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The cellular electrophysiological mechanisms underlying the ventricular arrhythmias that accompany myocardial infarction were studied in isolated, superfused infarcted myocardium excised from dogs previously subjected to a two-stage ligation of the anterior descending coronary artery. Ventricular arrhythmias frequently occurred in the intact heart 24 hours after coronary occlusion. Surviving subendocardial Purkinje fibers in infarcts excised at this time were highly arrhythmic when they were studied with intracellular microelectrodes in vitro. These arrhythmias consisted of rapid, repetitive depolarizations and occurred spontaneously or could be induced by premature electrical stimulation. Premature stimulation also resulted in single unstimulated responses. In such instances, premature impulses conducted extremely slowly through the infarcted region where surviving Purkinje fiber action potential durations were extraordinarily prolonged. Conduction block at some sites in the infarct caused phenomena which were interpreted as reentrant beats. Some surviving subendocardial Purkinje fibers in the infarct demonstrated spontaneous diastolic depolarization and appeared to function as pacemakers in the absence of electrical stimulation. In some instances, these fibers constituted typical parasystolic foci, demonstrating both entrance and exit block. These results suggest that subendocardial Purkinje fibers which survive in an infarct may be the site of origin of some of the ventricular arrhythmias that accompany myocardial infarction.
Friedman et al. (Thu,) studied this question.