Clinical meaning
Dilated cardiomyopathy (DCM) features eccentric ventricular remodeling with chamber dilation and reduced systolic function (EF <40%). Myocyte loss and interstitial fibrosis reduce contractile force. Causes include ischemia (most common), viral myocarditis, alcohol, peripartum, and genetic mutations (titin, lamin A/C). Hypertrophic cardiomyopathy (HCM) involves asymmetric septal hypertrophy from sarcomeric protein mutations (beta-myosin heavy chain, myosin-binding protein C), causing LV outflow tract obstruction (LVOTO) worsened by decreased preload/afterload or increased contractility. Restrictive cardiomyopathy (RCM) results from infiltration (amyloidosis, sarcoidosis, hemochromatosis) or fibrosis causing stiff, non-compliant ventricles with preserved EF but severe diastolic dysfunction. Each type has distinct hemodynamic profiles guiding management.
Diagnosis & workup
Diagnostics & workup: - Echocardiography: DCM shows dilated chambers with global hypokinesis and low EF; HCM shows asymmetric septal hypertrophy >15mm with SAM of mitral valve; RCM shows normal/small chambers with biatrial enlargement and diastolic dysfunction - Cardiac MRI with late gadolinium enhancement: identifies fibrosis patterns specific to each type; mid-wall enhancement in DCM, patchy in HCM, diffuse subendocardial in amyloid - BNP/NT-proBNP elevated in all types; troponin may be elevated in HCM and myocarditis - Genetic testing for HCM (sarcomeric mutations) and familial DCM; cascade screening of first-degree relatives - ECG: DCM shows low voltage or LBBB; HCM shows LVH with deep septal Q waves and T-wave inversions; RCM shows low voltage with pseudo-infarct pattern in amyloid - Endomyocardial biopsy for suspected infiltrative or inflammatory etiologies