This study evaluated the application of quantitative tissue velocity imaging (QTVI) in assessing regional myocardial systolic and diastolic functions in dogs with acute subendocardial ischemia. Animal models of subendocardial ischemia were established by injecting microspheres (about 300 microm in diameter) into the proximal end of left circumflex coronary artery in 11 hybrid dogs through cannulation. Before and after embolization, two-dimensional echocardiography, QTVI and real-time myocardial contrast echocardiography (RT-MCE) via intravenous infusion of self-made microbubbles, were performed, respectively. The systolic segmental wall thickening and subendocardial myocardial longitudinal velocities of risk segments before and after embolization were compared by using paired t analysis. The regional myocardial video intensity versus contrast time could be fitted to an exponential function: y=A.(1-exp(-beta.t)), in which the product of A and beta provides a measure of myocardial blood flow. RT-MCE showed that subendocardial normalized A.beta was decreased markedly from 0.99+/-0.19 to 0.35+/-0.11 (P<0.05) in 28 left ventricular (LV) myocardial segments after embolization, including 6 basal and 9 middle segments of lateral wall (LW), 8 middle segments of posterior wall (PW) and 5 middle segments of inferior wall (IW). However, there was no statistically significant difference in subepicardial layer before and after embolization. Accordingly, the ratio of A.beta of subendocardial myocardium to subepicardial myocardium in these segments was significantly decreased from 1.10+/-0.10 to 0.31+/-0.07 (P<0.05). Although the systolic wall thickening did not change 5 min after the embolization in these ischemic segments (29%+/-3% vs 31%+/-5%, P>0.05), the longitudinal peak systolic velocities (Vs) and early-diastolic peak velocities (Ve) recorded by QTVI were declined significantly (P<0.05). Moreover, the subendocardial velocity curves during isovolumic relaxation predominantly showed positive waves, whereas they mainly showed negative waves before the embolization. This study demonstrates that QTVI can more sensitively and accurately detect abnormal regional myocardial function and post-systolic systole caused by acute subendocardial ischemia.
Contrast Media ; Echocardiography/*methods ; Endocardium/physiopathology ; Microbubbles ; Myocardial Contraction/physiology ; Myocardial Ischemia/etiology ; Myocardial Ischemia/*physiopathology ; Myocardial Ischemia/*ultrasonography ; Myocardium/pathology ; Ventricular Function, Left/*physiology

Obesity is an independent risk factor of cardiovascular diseases. Epidemiological studies have shown that obesity induces the production of inflammatory factors and changes in cardiac hemodynamics, remodeling and function, leading to myocardial damage and heart diseases. The positive effect of exercise on the cardiovascular system has been widely confirmed, while the acute cardiovascular stress caused by exercise cannot be ignored. Compared with the general population, obese people were more prone to arrhythmia and have a higher risk of cardiovascular events during exercise, due to their abnormal cardiac function, myocardial pathological remodeling and low tolerance to corresponding stress. Studies have shown that the intervention of exercise preconditioning (EP) can effectively reduce such risks. EP increases myocardial oxygen consumption through short-term exercise, resulting in relative or absolute myocardial ischemia, inducing the intrinsic myocardial protective effect and reducing the continuous ischemia caused by subsequent long-term exercise. This article reviews the obesity-induced abnormal changes of cardiac function and structure, possible exercise- induced risks of cardiovascular events in obese people and the role of EP in reducing exercise-induced risks of cardiovascular events. We summarize the progress on EP models in obese people, EP prevention against adverse cardiovascular events in obese people, with the aim to provide a theoretical basis for the application of EP in obese people.
Humans ; Exercise ; Obesity ; Myocardium/pathology* ; Myocardial Ischemia ; Cardiovascular Diseases

Humans ; Ischemia ; metabolism ; pathology ; therapy ; Ischemic Postconditioning ; methods ; Myocardial Reperfusion Injury ; metabolism ; pathology ; therapy

Burns ; complications ; pathology ; physiopathology ; Humans ; Mitochondria, Heart ; pathology ; Myocardial Ischemia ; etiology ; prevention & control

Although coronary atherosclerosis occupies more than 90% of myocardial infarctions, anomalous coronary arteries are a potential cause of myocardial ischemia resulting in arrhythmia, angina, infarction, and sudden death. A medico-legal autopsy conducted on a 22 year-old healthy man who died suddenly after exercise, revealed that the right coronary artery ostium was situated higher the aortic ridge (sinotubular junction) with acute downward angulation of the proximal right coronary artery. There was no evidence of any other disease process. Coronary artery anomalies may be overlooked or misssed by the examining forensic pathologist. We described the pathology of this condition and briefly reviewed.
Arrhythmias, Cardiac ; Autopsy ; Coronary Artery Disease ; Coronary Vessels ; Death, Sudden* ; Humans ; Infarction ; Myocardial Infarction ; Myocardial Ischemia ; Pathology ; Young Adult

AIMTo study the varies and effects of ischemic preconditioning of myocardium on every part of adrenergic receptor-adenyl cyclase system in rats in vivo.

METHODSSD rats were randomly divided into three groups: CON group (n = 6), IP group (n = 12) and I/R group (n = 12). Surgical procedure included intermittent left coronary artery occlusion and reperfusion. After the procedure, the hearts were extracted. We analyzed the infarct size by TTC staining, measured serum myocardial enzymes, studied the beta-AR Bmax and KD by radioligand binding assay of receptors (RAB), and checked the activity of AC and the content of cAMP by radioimmunoassay (RIA).

RESULTSInfarct area were much smaller in IP group than in I/R group (P < 0.05). CK, CK-MB, LDH were significantly higher in I/R group (P < 0.01). The Bmax of beta-AR in IP group were much higher than in I/R group (P < 0.01). No difference of KD could be seen between IP and I/R group. In IP group, the activity of AC and the content of cAMP were higher than I/R group (P < 0.05).

CONCLUSIONIschemic preconditioning can protect the heart from necrosis and reduce endo-enzyme leakage. Ischemic preconditioning can increase the density of beta-AR, the activity of AC and the content of cAMP, which shows that the system of adrenergic receptor-adenyl cyclase system probably takes part in the protection of IP.

Adenylyl Cyclases ; metabolism ; Animals ; Female ; Ischemic Preconditioning, Myocardial ; Myocardial Ischemia ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta ; metabolism

BACKGROUNDSince the size of ischemic myocardium is closely related with both global and regional function of the myocardium, it is of great significance to measure the size of ischemic myocardium with non-invasive methods.

METHODSEleven mongrel dogs were subjected to occlusion of the left anterior descending coronary artery for acute ischemia. Strain rate imaging had M-mode of strain-rate (CAMM) curve pointed from the basal segment of the anterior wall to the basal segment of the inferior wall to detect the border of ischemia size. The strain rate (SR) defined the cut-off value of ischemic myocardium in a two-chamber apical view, and marked by the anterior and inferior wall on two-dimensional images respectively. Along the endocardium and epicardium, the ischemic size was curved on two-dimensional images by the trackball method and then compared with the pathologically ischemic size. And then longitudinal strain rates were compared in the cut-off value, adjacent non-ischemic and ischemic segments at which the cut-off point was defined by changing the curve M-mode of strain rate after ischemia.

RESULTSLinear correlation existed between pathology and strain rate ischemic size (r = 0.884, P < 0.001). The SR parameters were lower in ischemia and cut-off point than in non-ischemic segments. The peak SRs of systole (S(SR)), early diastole (E(SR)), late diastole (A(SR)), strain during ejection time (epsilon(et)), and the maximum length change during the entire heart cycle (epsilon(max)) in ischemic segments lowered (P < 0.05). Time to onset of regional relaxation (T(R)) was prolonged (P = 0.012).

CONCLUSIONSR imaging can accurately assess the size of ischemic myocardium.

Animals ; Dogs ; Echocardiography, Doppler ; methods ; Female ; Male ; Myocardial Ischemia ; diagnostic imaging ; pathology ; Ventricular Function, Left ; physiology

The effect of ginsenoside Rb1 on cardiomyocyte apoptosis after ischemia (30 min) and reperfusion (6 h) in rats was observed. The ischemia/reperfusion heart model was established by ligating left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were examined under transmission electron microscopy and counted by in situ nick end labeling (TUNEL) method and light microscopy. Results showed that (1) The apoptotic cardiomyocytes were found in ischemic regions in the ischemia/reperfusion group, but not in the sham-operating group under transmission electron microscopy; (2) The number of apoptotic cells were 134.45 +/- 45.61/field in the ischemia/reperfusion group, 0/field in the sham-operating group and 51.65 +/- 13.71/field in the ginsenoside Rb1-treated group. The differences were significant among the three groups (P < 0.01). It was concluded that myocardial ischemia-reperfusion could induce cardiomyocyte apoptosis, and ginsenoside Rb1 could significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats, indicating that ginsenoside Rb1 could inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion, thus alleviating ischemia-reperfusion injury.
Animals ; Apoptosis ; drug effects ; Female ; Ginsenosides ; pharmacology ; Male ; Myocardial Ischemia ; pathology ; Myocardial Reperfusion Injury ; pathology ; Myocytes, Cardiac ; pathology ; ultrastructure ; Panax ; chemistry ; Random Allocation ; Rats ; Rats, Wistar

The most effective ways to salvage ischemic myocardium threatened by infarction is to restore tissue perfusion as rapidly as possible. These are best accomplished by restoration of coronary flow(reperfusion) by thrombolysis, percutaneous transluminal conronary angioplasty(PTCA), coronary arterial bypass graft (CABG), or cardiac transplantation. Reperfusion of an ischemic area may result however, in paradoxical cardiomyocytes dysfunction, a phenomenon termed" reperfusion injury". Reperfusion injury has been observed in each of above situations. The myocardium can tolerate brief periods (up to 15 minutes) of severe and even total myocardial ischemia without resultant myocardial death. With increasing duration and severity of ischemia, greater cardiomyocytes damage develop with spectrum of reperfusionassociated pathologies, collectively called reperfusion injury. Here, we report a case of a sixty two-yearold female woman who was suffered cardiac surgery(bivalvular replacement and CABG) and died soon after. Post-mortem examination have revealed typical cardiac reperfusion injury in the background of diffuse myocardial infarction. So, authors report this case with literatures reviews, because we think that this is very good case of cardiac reperfusion injury, confirmed histologically by post-mortem examination.
Autopsy ; Coronary Artery Bypass* ; Coronary Vessels* ; Female ; Heart ; Heart Transplantation ; Heart Valves* ; Humans ; Infarction ; Ischemia ; Myocardial Infarction ; Myocardial Ischemia ; Myocardial Reperfusion Injury* ; Myocardial Reperfusion* ; Myocardium ; Myocytes, Cardiac ; Pathology ; Perfusion ; Reperfusion ; Reperfusion Injury ; Transplants

To explore the protective effects of right coronary artery ischemic preconditioning and post-conditioning on myocardial ischemia reperfusion injury in rabbit heart.
 Methods: A total of 30 rabbits were randomly divided into 4 groups: a control group (n=7), an ischemia reperfusion group (IR group, n=8), an ischemic preconditioning group (IPC group, n=8) and an ischemic post-conditioning group (IPO group, n=7). Venous blood samples were taken at pre-operation, 1 and 6 h post-operation, and the concentration of serum creatine kinase isoenzyme (CK-MB) and cardiac troponin-T (cTn-T) were measured. The infarct area of cardiac muscle was calculated.
 Results: Compared with the IR group, the levels of CK-MB and cTn-T at 1 and 6 h post-operation in the IPC group and the IPO group were reduced (all P<0.05). Compared with the IR group, the infarct size in the IPC group and the IPO group was significantly decreased, with significant difference (both P<0.05) .
 Conclusion: Right coronary artery ischemic preconditioning and post-conditioning exert significant protective effects on the myocardial ischemia reperfusion injury in New Zealand rabbits.
Animals ; Coronary Vessels ; Creatine Kinase, MB Form ; blood ; Heart ; Ischemia ; Ischemic Postconditioning ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Myocardial Infarction ; etiology ; pathology ; physiopathology ; prevention & control ; Myocardial Ischemia ; complications ; therapy ; Myocardial Reperfusion Injury ; prevention & control ; Myocardium ; Rabbits ; Troponin T ; blood