Longitudinal studies have demonstrated that this escalates the prevalence of cardiomyopathy from 25% at the age of 6 years to 59% by the age of 10 years, reaching near-universal penetrance (93%–100%) by 18 years; the phenotypic severity is strongly correlated with the DMD mutation type, where the frameshift variants in exons 45–50 (rod domain) confer delayed cardiac involvement compared to the C-terminal truncations that disrupt β-dystroglycan binding. This evidence concerns the gene DMD and cardiomyopathy.