Abstract
Malignant ventricular arrhythmias may occur in a variety of congenital or acquired heart diseases.1 By far the largest group of susceptible persons are patients who have had myocardial infarction, in whom the occurrence of complex ventricular ectopic activity is associated with an increase in mortality independent of other risk variables.2 Even simple ventricular premature beats seem to have an adverse effect on survival in this group. Because of the serious implications of ventricular ectopic activity, great attention has been given to the origin of these arrhythmias and to the development of pharmacologic agents to control ventricular ectopic activity. Among patients . . .