The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

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.

Acute effects of alcohol on cardiac electrophysiology and arrhythmogenesis: Insights from multiscale in silico analyses

“…Chronically, ethanol further impairs excitation-contraction coupling and promotes structural remodeling, including LV dilatation, reduced LV wall thickness and increased LV mass. In advanced stages, this leads to a reduction in LV ejection fraction and the development of an alcoholic cardiomyopathy [15,35]. Here, we confirmed the acute detrimental effects of high ethanol concentrations and provide new insights on the underlying mechanisms.…”

“…Structural remodeling, notably cardiac fibrosis, is a key feature of cAF and HF and may act as a substrate for cardiac arrhythmias, favoring reentrant waves to occur and persist [33,34]. In addition, long-term ethanol abuse can produce structural remodeling, promoting alcoholic cardiomyopathy [7,15,35]. As such, we assessed the acute effects of ethanol in the presence of mild (4% fibrotic tissue), moderate (11% fibrotic tissue) and extensive (20% fibrotic tissue) structural remodeling (Fig.…”

Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options

“…Excessive alcohol consumption leads to the severe failures of digestive, cardiovascular, and nervous (central and peripheral) systems [6][7][8][9][10]. The most frequent disorders related to alcohol abuse include alcoholic liver disease (including steatosis, steatohepatitis, cirrhosis, or hepatocellular carcinoma), pancreatitis, gastritis, hypertension, arrhythmia, or cardiomyopathy [11][12][13][14][15][16][17][18][19][20][21]. The prevalence of the alcoholic liver disease among heavy drinkers is estimated at 15-30% [22].…”

Heart pathomorphological changes in the long-term alcohol consumption

“…At present, the pathogenetic mechanisms of myocardial damage in chronic alcohol intoxication have been studied quite well [11,12], however, the description of pathomorphological changes in the heart of those who died in alcoholism is limited -in a few works of recent years [13].…”