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Several epidemiologic studies have shown that moderate intake of alcohol is associated with a lower risk of cardiovascular disease (CVD), but the mechanism is not fully elucidated. One of the proposed mechanisms of the protective effect of moderate alcohol intake is its beneficial effect on hemostasis. The aim of this review is to summarize the effect of ethanol intake on platelet aggregation and activation, coagulation factors including von Willebrand factor (vWF), and the fibrinolytic system. With regard to the effect of alcohol on platelet function, evidence in the literature suggests both platelet activation and platelet inhibition by ethanol. A unifying hypothesis is that platelets are partially activated by ethanol, with partial degranulation allowing for continued circulation of platelets with impaired function. Evidence also exists showing that ethanol intake decreases fibrinogen, factor VII, and vWF levels. In addition, alcohol intake has been found to increase fibrinolysis by increasing tissue plasminogen activator activity. The effect of ethanol on platelets, coagulation factors, and the fibrinolytic system is likely to contribute to protection against CVD.
Salem et al. (Wed,) studied this question.