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Alcohol and dilated cardiomyopathy
Insights
Alcohol-related heart disease remains poorly understood, with unclear causes and progression. While preclinical changes are common in alcoholics, clinical cardiomyopathy affects only a small percentage, possibly due to genetics or other risk factors.
Area of Science:
- Cardiology
- Toxicology
- Genetics
Background:
- Alcohol has been recognized as a cardiotoxin for over a century.
- The exact pathogenesis and natural history of alcohol-related heart disease are not fully understood.
- Diagnosis relies on identifying alcoholism alongside dilated cardiomyopathy without other identifiable causes.
Purpose of the Study:
- To review current understanding of alcohol's effects on the heart.
- To explore factors influencing the development of clinical cardiomyopathy in heavy drinkers.
- To highlight the diagnostic challenges and treatment limitations.
Main Methods:
- Review of existing literature on alcohol's cardiovascular effects.
- Analysis of haemodynamic and cellular effects of acute and chronic alcohol exposure.
- Examination of recent studies on preclinical changes in alcoholics.
Main Results:
- Preclinical changes in left ventricular (LV) dimensions and function are frequent in alcoholics.
- The development of clinical cardiomyopathy in heavy drinkers (1-2%) is not fully explained.
- Potential contributing factors include genetic predisposition and synergistic cardiovascular risk factors.
Conclusions:
- Abstinence is the primary treatment for alcohol-related heart disease.
- Prognosis remains poor once heart failure develops.
- Further research is needed to clarify the aetiology and natural history of this condition.
Abstract:
Alcohol has been considered a cardiotoxin for over a century, but the pathogenesis and natural history of alcohol-related heart disease remains obscure. The diagnosis still rests on the coincidence of alcoholism and a dilated hypocontractile heart in the absence of any other cause of dilated cardiomyopathy. Advances have been made in our understanding of the effects of acute and chronic alcohol administration both at a haemodynamic and cellular level, and recent studies have indicated that preclinical changes in LV dimensions and function are common in alcoholics. It is not known whether clinical cardiomyopathy, which develops in only 1-2% of heavy drinkers, occurs because of genetic predisposition, or the presence of synergistic cardiovascular risk factors. Abstinence remains the mainstay of treatment, but the prognosis is poor after development of frank heart failure.
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