Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to arrhythmias.

Abstract

We studied the effects of ischemia on transmembrane action potentials, conduction time, and refractory periods of both endocardial and epicardial muscle cells of coronary-perfused cat left ventricles. Oxygenated Tyrode's solution was perfused through the left anterior descending coronary artery, while the preparation was superfused with Tyrode's solution gassed with 95% N2 and 5% CO2. Transmembrane action potentials recorded simultaneously from endocardial and epicardial cells were normal during coronary perfusion. When perfusion was discontinued ("ischemia"), rapid deterioration of action potentials and prolongation of conduction time were observed in both endocardial and epicardial cells. The magnitude of the reduction of action potential amplitude and action potential duration (APD), and of prolongation of conduction time, was greater in epicardial cells than in endocardial cells, although the change in resting membrane potential was almost the same. However, APD of endocardial cells decreased progressively during 30 min of ischemia, whereas APD of epicardial cells was reduced maximally at 10 min and then partially recovered. Shortening of refractory periods of endocardial cells paralleled APD shortening, whereas refractory periods of epicardial cells decreased for the first 10 min and then increased. At 10 min of ischemia, APD and refractory periods of epicardial cells were significantly shorter than those of endocardial cells. At 30 min of ischemia, refractory periods of epicardial cells exceeded those of endocardial cells because of development of greater postrepolarization refractoriness in epicardial cells. Accompanying these different changes in APD and refractory periods of endocardial and epicardial cells, spontaneous extrasystolic impulses increased and rapid runs of extrasystolic impulses could be induced by extrastimuli. Our data suggest that dispersion of repolarization and refractory period between endocardial and epicardial cells is related to the development of arrhythmias during early ischemia. In addition, heterogeneities of both the initial change in refractory period paralleling APD shortening and the late-developed postrepolarization refractoriness may be involved in the occurrence of acute ischemic arrhythmias. Circulation 74, No. 2, 401-409, 1986. EXPERIMENTAL preparations of coronary artery occlusion have been extensively studied in an attempt to understand the mechanisms of ischemia-induced ventricular arrhythmias. 1A Study of the electrophysiologic events that occur at a cellular level during ischemia can provide a more precise understanding of the mechanisms of such arrhythmias. Indeed, some investigators

Effects of Pinacidil on Electrophysiological Properties of Epicardial Border Zone of Healing Canine Infarcts

“…14,16,20,21 The focus on the arrhythmogenic role of K ATP channel activation has been during acute ischemia. 4,14,17 During this period, epicardial muscle that eventually forms the EBZ undergoes more severe electrophysiological alterations than endocardial muscle, 22,23 partly related to greater activation of the K ATP channels. 24 During subsequent days, muscle cells in the EBZ undergo changes in ion channels that control repolarization, resting membrane potential, and depolarization and are related to changes in ion channel protein synthesis.…”

Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences

“…Other studies have demonstrated that, despite similar changes in resting membrane potential, ischemia induces a greater depression of the action potentials of ventricular Epi vs Endo tissues [6,7]. Additional studies have shown a greater Epi sensitivity to a fall of intracellular ATP-induced I K-ATP activation (in response to anoxia) and suggested that this effect may, at least in part, contribute to the greater deterioration of the ventricular Epi action potential to ischemia [8].…”

Initiation of Ventricular Fibrillation by a Single Ectopic Beat in Three Dimensional Numerical Models of Ischemic Heart Disease: Abrupt Transition to Chaos

“…Unless otherwise specified, gradients in conduction velocity and in refractory period ranging from endocardium to epicardium were established in keeping with published literature for normal and ischemic cardiac muscle [20]. The importance of such gradients in generating complex patterns of activation has been emphasized by Fenton [10].…”

“…Ischemic muscle physiology is simulated by adjusting the local abnormal conduction velocity between 0 and 100 percent of normal and the local refractory period between 50 and 100 percent of normal. Such changes in these physiologic parameters are characteristic of ischemic cardiac muscle [20,21]. The endocardial map of a typical local diseased region is presented in Figure 2.…”