![]() Secondary cardiomyopathies had myocardial involvement as part of a large number and variety of generalized systemic (multiorgan) disorders, including systemic diseases such as amyloidosis, hemochromatosis, sarcoidosis, autoimmune/collagen vascular diseases, toxins, cancer therapy, and endocrine disorders such as diabetes mellitus. Primary cardiomyopathies (ie, genetic, nongenetic, and acquired) were defined as those solely or predominantly confined to heart muscle. 5 With the development of molecular genetics, new classification schemes based on genomics such as the classification proposed by the AHA ensued, 6 which divided cardiomyopathies into 2 major groups based on predominant organ involvement. 5 Subsequently, the World Health Organization/International Society and Federation of Cardiology classification in 1996 added inflammatory and viral cardiomyopathies as new and distinct entities. The first classification on this topic categorized cardiomyopathies as heart muscle diseases with dilated (DCM), hypertrophic, restrictive, arrhythmogenic right ventricular (ARVC), or nonclassifiable cardiomyopathy in 1980. Current use of ischemic cardiomyopathy terminology implies ventricular dilation and depressed myocardial contractility caused by ischemia or infarction. 1, 5 Again, in general practice and clinical research trials, the term ischemic cardiomyopathy is defined as cardiomyopathy caused by ischemic heart disease. Although this approach might be practical, it fails to recognize that nonischemic cardiomyopathy can include cardiomyopathies caused by volume or pressure overload (such as hypertension or valvular heart disease) that are not conventionally accepted under the definition of DCM. The term nonischemic cardiomyopathy has been interchangeably used with DCM. In clinical practice, the pathogenesis of heart failure (HF) has often been placed into 2 categories: ischemic and nonischemic cardiomyopathy. The term dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders that are characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease. ![]() 4 The levels of evidence follow the AHA and ACC methods of classifying the level of certainty of the treatment effect. Although the format of our recommendations might resemble the ACC/AHA classification of recommendations used in the ACC/AHA practice guidelines, because of the preponderance of expert opinion or level of evidence C evidence in our document, we elected to use different terminology to provide a distinction from the practice guidelines, in which stronger levels and quality of evidence with randomized clinical trials or meta-analyses are usually present. Therefore, in this document, rather than using the standard ACC/AHA classification schema of recommendations and level of evidence, 4 we have included key management strategies at the end of each section and categorized our recommendations according to the level of consensus. Existing evidence in epidemiology, classification, diagnosis, and management of specific cardiomyopathies is usually derived from nonrandomized observational studies, registries, case reports, or expert opinion based on clinical experience, not large-scale randomized clinical trials or systematic reviews. Recommendations in this document are based on published studies, published practice guidelines from the American College of Cardiology (ACC)/AHA 1 and other organizations, 2, 3 and the multidisciplinary expertise of the writing group. There is special emphasis on recent developments in diagnostic approaches and therapies for specific cardiomyopathies. The intent of this American Heart Association (AHA) scientific statement is to summarize our current understanding of dilated cardiomyopathies.
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