Key result
Chronic daily alcohol exacerbates MI-induced cardiac dysfunction, reducing EF and promoting myocardial fibrosis versus vehicle.
Why the study?
Alcohol intake is a risk factor for cardiovascular diseases, but its effect on myocardial infarction-induced cardiac remodeling and heart failure was unclear.
Does chronic alcohol intake exacerbate cardiac dysfunction after myocardial infarction in a mouse model?
RCT
Randomly divided
Does chronic alcohol intake exacerbate cardiac dysfunction after myocardial infarction in a mouse model?
Chronic alcohol intake exacerbates post-myocardial infarction cardiac dysfunction and remodeling in mice by promoting fibrosis and inhibiting mitochondrial function.
Chronic alcohol may worsen post-MI dysfunction in mice; leaves open human relevance and need for clinical studies.
AIMS: Alcohol intake is a risk factor for cardiovascular diseases. This study was designed to investigate whether chronic alcohol intake affects myocardial infarction (MI)-induced cardiac remodeling and heart failure. METHODS: Eight-week-old male C57BL/6 mice were randomly divided into four groups: Sham group (Sham), MI plus drinking water group (MI + Vehicle), and MI plus daily alcohol intake for 6 weeks with or without gavage of additional alcohol every 3 days (MI + Alcohol and MI + Alcohol + G). The MI were induced by permanent left anterior descending (LAD) coronary artery ligation surgery before vehicle or alcohol treatment. The blood alcohol concentration (BAC), cardiac function, release of cardiac enzymes, pathological changes and mitochondrial function were measured. RESULTS: As expected, supplementation of alcohol in drinking water significantly increased random BAC in mice. Long-term exposure to alcohol further reduced body weight, ejection fraction and fractional shortening in comparison with the MI + Vehicle group. Histopathological data showed that alcohol increased fibrosis in infarct zone, which was well correlated with the functional decline. Also, as compared to the MI + Vehicle group, the adenosine diphosphate-supported respiratory function of freshly isolated cardiac mitochondria was inhibited in the MI + Alcohol + G group. Besides, upon MI-induced cardiac damage, we did not observe further changes in heart weight, cardiomyocyte enlargement in remote zone, exercise capacity, lung edema and the release of cardiac enzyme after chronic alcohol intake. CONCLUSIONS: Our study demonstrated that chronic daily alcohol exposure exacerbated MI-induced cardiac dysfunction, which is related to promoted myocardial fibrosis and inhibited mitochondrial function.
No takes yet. Share an insight, caveat, or question.
Liang et al. (2020) conducted an RCT in Myocardial infarction. Chronic alcohol intake vs. Vehicle (drinking water) was evaluated on Cardiac function, release of cardiac enzymes, pathological changes and mitochondrial function. Chronic daily alcohol exposure exacerbated MI-induced cardiac dysfunction, reducing ejection fraction and fractional shortening while promoting myocardial fibrosis compared to vehicle.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: