DCM is the most common cardiomyopathy, characterized by enlargement of one or both ventricles and systolic dysfunction. Broad spectrum of cardiac and systemic conditions are associated with DCM (variety of causes): 50% idiopathic and almost 40% are familiar or genetic, 35% and 40% of genetic DCM cases are thought to be caused by sarcomere gene mutations, with mutations in the giant protein titin estimated to be responsible for about 25%. Although genotype–phenotype correlations are lacking for most cases of DCM, mutations in genes such as LMNA (and DES) are known to be highly associated with conduction system disease.

If an inborn error of metabolism is diagnosed, treatment strategies can be directed toward the underlying metabolic abnormality and may include dietary management and supplementation to decrease the accumulation of toxic metabolic by-products. Duchenne muscular dystrophy is one of the rare genetic DCM diseases with a substantial focus on gene-directed therapies.

Evolution is different depending on the cause of DCM for that is important on finding the cause. Patients can have a period of clinical stability, ranging from years to decade. Reverse remodeling can be spontaneous or in response of medical or device therapy. Patients may have sudden deterioration and then have again a state of stability.