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). As early as 1961 (6) and certainly by the early 1980s, it had been shown that “fractionated electrograms” and “continuous electrical activity” could be identified in myocardial regions bordering healed infarcts, and they became manifest as fibrous tissue accumulated during infarct healing (7). Although it was also understood that slow conduction could be related to factors independent of those responsible for producing fractionated electrograms, the presence of fractionated electrograms in the setting of chronic ischemic heart disease was consistently linked to slowing of impulse propagation (7). At the same time, it was becoming apparent that fractionated electrograms persisted in healed infarct border zones once acute post-infarct derangements in resting membrane potential and active ionic currents had normalized (7). Taken together, these observations led to the conclusion that fractionated electrograms and slow conduction in the chronic infarct border zone were the result of diminished intercellular electrical coupling, associated with separation of fibers by peri-infarct scar tissue. This concept, articulated most lucidly by Josephson and Wit in the early 1980s (9) and later by de Bakker et al. (11), had its origins in seminal experimental work by Spach (4), Waldo and Kaiser (12), Boineau and Cox (13), El-Sherif et al. (14), Spear (15), Spear et al. (15), and others. It has since been strengthened by morphometric and immunohistochemical studies documenting gap junction remodeling in viable cardiac myocytes bordering healed infarcts (17) and ever more powerful in vitro and computational studies defining specific structural and electrophysiological determinants of slow conduction under various conditions and elucidating their pathophysiological consequences (20). Although it is true that these studies have differed in terms of the animal species, experimental protocols, and theoretical models used and have involved different types of measurements at different intervals after infarction, they have all converged on the idea that gap junction remodeling can reduce intercellular coupling and thereby slow conduction in ways that contribute importantly to the pathogenesis of re-entrant VT after myocardial infarction. Recognition of this concept has also raised the obvious possibility that preservation or enhancement of intercellular coupling in the infarct border zone might decrease the risk for re-entrant VT, an idea originally proposed in studies pre-dating the modern era of molecular biology and genetic engineering.