/R rats. More importantly, we revealed for the first time that sitagliptin pretreatment decreased cardiomyocyte apoptosis while increased the levels of GSH-Px and SOD in heart. Sitagliptin also increased GLP-1 level and enhanced cardiac function in I/R rats. Furthermore, sitagliptin pretreatment up-regulated Akt(serine473) and Bad(serine136) phosphorylation, reduced the ratio of Bax/Bcl-2, and decreased expression levels of cleaved caspase-3 and caspase-3. Interestingly, the above observed effects of sitagliptin were all abolished when co-administered with GLP-1 receptor antagonist exendin-(9-39) or PI3K inhibitor LY294002. Taken together, our data indicate that sitagliptin pretreatment could reduce myocardial injury and improve cardiac function in I/R rats by reducing apoptosis and oxidative damage. The underlying mechanism might be the activation of PI3K/Akt signaling pathway by GLP-1/GLP-1 receptor. Crown Copyright © 2013 Published by Elsevier B.V. All rights reserved.

  3. 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

  4. 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.

  5. THROMBOLYSIS OR PRIMARY PCI FOR MYOCARDIAL INFARCTION WITH ST-SEGMENT ELEVATION? THE STREAM TRIAL (STRATEGIC REPERFUSION EARLY AFTER MYOCARDIAL INFARCTION

    Directory of Open Access Journals (Sweden)

    V. A. Sulimov

    2013-01-01

    Full Text Available Ambiguous data about comparability regarding clinical outcomes for prehospital thrombolysis, coupled with timely coronary angiography, and primary percutaneous coronary intervention (PCI in the early after acute ST-segment elevation myocardial infarction (STEMI, there are now.In the STREAM trial 1892 patients with STEMI diagnosed within 3 hours after onset of symptoms, and whom it was impossible to perform primary PCI within 1 h after the first medical contact, were randomly assigned into two treatment groups: a primary PCI b prehospital thrombolytic therapy with bolus tenecteplase (dose decreased by half in patients aged ≥75 years in combination with clopidogrel and enoxaparin followed by admission to the hospital, where it was possible to perform PCI. Emergency coronary angiography performed if thrombolysis failed. Coronary angiography and PCI of the infarct-related artery were performed in the period from 6 to 24 hours after randomization and thrombolytic therapy in the case of an effective thrombolysis. Primary endpoints include a composite of death, shock, congestive heart failure, or reinfarction up to 30 days.The primary endpoint occurred in 116 of 939 patients (12.4 % of the thrombolysis group and in 135 of 943 patients (14.3% of the primary PCI group (relative risk in the group thrombolysis 0.86, 95% confidence interval 0.68-1.09, p=0.21. Emergency angiography was required in 36.3% of patients in the thrombolysis, and the remaining patients, coronary angiography and PCI were performed at a mean of 17 hours after randomization and thrombolytic therapy. Thrombolysis group had more intracranial hemorrhages than primary PCI group (1.0% vs 0.2%, p=0.04; after correction protocol and dose reduction by half of tenecteplase in patients ≥75 years: 0.5% vs. 0.3%, p=0.45. The rate of non- intracranial bleeding in two treatment groups did not differ.Prehospital thrombolysis followed by coronary angiography and timely PCI provide effective

  6. THROMBOLYSIS OR PRIMARY PCI FOR MYOCARDIAL INFARCTION WITH ST-SEGMENT ELEVATION? THE STREAM TRIAL (STRATEGIC REPERFUSION EARLY AFTER MYOCARDIAL INFARCTION

    Directory of Open Access Journals (Sweden)

    V. A. Sulimov

    2015-09-01

    Full Text Available Ambiguous data about comparability regarding clinical outcomes for prehospital thrombolysis, coupled with timely coronary angiography, and primary percutaneous coronary intervention (PCI in the early after acute ST-segment elevation myocardial infarction (STEMI, there are now.In the STREAM trial 1892 patients with STEMI diagnosed within 3 hours after onset of symptoms, and whom it was impossible to perform primary PCI within 1 h after the first medical contact, were randomly assigned into two treatment groups: a primary PCI b prehospital thrombolytic therapy with bolus tenecteplase (dose decreased by half in patients aged ≥75 years in combination with clopidogrel and enoxaparin followed by admission to the hospital, where it was possible to perform PCI. Emergency coronary angiography performed if thrombolysis failed. Coronary angiography and PCI of the infarct-related artery were performed in the period from 6 to 24 hours after randomization and thrombolytic therapy in the case of an effective thrombolysis. Primary endpoints include a composite of death, shock, congestive heart failure, or reinfarction up to 30 days.The primary endpoint occurred in 116 of 939 patients (12.4 % of the thrombolysis group and in 135 of 943 patients (14.3% of the primary PCI group (relative risk in the group thrombolysis 0.86, 95% confidence interval 0.68-1.09, p=0.21. Emergency angiography was required in 36.3% of patients in the thrombolysis, and the remaining patients, coronary angiography and PCI were performed at a mean of 17 hours after randomization and thrombolytic therapy. Thrombolysis group had more intracranial hemorrhages than primary PCI group (1.0% vs 0.2%, p=0.04; after correction protocol and dose reduction by half of tenecteplase in patients ≥75 years: 0.5% vs. 0.3%, p=0.45. The rate of non- intracranial bleeding in two treatment groups did not differ.Prehospital thrombolysis followed by coronary angiography and timely PCI provide effective

  7. Intracoronary autologous mononucleated bone marrow cell infusion for acute myocardial infarction: results of the randomized multicenter BONAMI trial

    Science.gov (United States)

    Roncalli, Jérôme; Mouquet, Frédéric; Piot, Christophe; Trochu, Jean-Noel; Le Corvoisier, Philippe; Neuder, Yannick; Le Tourneau, Thierry; Agostini, Denis; Gaxotte, Virginia; Sportouch, Catherine; Galinier, Michel; Crochet, Dominique P.; Teiger, Emmanuel; Richard, Marie-Jeanne; Polge, Anne-Sophie; Beregi, Jean-Paul; Manrique, Alain; Carrie, Didier; Susen, Sophie; Klein, Bernard; Parini, Angelo; Lamirault, Guillaume; Croisille, Pierre; Rouard, Hélène; Bourin, Philippe; Nguyen, Jean-Michel; Delasalle, Béatrice; Vanzetto, Gérald; Van Belle, Eric; Lemarchand, Patricia F.

    2011-01-01

    Aims Intracoronary administration of autologous bone marrow cells (BMCs) leads to a modest improvement in cardiac function, but the effect on myocardial viability is unknown. The aim of this randomized multicenter study was to evaluate the effect of BMC therapy on myocardial viability in patients with decreased left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI) and to identify predictive factors for improvement of myocardial viability. Methods and Results One-hundred one patients with AMI and successful reperfusion, LVEF ≤45%, and decreased myocardial viability (resting Tl201-SPECT) were randomized to either a control group (n=49) or a BMC group (n=52). Primary endpoint was improvement of myocardial viability 3 months after AMI. Baseline mean LVEF measured by radionuclide angiography was 36.3 ± 6.9%. BMC infusion was performed 9.3 ± 1.7 days after AMI. Myocardial viability improved in 16/47 (34%) patients in the BMC group compared to 7/43 (16%) in the control group (p = 0.06). The number of non-viable segments becoming viable was 0.8 ± 1.1 in the control group and 1.2 ± 1.5 in the BMC group (p = 0.13). Multivariate analysis including major post-AMI prognostic factors showed a significant improvement of myocardial viability in BMC vs. control group (p=0.03). Moreover, a significant adverse role for active smoking (p=0.04) and a positive trend for microvascular obstruction (p=0.07) were observed. Conclusions Intracoronary autologous BMC administration to patients with decreased LVEF after AMI was associated with improvement of myocardial viability in multivariate –but not in univariate – analysis. A large multicenter international trial is warranted to further document the efficacy of cardiac cell therapy and better define a group of patients that will benefit from this therapy. PMID:21127322

  8. Review of tenecteplase (TNKase) in the treatment of acute myocardial infarction.

    Science.gov (United States)

    Melandri, Giovanni; Vagnarelli, Fabio; Calabrese, Daniela; Semprini, Franco; Nanni, Samuele; Branzi, Angelo

    2009-01-01

    TNKase is a genetically engineered variant of the alteplase molecule. Three different mutations result in an increase of the plasma half-life, of the resistance to plasminogen-activator inhibitor 1 and of the thrombolytic potency against platelet-rich thrombi. Among available agents in clinical practice, TNKase is the most fibrin-specific molecule and can be delivered as a single bolus intravenous injection. Several large-scale clinical trials have enrolled more than 27,000 patients with acute myocardial infarction, making the use of this drug truly evidence-based. TNKase is equivalent to front-loaded alteplase in terms of mortality and is the only bolus thrombolytic drug for which this equivalence has been formally demonstrated. TNKase appears more potent than alteplase when symptoms duration lasts more than 4 hours. Also, TNKase significantly reduces the rate of major bleeds and the need for blood transfusions. The efficacy of TNKase may be further improved by enoxaparin substitution for unfractionated heparin, provided that enoxaparin dose adjustment is made for patients more than 75 years old. Hitherto, the small available randomized studies and international clinical registries suggest that pre-hospital TNKase is as effective as primary angioplasty, thus laying the foundations for a new fibrinolytic, TNKase-based strategy as the backbone of reperfusion in acute myocardial infarction.

  9. Thrombolysis in acute myocardial infarction: need for a change in strategy and future directions.

    Science.gov (United States)

    Pitt, B

    1990-01-01

    The results of several major trials of i.v. thrombolysis in patients with acute myocardial infarction have demonstrated the efficacy of the treatment in reducing mortality. Streptokinase and rt-PA have been shown to be effective (APSAC = anisoylated plasminogen streptokinase activator complex; GISSI = Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto miocardico, ASSET = Anglo Scandinavian study of early thrombolysis, rt-PA). This treatment is associated with the potential for cerebral and major bleeding, especially in elderly patients. The benefit of this treatment in patients with cardiogenic shock or hypotension (ISIS-2) is discussed. There is no convincing evidence that patients with ST-segment depression or those with an equivocal electrocardiogram had been benefited from i.v. thrombolysis. Further studies with i.v. thrombolysis and/or other strategies need to be explored. Overall the use of i.v. thrombolytic agents in combination with PTCA in patients with acute myocardial infarction have resulted in improvement in ventricular function and survival in patients eligible for this therapy. However, new techniques and therapeutic approaches to prevent reocclusion, to prevent reperfusion injury, to prevent restenosis after PTCA, to prevent atherosclerosis in the infarct and non-infarct related arteries, and to reduce the potential for ventricular arrhythmias and sudden death as well as the potential for mural thrombi and embolization after infarction are needed. The 1990's will see attempts to determine the optimum adjunctive therapy or "cocktail" of agents to be used with i.v. thrombolysis.

  10. Aromatase inhibition attenuates desflurane-induced preconditioning against acute myocardial infarction in male mouse heart in vivo.

    Directory of Open Access Journals (Sweden)

    Virginija Jazbutyte

    Full Text Available The volatile anesthetic desflurane (DES effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. We hypothesized that endogenous estrogens play a role as mediators of desflurane-induced preconditioning against myocardial infarction. In this study, we tested the hypothesis that desflurane effects local estrogen synthesis by modulating enzyme aromatase expression and activity in the mouse heart. Aromatase metabolizes testosterone to 17β- estradiol (E2 and thereby significantly contributes to local estrogen synthesis. We tested aromatase effects in acute myocardial infarction model in male mice. The animals were randomized and subjected to four groups which were pre-treated with the selective aromatase inhibitor anastrozole (A group and DES alone (DES group or in combination (A+DES group for 15 minutes prior to surgical intervention whereas the control group received 0.9% NaCl (CON group. All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94 ± 15.5% vs. 17.1 ± 3.62% without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model.

  11. Myocardial ischemia and reperfusion-induced cell death depends on JNK activation and leads to phosphorylation of mitochondrial p46

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    @@ Multiple signaling pathways, including the c-Jun N-terminal kinase (JNK) pathway, are activated in myocardial ischemia and reperfusion (MI/R) and correlate with cell death. However, the role of the JNK pathway with respect to protection or destruction in MI/R-induced cell death is poorly understood. In a rabbit model, we found that ischemia followed by reperfusion resulted in JNK activation which could be detected in cytosol as well as in mitochondria. To address the functional role of the JNK activation, we examined the consequences of blockade of JNK activation in isolated cardiomyocytes under conditions of simulated ischemia. The JNK activity was stimulated ~6-fold by simulated ischemia and reperfusion (simulated MI). When a dominant negative mutant of JNK kinase-2(dnJNKK2), an upstream regulator of JNK, and JNK-interacting protein-1 (JIP-1) were expressed in myocytes by recombinant adenovirus, the activation of JNK by simulated MI was reduced 53%. Furthermore, the TNFα-activated JNK activity in H9c2 cells was completely abolished by dnJNKK2 and JIP-1. In correlation, when dnJNKK2 and JIP-1 were expressed in cardiomyocytes, both constructs significantly reduced cell death after simulated MI compared to vector controls.

  12. Did clinical trials in which erythropoietin failed to reduce acute myocardial infarct size miss a narrow therapeutic window?

    Directory of Open Access Journals (Sweden)

    Mark I Talan

    Full Text Available BACKGROUND: To test a hypothesis that in negative clinical trials of erythropoietin in patients with acute myocardial infarction (MI the erythropoietin (rhEPO could be administered outside narrow therapeutic window. Despite overwhelming evidence of cardioprotective properties of rhEPO in animal studies, the outcomes of recently concluded phase II clinical trials have failed to demonstrate the efficacy of rhEPO in patients with acute MI. However, the time between symptoms onset and rhEPO administration in negative clinical trials was much longer that in successful animal experiments. METHODOLOGY/PRINCIPAL FINDINGS: MI was induced in rats either by a permanent ligation of a descending coronary artery or by a 2-hr occlusion followed by a reperfusion. rhEPO, 3000 IU/kg, was administered intraperitoneally at the time of reperfusion, 4 hrs after beginning of reperfusion, or 6 hrs after permanent occlusion. MI size was measured histologically 24 hrs after coronary occlusion. The area of myocardium at risk was similar among groups. The MI size in untreated rats averaged ~42% of area at risk, or ~24% of left ventricle, and was reduced by more than 50% (p<0.001 in rats treated with rhEPO at the time of reperfusion. The MI size was not affected by treatment administered 4 hrs after reperfusion or 6 hrs after permanent coronary occlusion. Therefore, our study in a rat experimental model of MI demonstrates that rhEPO administered within 2 hrs of a coronary occlusion effectively reduces MI size, but when rhEPO was administered following a delay similar to that encountered in clinical trials, it had no effect on MI size. CONCLUSIONS/SIGNIFICANCE: The clinical trials that failed to demonstrate rhEPO efficacy in patients with MI may have missed a narrow therapeutic window defined in animal experiments.

  13. 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.

  14. Reduced myocardial blood flow in acute and chronic digitalization.

    Science.gov (United States)

    Steiness, E; Bille-Brahe, N E; Hansen, J F; Lomholt, N; Ring-Larsen, H

    1978-07-01

    The myocardial blood flow was measured by the 133Xenon disappearance curve from the left ventricular wall following an injection of 133Xenon in the left coronary artery in 8 dogs without digoxin pretreatment and in 8 chronically digitalized dogs. The myocardial blood flow was significantly less (30%) in the digitalized dogs than in the dogs without pretreatment. In the digitalized dogs as well as in those without pretreatment an intravenous injection of digoxin resulted in a further significant decrease of the myocardial blood flow of about 20% and a significant increase of the coronary vascular resistance. The reduced myocardial blood flow both during acute and chronic digitalization is beleived to be of clinical importance.

  15. Management of cardiogenic shock complicating acute myocardial infarction.

    Science.gov (United States)

    Van Herck, Jozef L; Claeys, Marc J; De Paep, Rudi; Van Herck, Paul L; Vrints, Christiaan J; Jorens, Philippe G

    2015-06-01

    Cardiogenic shock complicates approximately 5-10% of cases with acute myocardial infarction and carries a poor prognosis. Early revascularization remains the cornerstone treatment of cardiogenic shock complicating myocardial infarction. Inotropic and/or vasopressor agents can be used for haemodynamic stabilization, although this comes at the expense of increased myocardial oxygen consumption and extended myocardial ischaemia. In recent years, the use of mechanical circulatory support has significantly increased. However, there is only limited data available from randomized trials evaluating the different percutaneous support systems. This review summarizes the available literature concerning the management of cardiogenic shock and gives an overview of the recommendations of the European and German-Austrian guidelines on cardiogenic shock.

  16. Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

    Science.gov (United States)

    la Garza, Francisco Javier Guzmán-de; Ibarra-Hernández, Juan Manuel; Cordero-Pérez, Paula; Villegas-Quintero, Pablo; Villarreal-Ovalle, Claudia Ivette; Torres-González, Liliana; Oliva-Sosa, Norma Edith; Alarcón-Galván, Gabriela; Fernández-Garza, Nancy Esthela; Muñoz-Espinosa, Linda Elsa; Cámara-Lemarroy, Carlos Rodrigo; Carrillo-Arriaga, José Gerardo

    2013-01-01

    OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion. PMID:23917671

  17. Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

    Directory of Open Access Journals (Sweden)

    Francisco Javier Guzmán-de la Garza

    2013-07-01

    Full Text Available OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student’s t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion.

  18. Myocardial oedema in acute myocarditis detected by echocardiographic 2D myocardial deformation analysis

    DEFF Research Database (Denmark)

    Løgstrup, Brian Bridal; Nielsen, Jan Møller; Kim, W Y;

    2015-01-01

    AIMS: The clinical diagnosis of acute myocarditis is based on symptoms, electrocardiography, elevated myocardial necrosis biomarkers, and echocardiography. Often, conventional echocardiography reveals no obvious changes in global cardiac function and therefore has limited diagnostic value....... Myocardial deformation imaging by echocardiography is an evolving method used to characterize quantitatively longitudinal systolic function, which may be affected in acute myocarditis. The aim of our study was to assess the utility of echocardiographic deformation imaging of the left ventricle in patients...... with diagnosed acute myocarditis in whom cardiovascular magnetic resonance (CMR) evaluation was performed. METHODS AND RESULTS: We included 28 consecutive patients (mean age 32 ± 13 years) with CMR-verified diagnosis of acute myocarditis according to the Lake Louise criteria. Cardiac function was evaluated...

  19. Classical and remote post-conditioning effects on ischemia/reperfusion-induced acute oxidant kidney injury.

    Science.gov (United States)

    Kadkhodaee, Mehri; Najafi, Atefeh; Seifi, Behjat

    2014-11-01

    The present study aimed to analyze and compare the effects of classical and remote ischemic postconditioning (POC) on rat renal ischemia/reperfusion (IR)-induced acute kidney injury. After right nephrectomy, male rats were randomly assigned into four groups (n = 8). In the IR group, 45 min of left renal artery occlusion was induced followed by 24 h of reperfusion. In the classical POC group, after induction of 45 min ischemia, 4 cycles of 10 s of intermittent ischemia and reperfusion were applied to the kidney before complete restoring of renal blood. In the remote POC group, 4 cycles of 5 min ischemia and reperfusion of left femoral artery were applied after 45 min renal ischemia and right at the time of renal reperfusion. There was a reduction in renal function (increase in blood urea and creatinine) in the IR group. Application of both forms of POC prevented the IR-induced reduction in renal function and histology. There were also significant improvements in kidney oxidative stress status in both POC groups demonstrated by a reduction in malondialdehyde (MDA) formation and preservation of antioxidant levels comparing to the IR group. We concluded that both methods of POC have protective effects on renal function and histology possibly by a reduction in IR-induced oxidative stress.

  20. Enalapril protects against myocardial ischemia/reperfusion injury in a swine model of cardiac arrest and resuscitation

    Science.gov (United States)

    Wang, Guoxing; Zhang, Qian; Yuan, Wei; Wu, Junyuan; Li, Chunsheng

    2016-01-01

    There is strong evidence to suggest that angiotensin-converting enzyme inhibitors (ACEIs) protect against local myocardial ischemia/reperfusion (I/R) injury. This study was designed to explore whether ACEIs exert cardioprotective effects in a swine model of cardiac arrest (CA) and resuscitation. Male pigs were randomly assigned to three groups: sham-operated group, saline treatment group and enalapril treatment group. Thirty minutes after drug infusion, the animals in the saline and enalapril groups were subjected to ventricular fibrillation (8 min) followed by cardiopulmonary resuscitation (up to 30 min). Cardiac function was monitored, and myocardial tissue and blood were collected for analysis. Enalapril pre-treatment did not improve cardiac function or the 6-h survival rate after CA and resuscitation; however, this intervention ameliorated myocardial ultrastructural damage, reduced the level of plasma cardiac troponin I and decreased myocardial apoptosis. Plasma angiotensin (Ang) II and Ang-(1–7) levels were enhanced in the model of CA and resuscitation. Enalapril reduced the plasma Ang II level at 4 and 6 h after the return of spontaneous circulation whereas enalapril did not affect the plasma Ang-(1–7) level. Enalapril pre-treatment decreased the myocardial mRNA and protein expression of angiotensin-converting enzyme (ACE). Enalapril treatment also reduced the myocardial ACE/ACE2 ratio, both at the mRNA and the protein level. Enalapril pre-treatment did not affect the upregulation of ACE2, Ang II type 1 receptor (AT1R) and MAS after CA and resuscitation. Taken together, these findings suggest that enalapril protects against ischemic injury through the attenuation of the ACE/Ang II/AT1R axis after CA and resuscitation in pigs. These results suggest the potential therapeutic value of ACEIs in patients with CA. PMID:27633002

  1. 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.)

  2. Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses.

    Science.gov (United States)

    Patanè, Salvatore; Marte, Filippo; Di Bella, Gianluca; Turiano, Giuseppe

    2009-05-29

    Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. It has been reported that subclinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes but increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. It has been also reported an acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism and with a myocardial bridge too. Moreover, it has been reported that simply measuring maximum P wave duration and P wave dispersion values, may help to determine the patients with subclinical hyperthyroidism and high risk for the development of atrial fibrillation. We present a case of an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism.

  3. Should primary percutaneous coronary intervention be always the first option for patients with an ST elevation myocardial infarction?

    Institute of Scientific and Technical Information of China (English)

    LI Jian-ping; HUO Yong

    2010-01-01

    @@ Acute ST elevation myocardial infarction, caused by the acute occlusion of a coronary artery, is a life-threating emergency. Reperfusion therapy, namely, using the mechanical or chemical method to open the infarction related artery (IRA), has become the key treatment for such patients. As the duration of a coronary occlusion is the main determinant of final infarct size, and the latter determines the outcome of acute myocardial infarction (AMI) patients, the time issue has long been the most important topic in reperfusion therapy. Besides the time issue, several other factors must be considered: the efficiency of the reperfusion therapy, and the availability of the reperfusion therapy.

  4. Pheochromocytoma mimicking an acute myocardial infarction.

    NARCIS (Netherlands)

    Menke-van der Houven van Oordt, C.W.; Twickler, T.B.; Asperdt, F.G. van; Ackermans, P.; Timmers, H.J.L.M.; Hermus, A.R.M.M.

    2007-01-01

    We report a 42-year-old female who presented with retrosternal pain, dyspnoea and nausea. Electrocardiography suggested a recent anterior myocardial infarction. However, emergency coronary angiography showed normal blood flow through all the coronary arteries. Paroxysmal hypertension raised the susp

  5. Assessment of microembolization associated with revascularization in acute myocardial infarction: MDCT cardiac perfusion and function study.

    Science.gov (United States)

    Saeed, Maythem; Hetts, Steven W; Do, Loi; Wilson, Mark W

    2013-12-01

    To use multi-detector computed tomography (MDCT) for assessing the effects of coronary microemboli on pre-existing acute myocardial infarct (AMI) and to compare this pathology to LAD microembolization and occlusion/reperfusion. An angioplasty balloon catheter was placed in the LAD coronary artery of pigs under X-ray guidance. Four animals served as controls without intervention (group A) and an additional 24 animals (8/group) were subjected to microembolization (group B), occlusion/reperfusion (group C) or combination of the two insults (group D). MDCT was used to assess perfusion, LV function and viability. At postmortem, the LV sections were stained with hematoxylin/eosin and triphenyltetrazolium chloride (TTC). Dynamic perfusion and helical cine MDCT demonstrated decline in regional LV perfusion and function, respectively, after all interventions. MDCT showed significant differences in ejection fraction between groups: A = 57.5 ± 4.7%, B = 40.3 ± 0.5% P 0.7). Microscopic examination confirmed the presence of patchy and contiguous necrosis, MVO, edema and calcium deposits. Dynamic and helical cine MDCT imaging can grade LV dysfunction and perfusion deficit, respectively. DE-MDCT demonstrated a large and persistent MVO zone after microembolization of pre-existing AMI. Furthermore, it has the potential to visualize patchy microinfarct, detect perfusion deficits and dysfunction at the border zone after microembolization of pre-existing AMI.

  6. History of Depression and Survival After Acute Myocardial Infarction

    NARCIS (Netherlands)

    Carney, Robert M.; Freedland, Kenneth E.; Steinmeyer, Brian; Blumenthal, James A.; de Jonge, Peter; Davidson, Karina W.; Czajkowski, Susan M.; Jaffe, Allan S.

    2009-01-01

    Objective: To compare survival in post-myocardial (MI) participants from the Enhancing Recovery In Coronary Heart Disease (ENRICHD) clinical trial with a first episode of major depression (MD) and those with recurrent MID, which is a risk factor for mortality after acute MI. Recent reports suggest t

  7. 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,

  8. 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...

  9. Acute myocardial infarction in a young man using anabolic steroids.

    Science.gov (United States)

    Wysoczanski, Mariusz; Rachko, Maurice; Bergmann, Steven R

    2008-01-01

    Anabolic-androgenic steroids are used worldwide to help athletes gain muscle mass and strength. Their use and abuse is associated with numerous side effects, including acute myocardial infarction (MI). We report a case of MI in a young 31-year-old bodybuilder. Because of the serious cardiovascular complications of anabolic steroids, physicians should be aware of their abuse and consequences.

  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...

  11. Prehospital thrombolysis for acute st-segment elevation myocardial infarction

    NARCIS (Netherlands)

    Lamfers, Evert Jan Pieter

    2003-01-01

    Early treatment of acute ST elevation myocardial infarction is associated with a good prognosis and a low incidence of complications. Prehospital administration of thrombolytic treatment is one of the ways of starting treatment early after onset of symptoms. Fifteen years of experience in prehospita

  12. Thrombolytic therapy preserves vagal activity early after acute myocardial infarction

    DEFF Research Database (Denmark)

    Lind, P; Hintze, U; Møller, M

    2001-01-01

    OBJECTIVE: The purpose of this study was to evaluate the effects of thrombolytic therapy on vagal tone after acute myocardial infarction (AMI). DESIGN: Holter monitoring for 24 h was performed at hospital discharge and 6 weeks after AMI in 74 consecutive male survivors of a first AMI, who fulfill...

  13. Myocardial stress in patients with acute cerebrovascular events

    DEFF Research Database (Denmark)

    Jespersen, Christian M; Fischer Hansen, Jørgen

    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...

  14. Sildenafil-mediated neovascularization and protection against myocardial ischaemia reperfusion injury in rats: role of VEGF/angiopoietin-1

    Science.gov (United States)

    Koneru, Srikanth; Varma Penumathsa, Suresh; Thirunavukkarasu, Mahesh; Vidavalur, Ramesh; Zhan, Lijun; Singal, Pawan K; Engelman, Richard M; Das, Dipak K; Maulik, Nilanjana

    2008-01-01

    Sildenafil citrate (SC), a drug for erectile dysfunction, is now emerging as a cardiopulmonary drug. Our study aimed to determine a novel role of sildenafil on cardioprotection through stimulating angiogenesis during ischaemia (I) reperfusion (R) at both capillary and arteriolar levels and to examine the role of vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1) in this mechanistic effect. Rats were divided into: control sham (CS), sildenafil sham (SS), control + IR (CIR) and sildenafil + IR (SIR). Rats were given 0.7 mg/kg, (i.v) of SC or saline 30 min. before occlusion of left anterior descending artery followed by reperfusion (R). Sildenafil treatment increased capillary and arteriolar density followed by increased blood flow (2-fold) compared to control. Treatment with sildenafil demonstrated increased VEGF and Ang-1 mRNA after early reperfusion. PCR data were validated by Western blot analysis. Significant reduction in infarct size, cardiomyocyte and endothelial apoptosis were observed in SC-treated rats. Increased phosphorylation of Akt, eNOS and expression of anti-apoptotic protein Bcl-2, and thioredoxin, hemeoxygenase-1 were observed in SC-treated rats. Echocardiography demonstrated increased fractional shortening and ejection fraction following 45 days of reperfusion in the treatment group. Stress testing with dobutamine infusion and echocardiogram revealed increased contractile reserve in the treatment group. Our study demonstrated for the first time a strong additional therapeutic potential of sildenafil by up-regulating VEGF and Ang-1 system, probably by stimulating a cascade of events leading to neovascularization and conferring myocardial protection in in vivo I/R rat model. PMID:18373738

  15. 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

  16. 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.

  17. 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.

  18. Cardioprotective Effects of Genistin in Rat Myocardial Ischemia-Reperfusion Injury Studies by Regulation of P2X7/NF-κB Pathway

    Directory of Open Access Journals (Sweden)

    Meng Gu

    2016-01-01

    Full Text Available The present study aimed to assess the effects and mechanisms of genistin in the rat model of myocardial ischemia reperfusion injury. The rat hearts were exposed to the left anterior descending coronary artery (LAD ligation for 30 min followed by 1 h of reperfusion. In the rat of myocardial ischemia/reperfusion (MI/R, it was found that genistin pretreatment reduced myocardial infarct size, improved the heart rate, and decreased creatine kinase (CK and lactate dehydrogenase (LDH levels in coronary flow. This pretreatment also increased catalase (CAT, superoxide dismutase (SOD activities but decreased glutathione (GSH, malondialdehyde (MDA levels. Furthermore, we determined that genistin can ameliorate the impaired mitochondrial morphology and oxidation system; interleukin-6 (IL-6, interleukin-8 (IL-8, interleukin-10 (IL-10, and tumor necrosis factor-α (TNF-α levels were also recovered. Besides, related-proteins of nuclear factor kappa-B (NF-κB signal pathway activated by P2X7 were investigated to determine the molecular mechanism of genistin and their expressions were measured by western blot. These results presented here demonstrated that genistin enhanced the protective effect on the rats with myocardial ischemia reperfusion injury. Therefore, the cardioprotective effects of genistin may rely on its antioxidant and anti-inflammatory activities via suppression of P2X7/NF-κB pathways.

  19. MicroRNAs regulate mitochondrial apoptotic pathway in myocardial ischemia-reperfusion-injury.

    Science.gov (United States)

    Makhdoumi, Pouran; Roohbakhsh, Ali; Karimi, Gholamreza

    2016-12-01

    MicroRNAs (miRNAs) are small non-coding RNAs that act as post-transcriptional gene regulators. They are involved in the pathogenesis of different disorders including heart diseases. MiRNAs contribute to ischemia/reperfusion injury (I/RI) by altering numerous key signaling elements. Together with alterations in the various potential signaling pathways, modification in miRNA expression has been suggested as a part of the response network following ischemia/reperfusion (I/R). In addition, cardiac mitochondrial homeostasis is closely associated with cardiac function and impairment of mitochondrial activity occurred after ischemia/reperfusion injury. MiRNAs play a key role in the regulation of mitochondrial apoptotic pathway and signaling proteins. In this review, we summarize the knowledge currently available regarding the molecular mechanisms of miRNA-regulated mitochondrial functions during ischemia/reperfusion injury. This regulation occurs in different stages of mitochondrial apoptosis pathway.

  20. Implications of ventricular arrhythmia "bursts" with normal epicardial flow, myocardial blush, and ST-segment recovery in anterior ST-elevation myocardial infarction reperfusion: a biosignature of direct myocellular injury "downstream of downstream".

    Science.gov (United States)

    Majidi, Mohamed; Kosinski, Andrzej S; Al-Khatib, Sana M; Smolders, Lilian; Cristea, Ecaterina; Lansky, Alexandra J; Stone, Gregg W; Mehran, Roxana; Gibbons, Raymond J; Crijns, Harry J; Wellens, Hein J; Gorgels, Anton P; Krucoff, Mitchell W

    2015-02-01

    Establishing epicardial flow with percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) is necessary but not sufficient to ensure nutritive myocardial reperfusion. We evaluated whether adding myocardial blush grade (MBG) and quantitative reperfusion ventricular arrhythmia "bursts" (VABs) surrogates provide a more informative biosignature of optimal reperfusion in patients with Thrombolysis in Myocardial Infarction (TIMI) 3 flow and ST-segment recovery (STR). Anterior STEMI patients with final TIMI 3 flow had protocol-blinded analyses of simultaneous MBG, continuous 12-lead electrocardiogram (ECG) STR, Holter VABs, and day 5-14 SPECT imaging infarct size (IS) assessments. Over 20 million cardiac cycles from >4500 h of continuous ECG monitoring in subjects with STR were obtained. IS and clinical outcomes were examined in patients stratified by MBG and VABs. VABs occurred in 51% (79/154) of subjects. Microcirculation (MBG 2/3) was restored in 75% (115/154) of subjects, of whom 53% (61/115) had VABs. No VABs were observed in subjects without microvascular flow (MBG of 0). Of 115 patients with TIMI 3 flow, STR, and MBG 2/3, those with VABs had significantly larger IS (median: 23.0% vs 6.0%, p=0.001). Multivariable analysis identified reperfusion VABs as a factor significantly associated with larger IS (p=0.015). Despite restoration of normal epicardial flow, open microcirculation, and STR, concomitant VABs are associated with larger myocardial IS, possibly reflecting myocellular injury in reperfusion settings. Combining angiographic and ECG parameters of epicardial, microvascular, and cellular response to STEMI intervention provides a more predictive "biosignature" of optimal reperfusion than do single surrogate markers. © The European Society of Cardiology 2014.

  1. Seabuckthorn Pulp Oil Protects against Myocardial Ischemia–Reperfusion Injury in Rats through Activation of Akt/eNOS

    Science.gov (United States)

    Suchal, Kapil; Bhatia, Jagriti; Malik, Salma; Malhotra, Rajiv Kumar; Gamad, Nanda; Goyal, Sameer; Nag, Tapas C.; Arya, Dharamvir S.; Ojha, Shreesh

    2016-01-01

    Seabuckthorn (SBT) pulp oil obtained from the fruits of seabuckthorn [Hippophae rhamnoides L. (Elaeagnaceae)] has been used traditionally for its medicinal and nutritional properties. However, its role in ischemia–reperfusion (IR) injury of myocardium in rats has not been elucidated so far. The present study reports the cardioprotective effect of SBT pulp oil in IR-induced model of myocardial infarction in rats and underlying mechanism mediating activation of Akt/eNOS signaling pathway. Male albino Wistar rats were orally administered SBT pulp oil (5, 10, and 20 ml/kg/day) or saline for 30 days. On the day 31, ischemia was induced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. SBT pulp oil pretreatment at the dose of 20 ml/kg observed to stabilize cardiac function and myocardial antioxidants such as glutathione, superoxide dismutase, catalase, and inhibited lipid peroxidation evidenced by reduced malondialdehyde levels as compared to IR-control group. SBT pulp oil also improved hemodynamic and contractile function and decreased tumor necrosis factor and activities of myocyte injury marker enzymes; lactate dehydrogenase and creatine kinase-MB. Additionally, a remarkable rise in expression of pAkt–eNOS, Bcl-2 and decline in expression of IKKβ/NF-κB and Bax was observed in the myocardium. The histopathological and ultrastructural salvage of cardiomyocytes further supports the cardioprotective effect of SBT pulp oil. Based on findings, it can be concluded that SBT pulp oil protects against myocardial IR injury mediating favorable modulation of Akt-eNOS and IKKβ/NF-κB expression. PMID:27445803

  2. Primary percutaneous coronary intervention ameliorates complete atrioventricular block complicating acute inferior myocardial infarction

    Directory of Open Access Journals (Sweden)

    Lee SN

    2014-11-01

    Full Text Available Su Nam Lee, You-Mi Hwang, Gee-Hee Kim, Ji-Hoon Kim, Ki-Dong Yoo, Chul-Min Kim, Keon-Woong MoonDepartment of Internal Medicine, St Vincent’s Hospital, The Catholic University of Korea, Suwon, South KoreaObjective: Complete atrioventricular block (CAVB in acute inferior ST-segment elevation myocardial infarction (STEMI is associated with poor clinical outcomes after noninvasive treatment. This study was designed to determine the effect of primary percutaneous coronary intervention (PCI in patients with CAVB complicating acute inferior STEMI, at a single center.Methods: We enrolled 138 consecutive patients diagnosed with STEMI involving the inferior wall; of these, 27 patients had CAVB. All patients received primary PCI. The clinical characteristics, procedural data, and clinical outcomes were compared in patients with versus without CAVB. Results: Baseline clinical characteristics were similar between patients with and without CAVB. Patients with CAVB were more likely to present with cardiogenic shock, and CAVB was caused primarily by right coronary artery occlusion. Door-to-balloon time was similar between those two groups. After primary PCI, CAVB was reversed in all patients. The peak creatinine phosphokinase level, left ventricular ejection fraction and in-hospital mortality rate were similar between the two groups. After a median follow up of 318 days, major adverse cardiac events did not differ between the groups (8.1% in patients without CAVB; 11.1% in patients with CAVB (P=0.702.Conclusion: We conclude that primary PCI can ameliorate CAVB-complicated acute inferior STEMI, with an acceptable rate of major adverse cardiac events, and suggest that primary PCI should be the preferred reperfusion therapy in patients with CAVB complicating acute inferior myocardial infarction. Keywords: major adverse cardiac events, PCI-capable hospital

  3. 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

  4. Rethinking the epidemiology of acute myocardial infarction: challenges and opportunities.

    Science.gov (United States)

    Yeh, Robert W; Go, Alan S

    2010-05-10

    During the previous decade, many strategies for preventing acute myocardial infarction found to be efficacious in randomized controlled trials have been adopted by physicians in the community. Although evaluations of quality improvement typically focus on process measures at the hospital, practice, or clinician level, assessment of improvements in health outcomes remains the true test for the successful translation of evidence into practice. We performed a review of the current literature examining trends in the incidence of myocardial infarction in communities. We focused specifically on the group of population-based studies that have examined trends in myocardial infarction incidence. Few population-based studies have examined recent temporal trends in the incidence of myocardial infarction, overall and by type. Existing studies have been largely limited by modest sample sizes, limited diversity within the study populations, the use of composite end points that combine disparate outcomes, and the inability to characterize the effect of long-term outpatient medication use on observed trends in incidence and severity of myocardial infarction. More contemporary assessments of community-wide changes in the epidemiology of myocardial infarction are needed to help assess the effectiveness of primary prevention and to identify areas for potential improvement.

  5. The impact of numeric and graphic displays of ST-segment deviation levels on cardiologists' decisions of reperfusion therapy for patients with acute coronary occlusion.

    Science.gov (United States)

    Nimmermark, Magnus O; Wang, John J; Maynard, Charles; Cohen, Mauricio; Gilcrist, Ian; Heitner, John; Hudson, Michael; Palmeri, Sebastian; Wagner, Galen S; Pahlm, Olle

    2011-01-01

    The study purpose is to determine whether numeric and/or graphic ST measurements added to the display of the 12-lead electrocardiogram (ECG) would influence cardiologists' decision to provide myocardial reperfusion therapy. Twenty ECGs with borderline ST-segment deviation during elective percutaneous coronary intervention and 10 controls before balloon inflation were included. Only 5 of the 20 ECGs during coronary balloon occlusion met the 2007 American Heart Association guidelines for ST-elevation myocardial infarction (STEMI). Fifteen cardiologists read 4 sets of these ECGs as the basis for a "yes/no" reperfusion therapy decision. Sets 1 and 4 were the same 12-lead ECGs alone. Set 2 also included numeric ST-segment measurements, and set 3 included both numeric and graphically displayed ST measurements ("ST Maps"). The mean (range) positive reperfusion decisions were 10.6 (2-15), 11.4 (1-19), 9.7 (2-14), and 10.7 (1-15) for sets 1 to 4, respectively. The accuracies of the observers for the 5 STEMI ECGs were 67%, 69%, and 77% for the standard format, the ST numeric format, and the ST graphic format, respectively. The improved detection rate (77% vs 67%) with addition of both numeric and graphic displays did achieve statistical significance (P numeric and/or graphic displays. Acute coronary occlusion detection rate was low for ECGs meeting STEMI criteria, and this was improved by adding ST-segment measurements in numeric and graphic forms. These results merit further study of the clinical value of this technique for improved acute coronary occlusion treatment decision support.

  6. Acute Myocardial Infarction Caused by Filgrastim: A Case Report

    Directory of Open Access Journals (Sweden)

    Cemil Bilir

    2012-01-01

    Full Text Available Common uses of the granulocyte-colony stimulating factors in the clinical practice raise the concern about side effects of these agents. We presented a case report about an acute myocardial infarction with non-ST segment elevation during filgrastim administration. A 73-year-old man had squamous cell carcinoma of larynx with lung metastasis treated with the chemotherapy. Second day after the filgrastim, patient had a chest discomfort. An ECG was performed and showed an ST segment depression and negative T waves on inferior derivations. A coronary angiography had showed a critical lesion in right coronary arteria. This is the first study thats revealed that G-CSF can cause acute myocardial infarction in cancer patients without history of cardiac disease. Patients with chest discomfort and pain who are on treatment with G-CSF or GM-CSF must alert the physicians for acute coronary events.

  7. Thrombolysis in acute myocardial infarction using intracoronary streptokinase: assessment by thallium-201 scintigraphy

    Energy Technology Data Exchange (ETDEWEB)

    Schuler, G.; Schwarz, F.; Hofmann, M.; Mehmel, H.; Manthey, J.; Maurer, W.; Rauch, B.; Herrmann, H.; Kubler, W.

    1982-09-01

    Twenty-one patients with acute myocardial infarction, admitted to the hospital within 4 hours after the onset of symptoms, were studied by seven-pinhole thallium-201 scintigraphy before and 1 hour and 24 hours after intracoronary fibrinolysis using streptokinase. The size of the thallium-201 perfusion defect was assessed from myocardial cross sections reconstructed from the riginal seven-pinhole data and expressed as a fraction of left ventricular circumference. Recanalization was achieved in 16 patients within 3.9 +/- 1.6 hours after onset of symptoms (group A). In these patients, the size of the perfusion defect had decreased from 36 +/- 17% to 19 +/- 15%(p<0.001) at 24 hours. No significant change was detected to redistribution at 1 hour after the intervention. In five patients, intracoronary fibrinolysis was unsuccessful, and the vessel remained occluded (group B). The thallium-201 perfusion defect affected 40 +/- 15% of the left ventricular circumference before the intervention; it remained virtually unchanged at 1 hour (37 +/- 16%) and at 24 hours (41 +/- 15%) after fibrinolysis. The perfusion defect was most reduced in patients with extensive collaterals supplying the ischemic area or with subtotal occlusion of the affected coronary artery. It is concluded that successful intracoronary fibrinolysis may reduce the size of the thallium-201 perfusion defect in many patients with acute myocardial infarction. One important factor in the final result may be the presence of residual coronary flow supplied by extensive collaterals or by subtotal occlusion of the affected coronary artery when reperfusion is achieved around 4 hours after the onset of symptoms.

  8. Mediated protective effect of electroacupuncture pretreatment by miR-214 on myocardial ischemia/reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Pei-Yu LIU; Yi TIAN; Shi-Yuan XU

    2014-01-01

    Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion (I/R) injury and microRNAs (miRNAs) could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation (OGD) on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase (LDH) and creatine kinase (CK) activities, intracellular free Ca2+concentration ([Ca2+]i) as well as the relative protein levels of sodium/calcium exchanger 1(NCX1), BCL2-like 11 (BIM), calmodulin-dependent protein kinase IIδ(CaMKIIδ) and Cyclophilin D (CypD). Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining (±dp/dt max). In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR (qPCR) results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9

  9. Holmium:YAG laser coronary angioplasty in acute myocardial infarction

    Science.gov (United States)

    Topaz, On; Luxenberg, Michael; Schumacher, Audrey

    1994-07-01

    Patients who sustain complicated acute myocardial infarction in whom thrombolytic agents either fail or are contraindicated often need mechanical revascularization other than PTCA. In 24 patients with acute infarction complicated by continuous chest pain and ischemia who either received lytics or with contraindication to lytics, a holmium:YAG laser (Eclipse Surgical Technologies, Palo Alto, CA) was utilized for thrombolysis and plaque ablation. Clinical success was achieved in 23/24 patients, with 23 patients (94%) surviving the acute infarction. Holmium:YAG laser is very effective and safe in thrombolysis and revascularization in this complicated clinical setting.

  10. Prognostic significance of transient myocardial ischaemia after first acute myocardial infarction: five year follow up study

    DEFF Research Database (Denmark)

    Mickley, H; Nielsen, J R; Berning, J

    1995-01-01

    OBJECTIVE: To assess the five year prognostic significance of transient myocardial ischaemia on ambulatory monitoring after a first acute myocardial infarction, and to compare the diagnostic and long term prognostic value of ambulatory ST segment monitoring, maximal exercise testing...... episodes of transient ST segment depression, of which 98% were silent. Over a mean of 5 (range 4 to 6) years of follow up, patients with ambulatory ischaemia were no more likely to have objective end points than patients without ischaemic episodes. If, however, subjective events were included...

  11. 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

  12. Ivabradine protects against ventricular arrhythmias in acute myocardial infarction in the rat.

    Science.gov (United States)

    Mackiewicz, Urszula; Gerges, Joseph Y; Chu, Sandy; Duda, Monika; Dobrzynski, Halina; Lewartowski, Bohdan; Mączewski, Michał

    2014-06-01

    Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). To elucidate effect of ivabradine, pure heart rate (HR) reducing drug, on ventricular arrhythmias within 24 h after non-reperfused MI in the rat. ECG was recorded for 24 h after MI in untreated and ivabradine treated rats and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. Forty-five minutes and twenty-four hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca(2+) handling was assessed and expression and function of ion channels were studied. Ivabradine reduced average HR by 17%. Combined VT/VF incidence and arrhythmic mortality were higher in MI versus MI + Ivabradine rats. MI resulted in (1) increase of Ca(2+) sensitivity of ryanodine receptors 24 h after MI; (2) increase of HCN4 expression in the left ventricle (LV) and funny current (IF) in LV cardiomyocytes 24 h after MI, and (3) dispersion of MAP duration both 45 min and 24 h after MI. Ivabradine partially prevented all these three potential proarrhythmic effects of MI. Ivabradine is antiarrhythmic in the acute MI in the rat. Potential mechanisms include prevention of: diastolic Ca(2+)-leak from sarcoplasmic reticulum, upregulation of IF current in LV and dispersion of cardiac repolarization. Ivabradine could be an attractive antiarrhythmic agent in the setting of acute MI.

  13. 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.

  14. 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 < 0.001). 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 < 0.05). Following reperfused STEMI, 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.

  15. 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

  16. RP105 Protects Against Apoptosis in Ischemia/Reperfusion-Induced Myocardial Damage in Rats by Suppressing TLR4-Mediated Signaling Pathways

    Directory of Open Access Journals (Sweden)

    Jun Yang

    2015-07-01

    Full Text Available Background: Myocardial apoptosis is heavily implicated in the myocardial damage caused by ischemia-reperfusion (I/R. Toll-like receptor 4 (TLR4 is a potent inducer of these apoptotic cascades. In contrast, the radioprotective 105 kDa protein (RP105 is a specific negative regulator of TLR4 signaling pathways. However, the precise mechanisms by which RP105 inhibits myocardium apoptosis via TLR4-associated pathways during I/R is not fully understood. Methods: We utilized a rat model of myocardial ischemic reperfusion injury (MIRI. Animals were pre-treated with Ad-EGFP adenovirus, Ad-EGFP-RP105 adenovirus, saline, or nothing (sham. After three days, rats underwent a 30min left anterior descending coronary artery occlusion and a 4h reperfusion. Mycardial tissue was assessed by immunohistochemistry, TUNEL-staining, Western blot, quantitative RT-PCR, and a morphometric assay. Results: RP105 overexpression resulted in a reduction in infarct size, fewer TUNEL-positive cardiomyocytes, and a reduction in mitochondrial-associated apoptosis cascade activity. Further, RP105 overexpression repressed I/R-induced myocardial injury by attenuating myocardial apoptosis. This was mediated by inhibiting TLR4 activation and the phosphorylation of P38MAPK and the downstream transcription factor AP-1. Conclusion: RP105 overexpression leads to the de-activation of TLR4, P38MAPK, and AP-1 signaling pathways, and subsequently represses apoptotic cascades and ensuing damage of myocardial ischemic reperfusion. These findings may become the basis of a novel therapeutic approach for reducing of cardiac damage caused by MIRI.

  17. Acute Anteroseptal Myocardial Infarction after a Negative Exercise Stress Test

    Directory of Open Access Journals (Sweden)

    Abdullah M. Al-Alawi

    2016-05-01

    Full Text Available A myocardial infarction is a rare complication which can occur after an exercise stress test. We report a 48-year-old male who was referred to the Mildura Cardiology Practice, Victoria, Australia, in August 2014 with left-sided chest pain. He underwent an exercise stress test which was negative for myocardial ischaemia. However, the patient presented to the Emergency Department of the Mildura Base Hospital 30 minutes after the test with severe retrosternal chest pain. An acute anteroseptal ST segment elevation myocardial infarction was observed on electrocardiography. After thrombolysis, he was transferred to a tertiary hospital where coronary angiography subsequently revealed significant left anterior descending coronary artery stenosis. Thrombus aspiration and a balloon angioplasty were performed. The patient was discharged three days after the surgical procedure in good health.

  18. 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.

  19. Depressive symptoms are associated with mental stress-induced myocardial ischemia after acute myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Jingkai Wei

    Full Text Available Depression is an adverse prognostic factor after an acute myocardial infarction (MI, and an increased propensity toward emotionally-driven myocardial ischemia may play a role. We aimed to examine the association between depressive symptoms and mental stress-induced myocardial ischemia in young survivors of an MI.We studied 98 patients (49 women and 49 men age 38-60 years who were hospitalized for acute MI in the previous 6 months. Patients underwent myocardial perfusion imaging at rest, after mental stress (speech task, and after exercise or pharmacological stress. A summed difference score (SDS, obtained with observer-independent software, was used to quantify myocardial ischemia under both stress conditions. The Beck Depression Inventory-II (BDI-II was used to measure depressive symptoms, which were analyzed as overall score, and as separate somatic and cognitive depressive symptom scores.There was a significant positive association between depressive symptoms and SDS with mental stress, denoting more ischemia. After adjustment for demographic and lifestyle factors, disease severity and medications, each incremental depressive symptom was associated with 0.14 points higher SDS. When somatic and cognitive depressive symptoms were examined separately, both somatic [β = 0.17, 95% CI: (0.04, 0.30, p = 0.01] and cognitive symptoms [β = 0.31, 95% CI: (0.07, 0.56, p = 0.01] were significantly associated with mental stress-induced ischemia. Depressive symptoms were not associated with ischemia induced by exercise or pharmacological stress.Among young post-MI patients, higher levels of both cognitive and somatic depressive symptoms are associated with a higher propensity to develop myocardial ischemia with mental stress, but not with physical (exercise or pharmacological stress.

  20. 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.

  1. Myocardial salvage after intracoronary thrombolysis with streptokinase in acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Markis, J.E.; Malagold, M.; Parker, J.A.; Silverman, K.J.; Barry, W.H.; Als, A.V.; Paulin, S.; Grossman, W.; Braunwald, E.

    1981-10-01

    Nine patients with acute myocardial infarction had cardiac catheterization and intracoronary infusions of streptokinase 2.3 to 4.3 hours (mean, 3.5) after the onset of symptoms. Occluded coronary arteries were opened within approximately 20 minutes in all patients, but reocclusion occurred in one patient. The immediate effect of thrombolysis on myocardial salvage was assessed with the intracoronary injection of thallium-201. Improved regional perfusion, indicating myocardial salvage after recanalization, was observed in seven of the nine patients. One patient, who had also sustained a nontransmural infarction one week before, had no change after thrombolysis. In the ninth patient, recanalization of a coronary artery was followed by reocclusion and worsening of the myocardial-perfusion defect. Intracoronary thallium-201 studies two weeks and three months after streptokinase infusion in two patients were unchanged in comparison with scintiscans performed 1.5 hours after thrombolysis. These short-term observations suggest that recanalization of obstructed coronary arteries after intracoronary thrombolysis can salvage jeopardized myocardium, However, evaluation of the long-term effects of this procedure on survival and myocardial function will require controlled clinical trials.

  2. 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.

  3. N-acetylcysteine and allopurinol synergistically enhance cardiac adiponectin content and reduce myocardial reperfusion injury in diabetic rats.

    Directory of Open Access Journals (Sweden)

    Tingting Wang

    Full Text Available BACKGROUND: Hyperglycemia-induced oxidative stress plays a central role in the development of diabetic myocardial complications. Adiponectin (APN, an adipokine with anti-diabetic and anti-ischemic effects, is decreased in diabetes. It is unknown whether or not antioxidant treatment with N-acetylcysteine (NAC and/or allopurinol (ALP can attenuate APN deficiency and myocardial ischemia reperfusion (MI/R injury in the early stage of diabetes. METHODOLOGY/PRINCIPAL FINDINGS: Control or streptozotocin (STZ-induced diabetic rats were either untreated (C, D or treated with NAC (1.5 g/kg/day or ALP (100 mg/kg/day or their combination for four weeks starting one week after STZ injection. Plasma and cardiac biochemical parameters were measured after the completion of treatment, and the rats were subjected to MI/R by occluding the left anterior descending artery for 30 min followed by 2 h reperfusion. Plasma and cardiac APN levels were decreased in diabetic rats accompanied by decreased cardiac APN receptor 2 (AdipoR2, reduced phosphorylation of Akt, signal transducer and activator of transcription 3 (STAT3 and endothelial nitric oxide synthase (eNOS but increased IL-6 and TNF-α (all P<0.05 vs. C. NAC but not ALP increased cardiac APN concentrations and AdipoR2 expression in diabetic rats. ALP enhanced the effects of NAC in restoring cardiac AdipoR2 and phosphorylation of Akt, STAT3 and eNOS in diabetic rats. Further, NAC and ALP, respectively, decreased postischemic myocardial infarct size and creatinine kinase-MB (CK-MB release in diabetic rats, while their combination conferred synergistic protective effects. In addition, exposure of cultured rat cardiomyocytes to high glucose resulted in significant reduction of cardiomyocyte APN concentration and AdipoR2 protein expression. APN supplementation restored high glucose induced AdipoR2 reduction in cardiomyocytes. CONCLUSIONS/SIGNIFICANCE: NAC and ALP synergistically restore myocardial APN and AdipoR2

  4. Berberine Attenuates Myocardial Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Inflammation Response: Role of Silent Information Regulator 1

    Directory of Open Access Journals (Sweden)

    Liming Yu

    2016-01-01

    Full Text Available Berberine (BBR exerts potential protective effect against myocardial ischemia/reperfusion (MI/R injury. Activation of silent information regulator 1 (SIRT1 signaling attenuates MI/R injury by reducing oxidative damage and inflammation response. This study investigated the antioxidative and anti-inflammatory effects of BBR treatment in MI/R condition and elucidated its potential mechanisms. Sprague-Dawley rats were treated with BBR in the absence or presence of the SIRT1 inhibitor sirtinol (Stnl and then subjected to MI/R injury. BBR conferred cardioprotective effects by improving postischemic cardiac function, decreasing infarct size, reducing apoptotic index, diminishing serum creatine kinase and lactate dehydrogenase levels, upregulating SIRT1, Bcl-2 expressions, and downregulating Bax and caspase-3 expressions. Stnl attenuated these effects by inhibiting SIRT1 signaling. BBR treatment also reduced myocardium superoxide generation, gp91phox expression, malondialdehyde (MDA level, and cardiac inflammatory markers and increased myocardium superoxide dismutase (SOD level. However, these effects were also inhibited by Stnl. Consistently, BBR conferred similar antioxidative and anti-inflammatory effects against simulated ischemia reperfusion injury in cultured H9C2 cardiomyocytes. SIRT1 siRNA administration also abolished these effects. In summary, our results demonstrate that BBR significantly improves post-MI/R cardiac function recovery and reduces infarct size against MI/R injury possibly due to its strong antioxidative and anti-inflammatory activity. Additionally, SIRT1 signaling plays a key role in this process.

  5. Antioxidant effects of ethyl acetate extract of Desmodium gangeticum root on myocardial ischemia reperfusion injury in rat hearts

    Directory of Open Access Journals (Sweden)

    Raman Archana

    2010-01-01

    Full Text Available Abstract Background This study aims to evaluate the antioxidant potential of the ethyl acetate extract of Desmodium gangeticum root for cardioprotection from ischemia reperfusion-induced oxidative stress. Methods The in vitro antioxidant potential of the extract was in terms of hydroxyl radical scavenging activity, lipid peroxide scavenging activity, nitric oxide scavenging activity and diphenylpicrylhydrazyl radical scavenging activity. The in vivo antioxidant potential of the extract was assessed in an isolated rat heart model. Results Free radicals were scavenged by the extract in a concentration-dependent manner within the range of the given concentrations in all models. Administration of the ethyl acetate extract of Desmodium gangeticum root (100 mg per kg body weight before global ischemia caused a significant improvement of cardiac function and a decrease in the release of lactate dehydrogenase in coronary effluent, as well as the level of malondialdehyde in myocardial tissues. Conclusion The ethyl acetate extract of Desmodium gangeticum root protects the myocardium against ischemia-reperfusion-induced damage in rats. The effects of the extract may be related to the inhibition of lipid peroxidation.

  6. Carbon monoxide increases inducible NOS expression that mediates CO-induced myocardial damage during ischemia-reperfusion.

    Science.gov (United States)

    Meyer, Grégory; André, Lucas; Kleindienst, Adrien; Singh, François; Tanguy, Stéphane; Richard, Sylvain; Obert, Philippe; Boucher, François; Jover, Bernard; Cazorla, Olivier; Reboul, Cyril

    2015-04-01

    We investigated the role of inducible nitric oxide (NO) synthase (iNOS) on ischemic myocardial damage in rats exposed to daily low nontoxic levels of carbon monoxide (CO). CO is a ubiquitous environmental pollutant that impacts on mortality and morbidity from cardiovascular diseases. We have previously shown that CO exposure aggravates myocardial ischemia-reperfusion (I/R) injury partly because of increased oxidative stress. Nevertheless, cellular mechanisms underlying cardiac CO toxicity remain hypothetical. Wistar rats were exposed to simulated urban CO pollution for 4 wk. First, the effects of CO exposure on NO production and NO synthase (NOS) expression were evaluated. Myocardial I/R was performed on isolated perfused hearts in the presence or absence of S-methyl-isothiourea (1 μM), a NOS inhibitor highly specific for iNOS. Finally, Ca(2+) handling was evaluated in isolated myocytes before and after an anoxia-reoxygenation performed with or without S-methyl-isothiourea or N-acetylcystein (20 μM), a nonspecific antioxidant. Our main results revealed that 1) CO exposure altered the pattern of NOS expression, which is characterized by increased neuronal NOS and iNOS expression; 2) cardiac NO production increased in CO rats because of its overexpression of iNOS; and 3) the use of a specific inhibitor of iNOS reduced myocardial hypersensitivity to I/R (infarct size, 29 vs. 51% of risk zone) in CO rat hearts. These last results are explained by the deleterious effects of NO and reactive oxygen species overproduction by iNOS on diastolic Ca(2+) overload and myofilaments Ca(2+) sensitivity. In conclusion, this study highlights the involvement of iNOS overexpression in the pathogenesis of simulated urban CO air pollution exposure.

  7. Coronary microvascular obstruction in acute myocardial infarction.

    Science.gov (United States)

    Niccoli, Giampaolo; Scalone, Giancarla; Lerman, Amir; Crea, Filippo

    2016-04-01

    The success of a primary percutaneous intervention (PCI) in the setting of ST elevation myocardial infarction depends on the functional and structural integrity of coronary microcirculation. Coronary microvascular dysfunction and obstruction (CMVO) occurs in up to half of patients submitted to apparently successful primary PCI and is associated to a much worse outcome. The current review summarizes the complex mechanisms responsible for CMVO, including pre-existing coronary microvascular dysfunction, and highlights the current limitations in the assessment of microvascular function. More importantly, at the light of the substantial failure of trials hitherto published on the treatment of CMVO, this review proposes a novel integrated therapeutic approach, which should overcome the limitations of previous studies.

  8. [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.

  9. Comparison of gadolinium polylysine and gadopentetate in contrast enhanced MR imaging of myocardial ischemia-reperfusion in cats

    Energy Technology Data Exchange (ETDEWEB)

    Lim, Tae Hwan [Asan Medical Center, University of Ulsan College of Medicine, Seoul (Korea, Republic of); Lee, Jung Hee; Lee, Tae Keun; Mun, Chi Woong [Asan Institute for Life Sciences, Seoul (Korea, Republic of)

    1995-07-15

    To assess the signal enhancement by gadolinium-DTPA-polylysine (Gd-polylysine) as compared to gadopentetate (Gd-DTPA) in MR imaging of heart that have undergone ischemia-reperfusion, and to estimate the extent of myocardial damage covered by the MR signal enhancement. A series of contrast enhanced cardiac MR images were obtained from 17 cats subjected to a 90 minutes of occlusion of the left anterior descending coronary artery (LAD) followed by a 90 minutes of reperfusion. Time courses of changes in the signal intensity (SI) of the ischemic area were measured in Gd-polylysine group (8 cats) and Gd-DTPA group (9 cats). The size of MR signal enhanced area was then compared to the sizes of infarction and the area at risk revealed by TTC histochemical staining. Maximum SIs were obtained at 60 minutes and 30 minutes after injection of the contrast material, respectively for Gd-polylysine group and Gd-DTPA group. Signal enhancement was stronger and persistent for a longer period in Gd-polylysine group than in GD-DTPA group. Sizes of the enhanced are, the infarction, and the area at risk were about 30%, 15%, and 50% of the total left ventricle (LV) area; the difference between the groups was statistically insignificant. Gd-polylysine can be used better for a blood pool marker than Gd-DTPA in MR imaging of myocardial ischemia, due to its strong and persistent signal enhancement. The MR signal enhanced area includes both the infarcted area and a portion of the area at risk.

  10. Attenuation of Myocardial Injury by HMGB1 Blockade during Ischemia/Reperfusion Is Toll-Like Receptor 2-Dependent

    Directory of Open Access Journals (Sweden)

    Jan Mersmann

    2013-01-01

    Full Text Available Genetic or pharmacological ablation of toll-like receptor 2 (TLR2 protects against myocardial ischemia/reperfusion injury (MI/R. However, the endogenous ligand responsible for TLR2 activation has not yet been detected. The objective of this study was to identify HMGB1 as an activator of TLR2 signalling during MI/R. C57BL/6 wild-type (WT or TLR2−/−-mice were injected with vehicle, HMGB1, or HMGB1 BoxA one hour before myocardial ischemia (30 min and reperfusion (24 hrs. Infarct size, cardiac troponin T, leukocyte infiltration, HMGB1 release, TLR4-, TLR9-, and RAGE-expression were quantified. HMGB1 plasma levels were measured in patients undergoing coronary artery bypass graft (CABG surgery. HMGB1 antagonist BoxA reduced cardiomyocyte necrosis during MI/R in WT mice, accompanied by reduced leukocyte infiltration. Injection of HMGB1 did, however, not increase infarct size in WT animals. In TLR2−/−-hearts, neither BoxA nor HMGB1 affected infarct size. No differences in RAGE and TLR9 expression could be detected, while TLR2−/−-mice display increased TLR4 and HMGB1 expression. Plasma levels of HMGB1 were increased MI/R in TLR2−/−-mice after CABG surgery in patients carrying a TLR2 polymorphism (Arg753Gln. We here provide evidence that absence of TLR2 signalling abrogates infarct-sparing effects of HMGB1 blockade.

  11. 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.

  12. Low-Level Tragus Stimulation for the Treatment of Ischemia and Reperfusion Injury in Patients With ST-Segment Elevation Myocardial Infarction: A Proof-of-Concept Study.

    Science.gov (United States)

    Yu, Lilei; Huang, Bing; Po, Sunny S; Tan, Tuantuan; Wang, Menglong; Zhou, Liping; Meng, Guannan; Yuan, Shenxu; Zhou, Xiaoya; Li, Xuefei; Wang, Zhuo; Wang, Songyun; Jiang, Hong

    2017-08-14

    The aim of this study was to investigate whether low-level tragus stimulation (LL-TS) treatment could reduce myocardial ischemia-reperfusion injury in patients with ST-segment elevation myocardial infarction (STEMI). The authors' previous studies suggested that LL-TS could reduce the size of myocardial injury induced by ischemia. Patients who presented with STEMI within 12 h of symptom onset, treated with primary percutaneous coronary intervention, were randomized to the LL-TS group (n = 47) or the control group (with sham stimulation [n = 48]). LL-TS, 50% lower than the electric current that slowed the sinus rate, was delivered to the right tragus once the patients arrived in the catheterization room and lasted for 2 h after balloon dilatation (reperfusion). All patients were followed for 7 days. The occurrence of reperfusion-related arrhythmia, blood levels of creatine kinase-MB, myoglobin, N-terminal pro-B-type natriuretic peptide and inflammatory markers, and echocardiographic characteristics were evaluated. The incidence of reperfusion-related ventricular arrhythmia during the first 24 h was significantly attenuated by LL-TS. In addition, the area under the curve for creatine kinase-MB and myoglobin over 72 h was smaller in the LL-TS group than the control group. Furthermore, blood levels of inflammatory markers were decreased by LL-TS. Cardiac function, as demonstrated by the level of N-terminal pro-B-type natriuretic peptide, the left ventricular ejection fraction, and the wall motion index, was markedly improved by LL-TS. LL-TS reduces myocardial ischemia-reperfusion injury in patients with STEMI. This proof-of-concept study raises the possibility that this noninvasive strategy may be used to treat patients with STEMI undergoing primary percutaneous coronary intervention. Copyright © 2017. Published by Elsevier Inc.

  13. Cancer risk of patients discharged with acute myocardial infarct

    DEFF Research Database (Denmark)

    Dreyer, L; Olsen, J H

    1998-01-01

    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......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...... 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...

  14. [Bradyarrhythmias in the acute phase of myocardial infarct].

    Science.gov (United States)

    Maroto Montero, J M; Lemus, J M; Marín-Huerta, E; Gorodezky, M; Cárdenas, M

    1975-01-01

    The functioning of the Intensive Care Units has permitted a better study and treatment of the arrhythmias which complicate the acute phase of myocardial infarction. 1,100 charts of patients admitted to the Coronary Unit of the National Institute of Cardiology of Mexico were reviewed. Acute myocardial infarction was demonstrated in 819 of them by the usual methods. The frequency and characteristics of the following bradiarrhythmias were studied: sinus bradicardia, sinus stoppage, seno-atrial block, migration of the atrial pacing, union rhythm and slow ventricular tachycardia. Sinus bradicardia was presented in 23.7% of the infarctions, sinus stoppage in 2.4%, migration of the atrial pacing in 9.4%, nodal rhythm in 7.2% and slow ventricular tachycardia in 7.8%. Bradiarrhythmias, generally considered as "lesser" arrhythmias, favor the appearance of lethal arrhythmias, regardless of the degree of mechanical failure, and thus should be treated actively.

  15. Evaluation of heart perfusion in patients with acute myocardial infarction using dynamic contrast-enhanced magnetic resonance imaging

    DEFF Research Database (Denmark)

    Hansen, Thomas Fritz; Dirks, Christina G; Jensen, Gorm B;

    2004-01-01

    PURPOSE: To investigate the diagnostic ability of quantitative magnetic resonance imaging (MRI) heart perfusion in acute heart patients, a fast, multislice dynamic contrast-enhanced MRI sequence was applied to patients with acute myocardial infarction. MATERIALS AND METHODS: Seven patients...... slices, each having 60 sectors, provided an estimation of the severity and extent of the perfusion deficiency. Reperfusion was assessed both by noninvasive criteria and by coronary angiography (CAG). RESULTS: The Ki maps clearly delineated the infarction in all patients. Thrombolytic treatment...... was clearly beneficial in one case, but had no effect in the two other cases. Over the time-course of the study, normal perfusion values were not reestablished following thrombolytic treatment in all cases investigated. CONCLUSION: This study shows that quantitative MRI perfusion values can be obtained from...

  16. Unsuccessful reperfusion in patients with ST-segment elevation myocardial infarction treated by primary angioplasty

    NARCIS (Netherlands)

    De Luca, G; van't Hof, AWJ; Ottervanger, JP; Hoorntje, JCA; Gosselink, ATM; Zijlstra, F; de Boer, M.J.; Suryapranata, H; Dambrink, Jan Hendrik Everwijn

    2005-01-01

    Background Several studies have shown that patency of the epicardial vessel does not guarantee optimal myocardial perfusion in patients undergoing primary angioplasty for ST-segment elevation myocardial infarction (STEMI). The aim of the current study was to identify clinical and angiographic correl

  17. 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.

  18. Acute Anterolateral Myocardial Infarction Due to Aluminum Phosphide Poisoning

    Directory of Open Access Journals (Sweden)

    Bita Dadpour

    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

  19. An unusual presentation of mad honey poisoning: acute myocardial infarction.

    Science.gov (United States)

    Akinci, Sinan; Arslan, Uğur; Karakurt, Kamber; Cengel, Atiye

    2008-09-26

    An unusual type of food poisoning is commonly seen in the Black Sea coast of Turkey due to grayanotoxin containing toxic honey so called "mad honey" ingestion. In cases of toxication bradycardia and rhythm disturbances are commonly observed. Herein, we present a case of a patient who was admitted to the hospital because of acute myocardial infarction with normal coronary arteries after "mad honey" ingestion.

  20. [Acute myocardial infarction during tocolytic treatment with ritodrine].

    Science.gov (United States)

    Fornet, I; Calvo, M; Gimeno, M; Canser, E; Alonso, E; Gilsanz, F

    2006-05-01

    Ritodrine, a beta2-adrenergic agonist with a selective effect on the uterine muscle, is prescribed to prevent premature labor and to treat a hypertonic uterus. At therapeutic doses ritodrine has chronotropic and peripheral vasodilator effects. At high doses it has been related to sporadic cases of subendocardial necrosis, pulmonary edema, and death in pregnancy. We report the case of a pregnant woman who had a non-Q wave acute myocardial infarction after administration of ritodrine.

  1. Early Biventricular Molecular Responses to an Acute Myocardial Infarction

    OpenAIRE

    Erdal, Cenk; Karakülah, Gökhan; Fermancı, Emel; Kunter, İmge; Silistreli, Erdem; Tülay CANDA; Erdal, Esra; Hepaguslar, Hasan

    2011-01-01

    Background: Acute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose. Objectives: The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI. Material and Methods: A rat model of left anter...

  2. Myocardial ischemia-reperfusion induces upregulation of contractile endothelin ETB receptor in rat coronary arteries

    DEFF Research Database (Denmark)

    Skovsted, Gry Freja; Sheykhzade, Majid; Trautner, Simon;

    2011-01-01

    ETB receptor upregulation. Methods and Results Thirteen Sprague-Dawley male rats (body weight 260-410 g) were anaesthetized with Hypnorm-Midazolam and subjected to 15 min occlusion of left anterior descending coronary artery (LAD) followed by 22 h of reperfusion. The contractile response...

  3. Myocardial ischemia-reperfusion induces upregulation of contractile endothelin ETB receptor in rat coronary arteries

    DEFF Research Database (Denmark)

    Skovsted, Gry Freja; Sheykhzade, Majid; Trautner, Simon

    2011-01-01

    ETB receptor upregulation. Methods and Results Thirteen Sprague-Dawley male rats (body weight 260-410 g) were anaesthetized with Hypnorm-Midazolam and subjected to 15 min occlusion of left anterior descending coronary artery (LAD) followed by 22 h of reperfus