Developmentally regulated SCN5A splice variant potentiates dysfunction of a novel mutation associated with severe fetal arrhythmia
Keywords: Arrhythmia; Sodium channel; SCN5A; Sudden death; Long-QT syndrome; Magnetocardiography; Alternative splicingAV, atrioventricular; LQTS, long-QT syndrome; TdP, torsades de pointes; WT, wild type