Cardiomyopathy denotes a heterogeneous group of diseases of the myocardium in which the heart muscle itself is structurally and functionally abnormal, in the absence of conditions sufficient to explain the impairment by coronary, valvular, hypertensive, or congenital causes alone. It is conventionally classified by …
Cardiomyopathy denotes a heterogeneous group of diseases of the myocardium in which the heart muscle itself is structurally and functionally abnormal, in the absence of conditions sufficient to explain the impairment by coronary, valvular, hypertensive, or congenital causes alone. It is conventionally classified by morphology and physiology into dilated cardiomyopathy, marked by ventricular enlargement and systolic dysfunction; hypertrophic cardiomyopathy, characterised by inappropriate myocardial thickening that may localise, as in apical variants; restrictive cardiomyopathy, defined by impaired ventricular filling; arrhythmogenic cardiomyopathy; and left ventricular non-compaction, a disorder of trabecular development. Aetiology spans inherited sarcomeric and cytoskeletal gene mutations as well as acquired causes including infection, toxins, infiltration, and metabolic disease. Clinically, cardiomyopathies predispose to heart failure, arrhythmia, thromboembolism, and sudden cardiac death, and their evaluation relies on imaging, electrophysiology, and increasingly genetic testing. Studies in this area examine apical hypertrophic cardiomyopathy through case-based characterisation, left ventricular non-compaction, the assessment of cardiac contractile function in cardiomyocyte cell lines, the progression to and management of heart failure, and congenital cardiac defects. The field connects molecular genetics, cellular physiology, cardiac imaging, and clinical management in understanding how primary muscle disease leads to mechanical and electrical dysfunction.
12 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 12 articles above have been cited 36 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
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