Preclinical models of Dravet syndrome demonstrate altered cardiac electrophysiology that may explain the increased risk of arrhythmogenesis and SUDEP.
These data from single cell and whole animal experiments suggest that altered cardiac electrical function in Dravet syndrome may contribute to the susceptibility for arrhythmogenesis and SUDEP. These mechanistic insights may lead to critical risk assessment and intervention in human patients.
Auerbach et al. (Mon,) studied this question.