Ectopic Ventricular Beats Originating in Ischemically‐Injured Left Ventricular Epicardium, 24 Hours Following Coronary Artery Occlusion in the Dog

Abstract

Epicardial Ectopics. Introduction: Ventricular ectopic beats demonstrating: (1) depolarization in ischemically‐injured anterior epicardium preceding His‐Purkinje activation by more than 25 msec; (2) initial delta waves on the anterior chest leads of the surface ECG coincident with presystolic epicardial activation; and (3) a left bundle branch block morphology were observed in 46 of 256 anesthetized dogs evaluated 18–24 hours following anterior descending coronary artery occlusion. Methods and Results: In 18 experiments, endocardial and epicardial recordings, and signal‐averaged recordings from the left ventricle were used to determine the earliest activation time/site for epicardial ectopic beats. In these ventricular ectopic beats, early epicardial activation was coupled to the preceding beat by a constant, fixed coupling interval. Electrical activity during the interectopic interval was not detected with composite or multiple bipolar recordings, or with signal averaging from the heart. The mean coupling interval was prolonged by lidocaine from 385 ± 24to 409 ± 45 msec (P < 0.01), and was decreased by epinephrine (364 ± 7 msec) and D‐600 (324 ± 32 msec)(P < 0.05). Spontaneous ventricular beats of epicardial origin could be reversibly suppressed by epicardial lidocaine administration or permanently suppressed with intracoronary latex injection, eliminating presystolic potentials. Histologic examination of the epicardium revealed surviving tissue bands (0.5–2.0 mm) distributed throughout transmural infarcted epicardium. Conclusion: The present experiments demonstrate constant‐coupled ectopic ventricular beats of epicardial origin, 18–24 hours following myocardial infarction. The ventricular ectopic beats may result from abnormal automaticity or electrotonic excitation from an initiating beat across an unexcitable gap with slow conduction from the “site of origin’ to reactivate the left ventricle. (JCardiovasc Electrophysiol, Vol. 3, pp. 315–333, August 1992)