Alcoholic cardiomyopathy pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Raviteja Guddeti, M.B.B.S. [2]

Pathophysiology

Alcoholic cardiomyopathy is a type of dilated cardiomyopathy. Both acute and chronic alcohol consumption, in excessive amounts, has been associated with adverse effects on the myocardium leading to nonischemic dilated cardiomyopathy. The maximum recommended dose of alcohol consumption in US men and women is 14 drinks and 7 drinks respectively. Consumption above these levels has been shown to be associated with the increased risk of alcoholic cardiomyopathy.

Excessive use of alcohol has a direct toxic effect on the heart muscle cells. The heart muscle becomes weakened, subsequently dilates, and cannot pumpblood efficiently. The lack of blood flow affects all parts of the body, resulting in damage to multiple tissues and organ systems. Alcohol may also simultaneously be causing direct damage to the liver..

Proposed mechanisms of myocardial injury in alcoholic cardiomyopathy include:

• Ethanol induced apoptosis
• Impaired contraction of myocardium due to direct toxicity
• Inhibition of protein synthesis
• Activation of renin-angiotensin system (RAS)
• Inhibition of oxidative phosphorylation
• Fatty acid ester accumulation
• Nutritional deficiency of thiamine
• Free radical damage
• Inflammation
• Inhibition of calcium-myofilament interaction