Functional modulation of atrio-ventricular conduction by enhanced late sodium current and calcium-dependent mechanisms in <i>Scn5a1798insD/+</i> mice

Abstract

Our findings indicate a detrimental role for enhanced INa,L and consequent calcium dysregulation on AV-conduction in Scn5a1798insD/+ mice, providing evidence for a functional mechanism underlying AV-conduction disturbances secondary to gain-of-function SCN5A mutations.