Abstract
Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.
Highlights
Ethyl alcohol, known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history [1]
We describe and discuss the global effects that ethanol exerts on the heart myocytes, the so-called alcoholic cardiomyopathy (ACM)
One of the relevant facts in Alcoholic-dilated Cardiomyopathy (ACM) is the existence of a clear gender difference, women being more susceptible to the toxic effects of alcohol than men at the same level of lifetime ethanol consumption [93,94]
Summary
Known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history [1]. There is an increasing consumption in particular groups, such as adolescents and young people [3,4] This ethanol misuse at high consumption rates causes a variety of health problems, ethanol being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths [5]. There is a relevant role on each organ, on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression [18,25,26] This multi-factorial effect is attributed to genetic factors [27] and ethnic [28] variability. We describe and discuss the global effects that ethanol exerts on the heart myocytes, the so-called alcoholic cardiomyopathy (ACM)
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