Alcohol Abuse And Cardiovascular Disease

Although there is considerable evidence that moderate drinking protects against mortality and morbidity from coronary heart disease [21,22], heavy consumption is shown to have deleterious cardiovascular effects. It exerts its adverse effects by increasing the risks of cardiomyopathy, hypertension, and stroke [23], Chronic ethanol consumption has been linked to the prevalence of hypertension, which contributes to an increased incidence of stroke. Heavy drinkers have alO mmHg higher systolic blood pressure than non-drinkers even though the relationship may differ between men and women [24], Stroke is a leading cause of death and morbidity. Alcohol may increase the risk of stroke through various mechanisms that include hypertension, hypercoagulable states, cardiac arrhythmias, and cerebral blood flow reductions [25], Hypertension, including borderline hypertension, is probably the most important stroke risk factor based on degree of risk and prevalence. Furthermore, cardiac morbidity, cigarette smoking, diabetes, physical inactivity, and high levels of alcohol consumption are also strongly related to stroke risk [26], Recently, chronic consumption of alcohol has proven detrimental to heart tissue and can lead to alcohol-induced heart muscle disease, a major cause of nonischemic cardio-myopathy in Western society [27], Alcohol-induced heart muscle disease yields abnormal contractile function and energy metabolism, sometimes resulting in arrhythmias, cardiomegaly, and congestive heart failure. A molecular mechanism underlying observed alcohol-induced heart failure is a nonoxidative pathway for alcohol metabolism in several target tissues including heart. Normally the mitochondria manufactures most of the cell's energy ATP via the tricarboxylic acid cycle (TCA cycle), beta-oxidation of fatty acids and oxidative phosphorylation. The very high-energy requirements ofheart muscle are mostly met by beta-oxidation of fatty acids. Fatty acids bound to albumin or from chylonmicrons and very low-density lipoproteins enter the myocyte where they are converted to acetyl CoA through beta-oxidation in the mitochondria matrix. Acetyl CoA then enters the TCA cycle. The products ofTCA cycle will enter the electron transport chain of the inner mitochondrial membrane, where most of the cell's ATP is produced. In alcoholics, it turns out that nonesterified fatty acids are esterified with ethanol to produce fatty acid ethyl esters (FAEEs), which can attach to mitochondria and uncouple oxidative phosphorylation and disrupt the energy process. Furthermore, electron-microscopic and histochemical analysis have revealed shrunken, disorganized myocytes, loss of myofibrils, a dilated and disordered sarcoplasmic reticulum, excessive accumulation of lipids, and enlarged mitochondria with chaotic cristae. It has also been indicated that chronic alcohol administration decreases activity of the Na~K+-ATPase pump that functions in providing the necessary ionic concentrations for membrane potentials needed for cardiac muscle contraction. In animal models, several weeks of chronic alcohol consumption by rats demonstrated in the myocytes a leaky sarcolemma and increases in cardiac intracellular calcium [28],

Similarly, in the alcoholic person ethanol represents on the average 50% of the total dietary energy intake [24], Consequently, alcohol consumption displaces many normal nutrients of the diet, resulting in primary malnutrition and associated symptomatology, foremost that of folate, thiamine and other vitamin B deficiencies. As alcohol impairs the activation and utilization of nutrients, secondary malnutrition may result from either maldigestion or malabsorption caused by gastrointestinal complications associated with alcoholism, mainly pancreatic insufficiency. In the absence of severe liver injury, high alcohol intake results in increased levels ofHDL, primarily HDL2, but at that level of alcohol intake there is no evidence of 'protection' against CHD. While alcohol consumption is associated with severe liver disease, levels of the HDL fractions decrease. Thus, with higher alcohol intakes, adverse effects predominate.

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