During remodeling, heterogeneous alterations in three factors contribute to increase the propensity to arrhythmias and to develop heart failure: (1) tissue architecture such as hypertrophy, fibrosis, fiber disarray, and cell size, (2) electrical coupling by means of gap junctions and especially those composed of Cx43, and (3) electrical excitability due to changes in sodium channels that are mainly composed of Nav1.5 (Kleber and Rudy, 2004; van Rijen et al., 2006; Bowers et al., 2010). This evidence concerns the gene GJA1 and heart failure.