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Basis for ventricular arrhythmias accompanying myocardial infarction: alterations in electrical activity of ventricular muscle and Purkinje fibers after coronary artery occlusion.

Investigations during the past several decades have indicated that the occurrence of cardiac arrhythmias associated with a variety of pathological states is a result of alterations in the basic cellular electrophysiological properties of the heart. This tenet obviously applies to the arrhythmias that accompany myocardial infarction as well. However, a definite documentation of the alterations in cardiac electrophysiology that are responsible for such arrhythmias in humans is still lacking. At present, our understanding of these mechanisms is derived from the results of laboratory investigations on animals. In this article, we discuss our own and related views on the mechanisms for the ventricular arrhythmias accompanying myocardial infarction based on such investigations. Our own data and that of others, which provides the basis for these hypotheses, has been mostly derived from microelectrode studies on isolated superfused canine myocardium exposed to environmental conditions simulating the conditions believed to be present after an acute