Up to 50 % of mortality in heart failure does not result from pump failure but from ventricular tachyarrhythmias (Grimm and Maisch 2002) that are the consequence of dysfunctions in cardiac Ca2+ homeostasis: Resting (diastolic) Ca2+ which is increased in heart failure(Gwathmey et al. 1990) as well as SR Ca2+ leak in a rare genetic disease called CPVT (Lehnart et al. 2008) can result in transient inward currents mediated by the sarcolemmal Na+/Ca2+ exchanger that, in turn, can lead to DADs and triggered activity. This evidence concerns the gene SLC8A1 and catecholaminergic polymorphic ventricular tachycardia.