Ventricular arrhythmias in healing myocardial infarction: Role of rhythm versus rate in re-entrant activation

Abstract

In 40 anesthetized dogs, malignant ventricular arrhythmias were studied in the late myocardial infarction period (3 to 20 days) after the phase of increased ventricular automaticity had subsided. Arrhythmias were induced by atrial pacing by means of regular stimulation or pacing with long-short cycle sequences. The latter involved the insertion of premature stimuli into regular pacing sequences as well as introduction of abrupt pauses into regular pacing rhythms. Arrhythmias could not be induced 10 to 20 days after infarction (eight dogs) or in sham-operated animals. In 27 dogs studied 3 to 9 days after myocardial infarction, re-entrant ventricular arrhythmias were consistently evoked by atrial pacing with long-short cycle sequences. Of these 27 dogs, only six had ventricular arrhythmias during regular pacing (50 to 350 beats per minute). The rate in each instance (115 to 260; average 200 beats per minute) remained within a critically narrow range (± 5 to 10 beats per minute). Activation delay in the epicardium of the infarct zone was consistently prolonged immediately after a long-short cycle sequence. Ventricular arrhythmias were always preceded by marked fractionation and delay of ischemic-zone epicardial electrograms when induced by long-short sequences in atrial pacing. In the six animals with critical, rate-dependent ventricular ectopia, complex patterns of underlying epicardial activation delay were recorded in the infarct zone. These included Wenckebach sequences of delayed portions of the electrograms and appeared as trigeminal and quadrigeminal rhythms on the standard electrocardiogram. This study indicates that in the dog, 3 to 9 days after myocardial infarction, re-entrant ventricular arrhythmias arising in the epicardium of the infarct zone are always evoked by atrial pacing with long-short cycle sequences. Abnormalities of refractoriness, particularly postrepolarization refractoriness, are related to both ischemia and abrupt heart rhythm changes, and they are implicated in the induction of these arrhythmias. Regular pacing over a wide range of heart rates less commonly resulted in arrhythmias. Re-entrant ventricular arrhythmias could not be provoked in dogs 10 to 20 days after myocardial infarction by either rapid heart rates or sudden changes in rhythm (long-short cycle sequences).