Myocyte interconnections at gap junctions and the development of anatomic substrates of ventricular arrhythmia's

Spontaneous ventricular tachyarrhythmias causing sudden death occur often in patients with healed myocardial infarcts. A reentrant mechanism has been implicated that depends, in part, on slow heterogeneous conduction and block in critical regions that have been mapped to the borders of the healed infarcts. The electrophysiological derangements responsible for initiation and maintenance of the reentrant tachycardia circuit appear to be attributable largely to abnormalities in current transfer between myocytes in the fibrotic border zone region. This review summarizes recent advances in understanding the role of gap junctions in intercellular electrical coupling in the normal heart and mechanisms of altered junctional coupling in the pathogenesis of reentrant ventricular tachycardia.