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In 20 anesthetized open-chest dogs, epicardial electrograms were recorded from ischemic and nonischemic zones of the left ventricle during acute occlusion of the left anterior descending artery. The average time to onset of ventricular tachycardia during atrial pacing (150-200 beats/min) was 4 min, 18 sec. In 18 dogs, ventricular ectopic beats were induced in normal and ischemic zones after every tenth atrial stimulus. Those induced in the ischemic zone consistently caused ventricular tachycardia earlier (mean: 3 min, 22 sec) than those in the normal zone (mean: 4 min, 11 sec) (P < 0.01). This arrhythmia, whether spontaneous or induced, always followed the complex which demonstrated the greatest delay of the ischemic zone potential and increased ventricular activation time. Ventricular tachycardia was repeatedly produced by ectopic beats with late diastolic coupling. Analysis of the episodes of tachycardia leading to fibrillation revealed a progressive increase in the ventricular activation time of the successive beats, whereas in those self-terminating episodes ventricular activation time progressively decreased. These data suggest that the major determinant of malignant ventricular arrhythmias in acute ischemia may be the related abnormalities of ventricular activation rather than the coupling of the premature ectopic beats.

The Pathophysiology of Malignant Ventricular Arrhythmias During Acute Myocardial Ischemia