Key result
Excessive alcohol consumption is a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy, with pathophysiological mechanisms involving myocyte loss and dysfunction.
This review summarizes the epidemiology, pathophysiology, clinical presentation, prognosis, and treatment of alcoholic cardiomyopathy.
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ACM mechanisms remain poorly understood; leaves open mechanistic research to refine diagnosis and management in dilated cardiomyopathy.
The myocardial depressant effects of excessive ethanol consumption have long been known. Excessive alcohol intake is reported in a wide range (3-40%) of patients with idiopathic dilated cardiomyopathy; furthermore, chronic excessive alcohol consumption may lead to progressive and chronic cardiac dysfunction and can be a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy (ACM). The pathophysiological mechanisms underlying ACM are poorly understood. Excessive alcohol consumption has been associated with left-ventricular myocyte loss in some animal models but not in all studies. In addition, heavy drinking may cause myocyte dysfunction, due to abnormalities in calcium homeostasis, and cause elevated levels of norepinephrine. Increasing doses of ethanol have been associated with a negative inotropic effect on myocytes in animal experiments. In this review, we evaluate the epidemiology, current pathophysiological mechanisms and possible role of factors that influence ACM and discuss its clinical presentation, prognosis and treatment.
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Iacovoni et al. (2010) conducted a review in Alcoholic cardiomyopathy. Excessive alcohol consumption was evaluated. Excessive alcohol consumption is a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy, with pathophysiological mechanisms involving myocyte loss and dysfunction.
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