United We Stand; Divided We Fibrillate?
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The heart is an electric and biochemical syncytium with its cardiac myocytes coupled by gap junctions that allow the passage of both ionic current and small molecules.1 Electric coupling allows the rapid spread of depolarization through the atrium, ventricle, and specialized conduction system that is required for coordinated and efficient mechanical function. In addition, these low-resistance intercellular connections help to prevent arrhythmias in several ways. First, tight coupling leads to synchronization of repolarization across the cardiac chambers that decreases dispersion of repolarization and refractoriness and prevents functional reentry.2 Second, the flow of ions and metabolites minimizes the differences at the single cell level that could result from variations in ion channel expression and metabolic state, stabilizing electric propagation and preventing triggered activity. Third, if an aberrant action potential is triggered in a cell or small group of cells, the source–sink mismatch of the electric syncytium will often prevent propagation. In fact, both theoretical and experimental studies have estimated the number of synchronized myocytes required to initiate a premature ventricular beat.3,4
Article, see p 1379
Although coupling between cardiac myocytes is important, the absence of coupling is also critical in some circumstances. Electric isolation is required …