Why the study?
The study was conducted to characterize modern concepts regarding the pathogenetic mechanisms underlying the development of alcoholic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
This review highlights that alcoholic cardiomyopathy is primarily driven by metabolic disorders and oxidative stress-induced apoptosis in cardiomyocytes, ultimately leading to progressive heart failure.
Aim. The aim of the study was to characterize the modern concepts of alcoholic cardiomyopathy development pathogenetic mechanisms. Material and methods. Review of research medical publications on alcoholic cardiomyopathy pathogenesis and clinical manifestations. Results and discussion. Long time alcohol abuse is one of the common causes of cardiovascular mortality, along with smoking, hyperlipidemia, and hypertension, which is associated with the prevalence of alcohol dependence. Every third adult had at least one period of excessive alcohol consumption during one's lifetime. The treatment cost in such patients is ten times higher than such in ones with the heart failure. A common effect of alcohol on the cardiovascular system is alcoholic cardiomyopathy, which remains asymptomatic for a long time, but at the fi nal stage of the disease it is manifested by progressive heart failure. Alcoholic cardiomyopathy is expressed in an increase in the heart chamber size, mainly in the left ventricle, diffuse myocardial hypokinesis development, and a decrease in its integral contractility. Complications of alcoholic cardiomyopathy can be heart rhythm disturbances and thromboembolism. The leading causes of increased cardiovascular morbidity and mortality in people who consume alcohol are the factors leading to heart failure development. The main ones are viable cardiomyocyte loss, common cardiosclerosis, and a decreased function in the remaining contractile elements. Conclusion. The main damaging mechanism of alcohol exposure to the myocardium is metabolic disorders in the cardiomyocytes, leading to their irreversible dystrophic changes and cardiosclerosis. An increase in cell active oxygen radical amount not only destroys it chemically, but also initiates and completes apoptotic cell death process through intracellular signaling system modifi cation.
No takes yet. Share an insight, caveat, or question.
FADEEV et al. (2019) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: