The origin of ventricular arrhythmias 24 hours following experimental anterior septal coronary artery occlusion

Abstract

The anterior septal coronary artery was acutely ligated in 16 open chest anesthetized dogs to produce an infarct of the septal myocardium. Twenty four hours following occlusion complete epicardial mapping and extensive plunge electrode recording techniques were used to localize the sites of origin and patterns of activation of the ventricular tachyarrhythmias that developed during recovery. The earliest electrical activity for 13 individual rhythms was recorded from surviving septal subendocardial Purkinje fibers at the margins of the infarct, in the right or left ventricle, directly underlying the sites of earliest epicardial breakthrough. The sites of origin were verified by demonstrating unchanged activation sequences during pacing through the electrode sites which recorded the earliest activity. None of the arrhythmias arose from the His bundle or bundle branches despite the fact that these tissues course directly through the necrotic septum. The data presented supports the hypothesis that ventricular arrhythmias occurring in the 24-36 hour post acute infarction period may originate in the surviving subendocardial Purkinje system. This experimental model shows that in cases in which a malignant rhythm arises from a focus, whether it is due to enhanced automaticity or local re entry, epicardial mapping alone may not identify the source of the arrhythmias. Extensive endocardial mapping may provide a more rational basis for surgical interventions designed to abolish these arrhythmias.