Abstract
Conduction dependence on ephaptic coupling (EpC) is mediated by voltage gated sodium channels (Nav1.5) localized to the gap junction adjacent extracellular nanodomain: the perinexus. Pharmacologic Nav1.5 inhibition exacerbates conduction slowing due to reduced EpC. Yet, a 50% reduction of the SCN5a gene encoding Nav1.5 either modestly slows or does not change conduction velocity (CV) in genetically modified mice. Thus, the mechanism by which predicted dramatic conduction slowing during Nav1.5 LOF is attenuated in hearts is unknown.
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