Abstract
Several studies have reported inconsistent results regarding cardiac conduction velocity (CV) in mice with a heterozygous knockout of the gene SCN5A. This mutation results in a 50% reduction in inward sodium current. Previous results from our lab suggest that reducing ephaptic coupling (EpC) in ex vivo hearts exacerbates Nav1.5 loss of function (LOF). However, these results were from a pharmacologically induced model of Nav1.5 LOF; it has yet to be determined whether this effect is consistent in a genetic Nav1.5 LOF model.
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