Dravet syndrome (DS), a severe childhood epilepsy caused primarily by SCN1A mutations, is associated with a dramatically elevated risk of sudden unexpected death in epilepsy (SUDEP). While seizures are central to the disorder, increasing evidence implicates cardiac dysfunction in SUDEP pathogenesis. The proposed project aims to investigate the cardiac phenotype of DS using patient-derived induced pluripotent stem cells (iPSCs) differentiated into ventricular and atrial cardiomyocytes. By combining patch-clamp electrophysiology, calcium and sodium imaging, and advanced confocal microscopy, we will identify arrhythmogenic mechanisms specific to SCN1A mutations. The project’s long-term goal is to establish a pathophysiological link between SCN1A dysfunction, cardiac excitability, and SUDEP risk, providing new insights for therapeutic strategies.