The arrhythmogenic substrates in structurally normal hearts and in non-ischemic myocardial disorders are less well-understood; therefore, we assessed the CI variability of PVCs in the following three groups: (i) patients with idiopathic VAs (idiopathic group), who exhibited PVCs in the absence of apparent SHD; (ii) patients with non-ischemic dilated cardiomyopathy (NIDCM group); and (iii) patients with familial dilated cardiomyopathy due to mutations in the genes encoding lamin A/C or phospholamban (PLN/LMNA group). This evidence concerns the gene PLN and familial dilated cardiomyopathy.