Ventricular ectopic rhythms following vagal stimulation in dogs with acute myocardial infarction.

SUMMARY Vagal stimulation inducing significant bradyeardia did not precipitate ventricular fibrillation in any of 34 dogs subjected to ligation of the left anterior descending coronary artery. Vagal stimulation , however, did result in two distinct types of ventricular arrhythmias occurring at different times following coronary occlusion. Within 3 hours, couplets and salvos were provoked which were overdriven by pacing at slow rates. From 4.5 to 9 hours ventricular tachycardia resulted which was slower in rate than the intrinsic sinus rhythm and could be overdriven only by pacing at rates faster than the ectopic mechanism. The response to acetylcholine administration was similar to that of vagal stimulation. By pacing in the presence of complete heart block or by the use of beta-adrenergic blockade, bradyeardia was shown to be the basis for the ventricular ar-rhythmias. Reentry is believed to be the mechanism for the ectopics provoked by bradyeardia early after coronary acclusion, while enhanced Purkinje fiber automaticity may account for the late ar-rhythmias. Coronary occlusion Bradyeardia Ventricular premature beats BRADYCARDIA is known to facilitate ventricu-lar ectopic activity. This has been noted in man after carotid sinus massage,' during digitalis intoxication,2 3 after the long cycle of sinus arrhythmia,4 and after pauses in atrial fibrillation,5 as well as during slowing of heart rate in acute myocardial infarction.6 In animal studies bradyear-dia has been demonstrated to facilitate ectopic beat formation,7 to increase temporal dispersion of refractory period duration, and to reduce significantly the threshold for ventricular fibrillation.8 Bradyeardia is common in the early stages of acute myocardial infarction.9 It is believed to be due to vagal reflexes originating in the region of the 44 coronary sinus and posterior portions of the interatrial septum'0 as well as the immediate area around the left coronary artery."' 12 Since the risk of sudden death is highest at the very inception of acute myocardial infarction when bradyeardia is also most common, it has been suggested that bradyeardia may predispose to ventricular fibrilla-tion. This question was examined in dogs with myocardial infarction by determining the effects of vagal stimulation on ventricular rhythm. Harris13 has described three sequential phases following coronary artery ligation in the dog. Within 10-30 sec after occlusion of the LAD frequent ventricular premature beats and ventricular tachycardia emerge. This is followed by a quiescent period lasting 6-12 hours during which ectopic activity diminishes or disappears entirely. Thereafter, ven-tricular ectopic activity recurs most commonly in the form …