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Alcoholic cardiomyopathy: aspects of pathogenesis and clinic

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Alcoholic cardiomyopathy is the most common form of myocardial damage caused by ethanol. Ethanol and its main active metabolite acetaldehyde have a direct toxic effect on the myocardium. The mechanisms of the cardiotoxic effect of ethanol are diverse and include membranotropic action, damage to cellular organelles, activation of lipid peroxidation, and a number of others. Dissolving in the lipids of biological membranes, ethanol changes their physico-chemical properties, disrupts the activity of membrane receptors, eventually disconnecting the connection of excitation with the contraction of cardiomyocytes. Particular importance in the pathogenesis of alcoholic cardiomyopathy is attached to the ability of ethanol to cause structural and functional changes in mitochondria, which is directly related to the violation of oxidative processes and energy supply of the myocardium as a whole. Under the influence of alcohol, free-radical lipid oxidation products content increases and antioxidants activity decreases, which indicates oxidative stress development. The deterioration of myocardial contractility due to chronic alcohol intoxication triggers a cascade of compensatory mechanisms in the form of cardiomyocyte hypertrophy and progressive fibrosis, while adaptive reactions become a factor in further pathological changes. Ethanol causes myocardial damage in a dose-dependent manner.The probability of alcoholic cardiomyopathy occurrence is a derivative of the total accumulated dose of alcohol and individual predisposition. Alcoholic cardiomyopathy is considered as a variant of secondary dilated cardiomyopathy with all its clinical manifestations and consequences: dilation of the heart chambers, low left ventricular ejection fraction, progressive circulatory insufficiency, and cardiac arrhythmias. A relatively favorable prognosis in alcoholic cardiomyopathy is provided due to partial reversibility of myocardial damage under the condition of abstinence from alcohol consumption. Specific drugs for the treatment of alcoholic cardiomyopathy have not been developed. New treatment strategies include the use of myocardial growth and regulation factors synthesized by cardiomyocytes, as well as the stimulation of heart muscle regeneration and repair processes.
Publishing House ABV Press
Title: Alcoholic cardiomyopathy: aspects of pathogenesis and clinic
Description:
Alcoholic cardiomyopathy is the most common form of myocardial damage caused by ethanol.
Ethanol and its main active metabolite acetaldehyde have a direct toxic effect on the myocardium.
The mechanisms of the cardiotoxic effect of ethanol are diverse and include membranotropic action, damage to cellular organelles, activation of lipid peroxidation, and a number of others.
Dissolving in the lipids of biological membranes, ethanol changes their physico-chemical properties, disrupts the activity of membrane receptors, eventually disconnecting the connection of excitation with the contraction of cardiomyocytes.
Particular importance in the pathogenesis of alcoholic cardiomyopathy is attached to the ability of ethanol to cause structural and functional changes in mitochondria, which is directly related to the violation of oxidative processes and energy supply of the myocardium as a whole.
Under the influence of alcohol, free-radical lipid oxidation products content increases and antioxidants activity decreases, which indicates oxidative stress development.
The deterioration of myocardial contractility due to chronic alcohol intoxication triggers a cascade of compensatory mechanisms in the form of cardiomyocyte hypertrophy and progressive fibrosis, while adaptive reactions become a factor in further pathological changes.
Ethanol causes myocardial damage in a dose-dependent manner.
The probability of alcoholic cardiomyopathy occurrence is a derivative of the total accumulated dose of alcohol and individual predisposition.
Alcoholic cardiomyopathy is considered as a variant of secondary dilated cardiomyopathy with all its clinical manifestations and consequences: dilation of the heart chambers, low left ventricular ejection fraction, progressive circulatory insufficiency, and cardiac arrhythmias.
A relatively favorable prognosis in alcoholic cardiomyopathy is provided due to partial reversibility of myocardial damage under the condition of abstinence from alcohol consumption.
Specific drugs for the treatment of alcoholic cardiomyopathy have not been developed.
New treatment strategies include the use of myocardial growth and regulation factors synthesized by cardiomyocytes, as well as the stimulation of heart muscle regeneration and repair processes.

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