Mechanisms of Ectopic Rhythm Formation due to Myocardial Ischemia: Effects of Heart Rate and Ventricular Premature Beats

Abstract

Almost 10 years ago when we started our investigations on arrhythmias due to myocardial ischemia, the prevailing concepts of ectopic impulse formation were based on the studies of Harris and his coworkers (340). After occlusion of the left anterior descending artery in the dog, ventricular premature beats, ventricular tachycardia and ventricular fibrillation were suddenly seen within the first few minutes (early phase) and then another period of similar arrhythmias was observed 24–48 hours later (late phase). Soon the idea of two phases of ventricular arrhythmias attracted the attention of clinicians. The pre-hospital phase of clinical, acute myocardial infarction with its sudden onset and high mortality seemed to be closely analogous to the early phase in the experimental setting. Whereas the ventricular arrhythmias seen in the coronary care unit were likened to the later phase of the experimental studies. Harris postulated (340,343) that the mechanism and site of origin of both the early and late ventricular arrhythmias were related to rapidly discharging automatic foci arising at the borders of the ischemic or infarcted myocardium. Our aim was to test this hypothesis and clarify whether automaticity or reentry or both were the responsible mechanisms. Also, we attempted to test whether Purkinje or muscle tissue at the borders or within the ischemic or infarcted zones were the sites of origin of these arrhythmias. In keeping with the title of this report and on the basis of the relatively great interest in the prehospital phase arrhythmias, we will confine ourselves to the ventricular arrhythmias occurring during the early ischemic phase. Information regarding the later phase arrhythmias can be found elsewhere (82,218,226,437,474,739).

This work supported in part by NIH-NHLI Contract No. 72-2972-M.