The origin of most cardiomyopathies is unknown. Occasionally, dilated cardiomyopathy results from myocardial destruction by toxic, infectious, or metabolic agents, such as certain viruses, endocrine and electrolyte disorders, and nutritional deficiencies. Other causes include muscle disorders (myasthenia gravis, progressive muscular dystrophy, myotonic dystrophy), infiltrative disorders (hemochromatosis, amyloidosis), and sarcoidosis.

Cardiomyopathy may be a complication of alcoholism. Although the condition may improve if the patient abstains from alcohol, it will recur when he resumes drinking.

How viruses induce cardiomyopathy is unclear, but investigators suspect a link between viral myocarditis and subsequent dilated cardiomyopathy, especially after infection with poliovirus, coxsackievirus B, influenza virus, or human immunodeficiency virus.

Metabolic cardiomyopathies are related to endocrine and electrolyte disorders and nutritional deficiencies. Thus, dilated cardiomyopathy may develop in patients with hyperthyroidism, pheochromocytoma, beriberi (thiamine deficiency), or kwashiorkor (protein deficiency). Cardiomyopathy may also result from rheumatic fever, especially among children with myocarditis.

Antepartal or postpartal cardiomyopathy may develop during the last trimester or within months after delivery. Its cause is unknown, but the condition is most common in multiparous women older than age 30, particularly those with malnutrition or preeclampsia. In these patients, cardiomegaly and heart failure may reverse with treatment, allowing a subsequent normal pregnancy. If cardiomegaly persists despite treatment, the prognosis is extremely poor.