Electrocardiography ; Humans ; Myocardial Ischemia ; physiopathology

Animals ; Autophagy ; Humans ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology

Torsades de Pointes is a kind of severe ventricular arrhythmia. Myocardial ischaemia is one of the major causes leading to TdP. In this paper the mechanisms of the TdP were quantitatively studied under the condition of ischaemia based on the Noble98 dynamic model of the ventricular action potential. The study was conducted on one-dimensional homogeneous myocardium with the method of computer simulation. The models were firstly developed to simulate the lower excitability, extracellular accumulation of the K+ concentration or the decreased gap junctions in ischaemic myocardium. By separately reducing the Na+ conductance, increasing the extracellular K+ concentration or decreasing the conductance of the gap junctions enabled us to study the effect of each change in isolation. Then different degrees of ischaemic models were established to study their physiological features. The study showed that the conduction velocity became slower with the ischaemia aggravation, the action potential duration became shorter and the width of the vulnerable window obviously became larger than the normal conditions. The results illustrated that ischaemia was easily leading to unidirectional conduction block and resulted in re-entry and arrhythmias.
Computer Simulation ; Models, Cardiovascular ; Myocardial Ischemia ; physiopathology

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

Aged ; Electrocardiography ; Female ; Humans ; Hyperkalemia ; complications ; physiopathology ; Myocardial Ischemia ; etiology

Fractional Flow Reserve, Myocardial ; physiology ; Humans ; Mesenteric Ischemia ; physiopathology

Renalase, a novel amine oxidase, is secreted by kidney. It regulates heart function and blood pressure by degrading catecholamines. Hormones secreted by the kidney are associated with cardiovascular disease. Renalase, as a new biomarker of heart and kidney functional correlation, can lower blood pressure, protect ischemic heart muscle, improve heart function and degrade catecholamine.
Animals ; Cardiovascular Diseases ; physiopathology ; Heart Failure ; physiopathology ; Humans ; Hypertension ; physiopathology ; Monoamine Oxidase ; genetics ; physiology ; Myocardial Ischemia ; physiopathology

Coronary vasospasm of the left main coronary artery (LMCA) is a rare condition with potentially devastating consequences. We present 2 patients with LMCA vasospasm-related angina, the first being a 46-year-old woman and the second a 51-year-old woman. Both of them developed ST-segment ischemic changes on treadmill exercise tests. Coronary angiography showed spontaneous LMCA vasospasm in one patient and methylergonovine-induced LMCA vasospasm in the other patient. Follow-up treadmill exercise tests revealed no exercise-induced ischemia after calcium antagonist monotherapy. These cases demonstrate the importance of identifying LMCA vasospasm, as the treatment of choice varies in patients with angina pectoris. Reversible myocardial ischemia caused by LMCA vasospastic angina can be controlled by calcium antagonist monotherapy and detected by repeat non-invasive stress testing.
Coronary Vasospasm ; diagnosis ; physiopathology ; Exercise Test ; Female ; Humans ; Middle Aged ; Myocardial Ischemia ; diagnosis ; physiopathology

The aim of this study was to determine if the potassium aspartate and magnesium (PAM) prevent reperfusion-induced ventricular arrhythmias (RIVA) in ischemia-reperfusion (IR) rabbit heart. Thirty rabbits were randomly divided into control, ischemia and PAM groups. Arterially-perfused rabbit left ventricular preparations were made, and transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments. In control group rabbit ventricular wedge preparations were continuously perfused with Tyrode's solution, and in ischemia group and PAM groups the perfusion of Tyrode's solution was stopped for 30 min. Then the ischemia group was reperfused with Tyrode's solution and the PAM group with Tyrode's solution containing 2.42 mg/L PAM, respectively. ECG, QT interval, transmural repolarization dispersion (TDR) and action potentials from epicardium and endocardium were simultaneously recorded, and the RIVA of the wedge preparation was observed. Compared with control group, TDR and incidence of RIVA were significantly increased in ischemia group (P<0.05). The incidence of RIVA in control, ischemia and PAM group was 0/10, 9/10 and 1/10, respectively. Compared with ischemia group, TDR and incidence of RIVA were significantly reduced in PAM group (P<0.05). Potassium aspartate and magnesium significantly reduce TDR and prevent ventricular arrhythmia in ischemic rabbit heart.
Arrhythmias, Cardiac/etiology ; Arrhythmias, Cardiac/*prevention & control ; Myocardial Ischemia/*complications ; Myocardial Ischemia/physiopathology ; Myocardial Reperfusion Injury/*complications ; Potassium Magnesium Aspartate/*therapeutic use ; Random Allocation

In this paper, to analyze the functional influence of ischemia on cardiac cell electrical activity and subsequently on ventricular electrical wave conduction, a human ventricular ischemic model was developed, which took into account three major pathophysiological components of ischemias hyperkalaemia, acidosis, and anoxia. This model simulated the action potential (AP) propagations of endocardial, midmycardial and epicardial cells with different levels of ischemia, and the influence of each factor on cell AP was analyzed. Finally the ECG waveform under ischemia was quantified by using a 2D model of human left ventricular tissue based on the anatomical structure of human heart. The experimental results showed that under ischemia action potential durations (APD) were reduced. In most cases, the larger the size of ischemic region or the more severe the ischemic level, the more dramatic the changes in the amplitude of ST-T wave were observed. For the three components of ischemia, hyperkalaemia was the dominant contributor to ST-T wave changes, which was in agreement with the results obtained on animal models.
Action Potentials ; physiology ; Computer Simulation ; Electrocardiography ; Heart Ventricles ; physiopathology ; Humans ; Hyperkalemia ; physiopathology ; Models, Cardiovascular ; Myocardial Ischemia ; physiopathology