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Ventricular Activation Patterns of Spontaneous and Induced Ventricular Rhythms in Canine One‐Day‐Old Myocardial Infarction: Evidence for Focal and Reentrant Mechanisms

We studied isochronal maps of ventricular activation during spontaneous multiform ventricular rhythms (rates 120–190/min) and pacing-induced ventricular tachyarrhythmias (rate 230–450/min) in dogs 1 day after myocardial infarction. Recordings were obtained from the entire epicardial surface and from selected endocardia! and intramural sites utilizing a computerized multiplexing technique. Spontaneous ventricular rhythms had a focal origin from the surviving subendocardial Purkinje network underlying the infarction and showed frequent shift of the pacemaker site. On the other hand, fast ventricular tachyarrhythmias were consistently induced in the same dogs by bursts of rapid ventricular pacing or programmed premature stimulation and had a tendency to degenerate into ventricular fibrillation. Pacing-induced rhythms were due to reentrant activation that developed mainly in the surviving, electrophysiologically abnormal, epicardial layer overlying the infarction. The last stimulated beat that initiated reentry resulted in a continuous arc of functional conduction block and two slowly circulating activation fronts around both ends of the arc of block. The activation fronts rejoined on the distal side of the arc of block before breaking through the arc to reactivate an area proximal to the block. This resulted in splitting of the initial single arc of block into two separate arcs. Reentrant activation subsequently continued as two synchronous circuits which conducted in clockwise and counterclockwise directions, respectively. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue and failed to advance. The presence of two synchronous circuits was the hallmark of a stable reentrant activation. The development of three or more asynchronous circuits resulted in an activation pattern that was “prefibrillatory.” This pattern was seen to develop during pleomorphic ventricular rhythms and ventricular tachycardias of the torsades de pointes type that degenerated into ventricular fibrillation. Ventricular fibrillation was maintained by continuously changing multiple asynchronous circuits. The transition from a stable reentrant activation pattern to that of ventricular fibrillation was probably related to nonhomogeneous shortening of refractoriness in different parts of the myocardium.