Pathobiochemical aspects of alcoholic cardiomyopathy. The role of hydrogen sulfide in the mechanism of cardiocytoprotection (a review)

Abstract

Aim: systematization of knowledge about the pathobiochemical mechanisms of heart disease in alcoholic cardiomyopathy (ACMP) and the search for promising ways of cardiocytoprotection. Alcohol abuse is an important medical and social problem, risk factor for metabolic disorders, malnutrition, cancers, dementia, neuropathy, and others. Consumption of large amounts of ethanol increases a risk of sudden cardiac death and cardiac arrhythmias. The term “alcoholic cardiomyopathy” describes a heart disease in people with a history of long-term alcohol use. ACMP is characterized by left ventricular dilatation, decreased wall thickness and (at the later stages) decreased left ventricular ejection fraction (less than 40 %). Analysis of literature data about the mechanisms of alcohol-induced cardiotoxicity revealed trigger factors for myocardial damage. Negative effect of ethanol on the heart is realized through induction of oxidative-nitrosative stress, apoptosis, inflammation, fibrogenesis, hypoenergetic state and ion pump dysfunction, development of endothelial dysfunction, impaired ribosomal synthesis. In-depth study of biochemical mechanisms and identification of new molecular targets, integrated into the pathogenesis of ACMP, will optimize the pharmacotherapy for this pathology. Hydrogen sulfide (H2S), is a metabolic factor involved in the regulation of cardiovascular activity. Use of exogenous H2S has potent cardioprotective properties in cardio-vascular diseases. Donors of H2S and H2S-releasing drugs (hybrid molecules – H2S-aspirin, H2S-NO) show a powerful cardioprotective role in various pathological conditions. Therefore, it is advisable to further study the role of H2S system in the pathogenesis of ACMP to develop new approaches to more effective treatment of this disease. Conclusions. Modulation of the H2S level in the organism may be a predictor of the severity of myocardial damage, as well as a promising vector in pharmacotherapy, including alcoholic cardiomyopathy.