If this beneficial response remains absent, one must consider other factors influencing the arrhythmic phenotype such as genetic mutations (ie, LMNA or SCN5A mutations).45 To date, the exact mechanisms of most genetic and nongenetic arrhythmias in DCM are not completely understood, but involve the loss of normal extracellular matrix and contractile dysfunction, alterations in cellular growth and viability, defects in Ca2+ handling, and neurohormonal activation results in DCM.77 Here, SCN5A is linked to familial dilated cardiomyopathy.