Enhanced late sodium current underlies pro-arrhythmic intracellular sodium and calcium dysregulation in murine sodium channelopathy

摘要

Background: Long QT syndrome mutations in the SCN5A gene are associated with an enhanced late sodium current (I-Na,I-L) which may lead to pro-arrhythmic action potential prolongation and intracellular calcium dysregulaLion. We here investigated he dynamic relation between I-Na,I-L intracellular sodium [Na+](i)) and calcium ([Ca2+](i) homeostasis and pro-arrhythmic events in he setting of a SCN5A mutation.