Myocardial hypertrophy in relevant animal models has been shown to result in electrophysiological remodeling where the expression of potassium channels critical for repolarization and repolarization reserve (such as IKs), is significantly reduced, creating an arrhythmia substrate of increased spatial heterogeneity and temporal instability of repolarization and leading to increased arrhythmia susceptibility in the heart [14,30–32]. This evidence concerns the gene KCNA3 and hypertrophy.