The different etiologies of<unk>  (CM), resulting in abnormal heart structure and function are myriad. Our knowledge of this disease entity has progressed significantly since the term was first used in 1957. Historically, CM has been grouped in three different categories by phenotype or symptomatic presentation (later confirmed through echocardiographic and autopsy studies), ranging from dilated to restrictive to hypertrophic forms of CM. Emerging additional categories include arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) and unspecified CM. Dilated and Hypertrophic CM, which share symptoms of left heart failure, can be distinguished by a patient's ejection fraction (EF), left ventricular (LV) wall thickness, and LV end diastolic volume (LVEDV). Restrictive CM is relatively uncommon and presents largely with symptoms of right-sided heart failure (HF) and diastolic dysfunction. Some etiologies (e.g. inherited metabolic disorders, sarcoidosis, hemachromatosis, etc.) may cause more than one type of CM. This overlap in classification underscore the limitations of phenotypic classification system. For this reason, and with improving technology, the American Heart Association proposed a classification of CM emphasizing primary and secondary (to other systemic diseases) etiologies. Primary CM is subdivided into genetic, acquired, and mixed causes. Genetic cause include HCM, ARVD/C, ion channel disorders, storage and infiltrative diseases. Genetics play an important and increasing role in the pathophysiology of CM. The genetic basis of hypertrophic<unk>  (HCM) is well established.  Approximately 30% of Dilated CM (DCM) cases are familial. Mutations in over 40 different genes have been described (locus heterogeneity). Various mutations within those genes have produced CM (allelic heterogeneity), and the same mutation can manifest differently within different family members (incomplete penetrance).  The clinical presentation of patients with<unk>  can vary widely, depending on the underlying mechanism of disease.  Symptoms range from exercise intolerance and progressive heart failure to fatal arrhythmias and sudden cardiac death. Currently, treatment of CM is driven primarily by phenotype. Therefore, the discussion below will focus on this classification.
Cardiomyopathy pathophysiology
Ventricular remodeling pathophysiology
Alcoholic cardiomyopathy pathophysiology
Dilated cardiomyopathy pathophysiology
Stress cardiomyopathy pathophysiology
Pacemaker syndrome pathophysiology
Endocarditis pathophysiology
Myocarditis pathophysiology