Gap junctions, slow conduction, and ventricular tachycardia after myocardial infarction.

Over the past 30 years, the cumulative results of clinical, experimental, and theoretical studies have validated the concept that slow conduction, related at least in part to changes in intercellular coupling via gap junctions, plays an important role in the pathogenesis of ventricular tachycardia (VT) after myocardial infarction. Long before the major cardiac gap junction protein, connexin43 (Cx43), was first cloned by Beyer et al. (1) in 1987, the basic relationship between electrical coupling and the speed of impulse propagation had been recognized through the pioneering work of Barr, Dewey, Lieberman, Kootsey, Johnson, Spach, and many others (2–5).