The effects of alcohol on the heart are complex. Meta-analyses have suggested that there is a reduction in risk for coronary heart disease associated with moderate consumption and increased risk with both more and less consumption, described by a J curve. This risk is influenced by the effects of alcohol on multiple thrombotic, inflammatory, and oxidative pathways. Oxidative metabolic processes appear to play a role in both the potentially beneficial and adverse cardiovascular effects of alcohol. Clinical and experimental evidence suggest that protective mechanisms include increased HDL-cholesterol, decreased oxidation of LDL-C, increased insulin sensitivity, decreased thrombosis and platelet aggregation, increased fibrinolysis, decreased fibrinogen, and reduced inflammatory activity. Excessive alcohol intake is associated with potentially adverse effects through generation of increased acetaldehyde, oxidative stress, triglycerides, reactive oxygen species, and decreased HDL-C. Alcohol-mediated cardiac protection may be related to ethanol as well as to polyphenolic antioxidant vasodilators in alcoholic beverages such as wine. Polyphenols block endothelin production, thereby reducing its vasoconstrictor and atherogenic activity. Resveratrol, a polyphenolic compound found in wine, has potent antioxidant actions, decreases thromboxane levels, reduces platelet aggregation, inhibits the lipoxygenase pathway and induces NO and vasorelaxation. Mitochondria generate reactive oxygen species that contribute to both physiologic cardiac function and myocardial tissue damage. The cellular mechanisms of alcohol's protective actions may relate to its influence on opening of mitochondrial ATP-sensitive potassium channels through which ethanol may prevent oxidant-induced experimental mitochondrial damage. There is also evidence that it activates signal transduction pathways and effector molecules that may be involved in ischemic preconditioning. Alcoholic cardiomyopathy may result from mechanisms that include oxidative damage mediated by decreased myofilament calcium sensitivity and impaired protein synthesis. The oxidation of ethanol to acetaldehyde by alcohol dehydrogenase is accompanied by generation of free radicals that can damage both the heart and liver.
|Original language||English (US)|
|Title of host publication||Oxidative Stress: A Focus on Cardiovascular Disease Pathogenesis|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||17|
|State||Published - 2011|
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