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Vagal stimulation inducing significant bradycardia 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, bradycardia was shown to be the basis for the ventricular arrhythmias. Reentry is believed to be the mechanism for the ectopics provoked by bradycardia early after coronary acclusion, while enhanced Purkinje fiber automaticity may account for the late arrhythmias.
Kerzner et al. (Mon,) studied this question.