Electrophysiological effects of acute ischaemia on electrically stable myocardial infarction.

The purpose of this study was to examine the effects of acute ischaemia superimposed on an electrophysiologically stable, small myocardial infarction, and to determine the mechanisms of induced ventricular arrhythmias, using a canine infarction model. Ten dogs without inducible ventricular tachycardia or fibrillation on the 7th day post-myocardial infarction (Group 1) and 14 control dogs (Group 2) were subjected to 30 min acute ischaemia by occlusion of the proximal left anterior descending artery. The areas of infarcted myocardium ranged from 1.0 to 20.4% (mean 8.9, SD 7.7) of total left ventricular weight. Ventricular arrhythmias were inducible by programmed electrical stimulation in eight of 10 dogs (80%) after acute ischaemia, but in only one of 14 control dogs (7%) (p less than 0.005). In seven of eight Group 1 dogs, epicardial mapping showed that ventricular arrhythmias did not originate from the epicardial region. In one dog, in which there was simultaneous epicardial and endocardial mapping, an endocardial electrogram from the boundary area between infarcted and acutely ischaemic zones recorded continuous fragmented activity. It was thus suggested that re-entry in a relatively isolated endocardial site could be attributed to the induction of ventricular tachyarrhythmias, and that the electrical instability could be significantly enhanced during acute ischaemia when underlying myocardial infarction was present.