Etiology

• Idiopathic

• Familial, due to mutations in genes that encode components for sarcomeres and desmosomes, such as:

  • TTN gene: encodes the intrasarcomeric protein titin (connectin)

  • MYH7 gene: encodes the beta-myosin heavy chain

• ubstance use

  • Alcohol use disorder

  • Cocaine

  • Amphetamines

• Cardiotoxic medications, e.g., anthracyclines (such as doxorubicin and daunorubicin), AZT, trastuzumab

• Infection (infectious myocarditis)

  • Coxsackie B virus infection

  • Chagas disease

  • HIV infection

• Infiltrative and autoimmune disorders

  • Systemic lupus erythematosus

  • Sarcoidosis

  • Vasculitides, e.g., eosinophilic granulomatosis with polyangiitis, polyarteritis nodosa

• Hemochromatosis

• Peripartum cardiomyopathy (can occur in the last trimester or up to 6 months postpartum)

• Chronic tachycardia, e.g., atrial fibrillation

• Radiation [9]

• Endocrinopathies, e.g., pheochromocytoma, acromegaly, hyperthyroidism

• Neuromuscular diseases, e.g., myotonic dystrophy, Duchenne muscular dystrophy

• Nutritional deficiencies, e.g., thiamine (wet beriberi), selenium, carnitine

Volume and pressure overload secondary to conditions such as hypertension and valvular heart disease can cause dilation of the myocardium; however, these are not considered forms of DCM, as filling pressures are abnormal. [1]

To remember some high-yield secondary causes of dilated cardiomyopathy, think ABCCCDD: Alcohol use, Beriberi, Cocaine, Coxsackie B virus, Chagas, Doxorubicin/Daunorubicin

• Causative factors decrease the contractility of the myocardium → activation of compensatory mechanisms (Frank-Starling law) to maintain cardiac output → ↑ end-diastolic volume (preload) → myocardial remodeling → eccentric hypertrophy (sarcomeres added in series) and dilation of the ventricle → reduced myocardial contractility → systolic dysfunction and ↓ ejection fraction → heart failure

• Decreased LV contractility due to dilation leads to left heart failure and eventually right heart failure