TY - CHAP M1 - Book, Section TI - Dilated Cardiomyopathy A1 - Arbustini, Eloisa A1 - Di Toro, Alessandro A1 - Giuliani, Lorenzo A1 - Urtis, Mario A1 - Dec, G. William A1 - Narula, Jagat A2 - Fuster, Valentin A2 - Narula, Jagat A2 - Vaishnava, Prashant A2 - Leon, Martin B. A2 - Callans, David J. A2 - Rumsfeld, John S. A2 - Poppas, Athena PY - 2022 T2 - Fuster and Hurst's The Heart, 15e AB - Chapter SummaryThis chapter summarizes the pathogenesis, diagnosis, and management of dilated cardiomyopathy (DCM). The term DCM covers a wide spectrum of heart muscle disease phenotypes characterized by dilatation and systolic impairment of the left or both ventricles unexplained by abnormal loading conditions (such as hypertensive, diabetic, valvular, or congenital heart disease) or coronary artery disease sufficient to induce the observed phenotype (see Fuster and Hurst’s Central Illustration). The causes of DCM are heterogeneous; genetic in up to 50% (familial DCM), autoimmune/immune-mediated and inflammatory (usually postmyocarditic), and, less commonly, cardiotoxicity (anticancer drugs, alcohol abuse, and cirrhosis). DCM is diagnosed by clinical presentation and morphofunctional echocardiographic and magnetic resonance imaging. Tissue diagnosis is needed for inflammatory cardiomyopathies. The genetic diagnosis is based on testing of genes coding for proteins of the sarcomere, nuclear lamina, intermediate filaments, sarcolemma, sarcoplasmic reticulum and Golgi, desmosomes, and mitochondria. Familial DCM is considered when two or more family members are affected, and diagnosed by family history, clinical screening of relatives, and cascade genetic testing. Early diagnosis in relatives can be framed in the context of nondilated hypokinetic cardiomyopathy based upon the recommended major or minor criteria. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accesscardiology.mhmedical.com/content.aspx?aid=1202448218 ER -