Ethanol has long been recognized as a toxic agent affecting different organ functions both acutely and chronically , A prospective study of middle-aged Swedish males registered for alcohol addiction revealed a two-fold greater increase in the incidence of clinical cardiac events than for liver cirrhosis , Several factors may be responsible for the deleterious effects of alcohol on the myocardium, including (i) a direct toxic effect of ethanol or its metabolites; (ii) associated nutritional deficiencies (i.e., thiamine); or (iii) direct toxicity of additives in the alcoholic beverage (i.e., lead or cobalt) ,
Social drinking is often associated with a small rise of systolic blood pressure, which may have negligible effects in healthy adults. Cardiovascular events such as hypertension, stroke, arrhythmia, heart failure, and sudden death have been associated with heavy alcohol drinkers. In fact, chronic alcohol ingestion is a major cause of nonischemic cardiomyopathy in the Western world with an incidence ranging from 21-32% , Most common in middle-aged individuals who have consumed large amounts of alcohol for more than 10 years resulting in heart failure , there is also an increased incidence of sudden death that apparently peaks about 50 years of age in the alcoholic population without heart failure.
Acute ingestion of ethanol resulting in blood levels of approximately 100 mg %, produces transient cardiac dysfunction in normal non-addictive subjects. By contrast, in chronic ethanol abusers asymptomatic but stable cardiac dysfunction has been observed for some years before evidence of heart failure appeared , Early manifestations of the subclinical abnormality in chronic alcohol abusers include increased diastolic stiffness of the left ventricle, as indicated by an elevated end-diastolic pressure and diminished end-diastolic volume [12-15], This process has been attributed to increased interstitial fibrosis. In a canine model without other risk factors, diastolic dysfunction and interstitial fibrosis were observed in studies lasting 6 months , Improved basal contractility was not observed until after a period of 4 years consuming 36% of calories as ethanol ,
In chronic studies, ethanol causes a reduction in the amount of contractile proteins, and two dimensional protein profiling implicates selective loss of individual myocardial proteins. The differential activities of lysosomal proteases may contribute to this patterned response. However, in chronic ethanol feeding, adaptive mechanisms also become important, as the synthesis of the myofibrillary proteins increases , Ethanol has been shown to affect a number of molecular processes in heart muscle, including neurotransmitter receptors for amines, amino acids, and opioids and enzymes such as Na/K ATPase, acetylcholin esterase, adenylyl cyclase, as well as ion channels involved in calcium transport , In a chronic canine model, increased concentrations of norepinephrine have been observed in the coronary venous effluent associated with a decrease in the ventricular fibrillatory threshold ,
At the myocyte level, alcohol decreases the binding of calcium by the sarcoplasmic reticulum and decreases the sodium-potassium ATPase pump activity resulting in increased intracellular sodium, but these abnormalities at the levels observed are insufficient to produce systolic dysfunction [16,20,21],
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...