RESUMEN
Slow conduction leading to reentrant ventricular tachycardias in patients with healed myocardial infarcts appears to depend primarily on alterations in intercellular coupling at gap junctions of myocytes bordering the infarct scar. Results of correlative morphometric and electrophysiologic studies indicate that the elongated shape of individual myocytes, their complex overlapped packing in myocardium, and the number and distribution of gap junctions that electrically couple myocytes are all important structural determinants of anisotropic patterns of current spread in normal myocardium. Alterations of these structural features likely contribute to electrophysiologic derangements critical in reentrant arrhythmogenesis. Recent observations that cardiac myocytes may be coupled by multiple gap junction channel proteins having unique electrophysiologic properties provide new insights into potential mechanisms regulating intercellular current transfer in the heart.
