Key result
An increase in late INa facilitates the formation of early and delayed afterpolarizations, triggered arrhythmias, and cellular Ca2+ loading, potentially leading to reentrant arrhythmias.
Population
Cardiomyocytes
Design
Review
Authors
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May support late INa inhibition to suppress triggered arrhythmias; leaves open clinical translation in prospective trials.
Increased late sodium current (late INa) in cardiomyocytes contributes to arrhythmogenesis by prolonging action potential duration and increasing cellular sodium and calcium loading.
Shryock et al. (2013) conducted a review in Arrhythmias. Late INa was evaluated. An increase in late INa facilitates the formation of early and delayed afterpolarizations, triggered arrhythmias, and cellular Ca2+ loading, potentially leading to reentrant arrhythmias.
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