TLX2 and heart failure: In contrast, enhanced NCX expression, which occurs in heart failure, can hasten diminished contractile function by reducing SR Ca2+ stores available for excitation-contraction coupling and contribute to arrhythmogenic delayed after depolarizations triggered by increased NCX-mediated Na+ influx concomitant with Ca2+ efflux (Lytton, 2007; Ottolia et al., 2013).