SCN5A and Brugada syndrome: The present findings thus implicate conduction velocity secondary to compromised Na+ current as a source for arrhythmic substrate under conditions of acutely perturbed cytosolic Ca2+ homeostasis, reconstructing the altered conduction previously reported in Nav1.5 haplo‐insufficient, Scn5a+/− murine models for Brugada Syndrome.1, 2, 3, 4, 5 They also complement previous findings in murine hearts chronically modelling catecholaminergic polymorphic ventricular tachycardia (CPVT).