Alcohol and fibrinolysis

Abstract

Epidemiological studies have shown an inverse relation between moderate alcohol use and the incidence of coronary heart disease. Potential mechanisms explaining that relation may be found in the haemostatic processes. One possible candidate is the fibrinolytic system which, as the natural anticoagulant system in the body, may be reinforced by moderate alcohol consumption. Such an effect might protect against thrombo-embolic complications.From epidemiological and experimental studies into the effects of alcohol consumption it can be concluded that the long-term effects of alcohol consumption on Fibrinolytic variables are moderate. The short-term or acute effects, however, are marked and involve two-to ten-fold changes in blood levels of some components.A recent study has shown that alcohol induces significant short-term increases in levels of the tissue-type plasminogen activator (t-PA). The data further support the notion that this increase is mainly effective with moderate alcohol consumption.It is postulated that this increased fibrinolysis potential can contribute to a reduction of the risk for thrombo-embolic disease in two ways. 1 ) The increase of t-PA, which lasts for 10-15 hours, can counteract new thrombotic events and enhance the removal of old clots locally in the vessels where t-PA is released by the endothelium. 2) The t-PA increase reaches a peak, in systemic activity in the early morning following an evening of moderate alcohol consumption. This peak coincides with the period of highest risk for myocardial infarction. It can be postulated that in moderate alcohol consumers the morning peak in frequency of infarctions is blunted, thus possibly explaining the lower risk in this group.Abbreviations dDAVP, desamino-D-arginine vasopression; LP(a), lipoprotein (a); PA, plasminogen activator; PAI-1, plasminogen activator inhibitor-1; t-PA, tissue-type plasminogen activator: u-PA, urokinase-type plasminogen activator.

Relationship between plasma plasminogen activator inhibitor-1 activity and VLDL triglyceride concentration, insulin levels and insulin sensitivity: studies in randomly selected normo- and hypertriglyceridaemic men

“…One possible explanation for this discrepancy may be that the pattern of alcohol consumption, e. g. daily moderate intake as opposed to binge drinking, seems to influence PAI-1 activity differently. Regular daily alcohol consumption has been shown to be followed by increased plasma PAI-1 activity [35] while binge drinking appeared to have no effect on PAI-1 levels [34,35].…”

“…In epidemiological studies alcohol consumption has been positively associated with fibrinolytic capacity [34]. By contrast, experimental studies have shown decreased fibrinolysis after alcohol intake [34].…”

“…In epidemiological studies alcohol consumption has been positively associated with fibrinolytic capacity [34]. By contrast, experimental studies have shown decreased fibrinolysis after alcohol intake [34]. One possible explanation for this discrepancy may be that the pattern of alcohol consumption, e. g. daily moderate intake as opposed to binge drinking, seems to influence PAI-1 activity differently.…”

Relationship of Light to Moderate Alcohol Consumption and Risk of Hypertension in Japanese Male Office Workers

“…Considering the beneficial effect of reduced alcohol consumption on BP, such a reduction may prove to be a factor in the primary prevention of hypertension for this population. Established light to moderate drinkers should not be advised to omit their drinking because of hypertension risk, especially for white subjects; they are at the lowest overall risk of mortality because of less coronary heart disease (Friedman and Klatsky, 1993;Pearson and Terry, 1994) through the beneficial effects of alcohol consumption on lipid metabolism Gordon et al, 1977), thrombogenesis, and fibrinolytic activity (Meade et al, 1979;Veenstra et al, 1990). However, Japanese may be at higher risk of adverse alcohol reaction than white subjects because of genetic differences in how they metabolize alcohol.…”

Alcohol‐Induced Up‐Regulation of Fibrinolytic Activity and Plasminogen Activators in Human Monocytes

“…Some proposed mechanisms for the protective effect of moderate alcohol include its antiatherogenic role in changes in lipid profile and cholesterol subtypes, as well as its role in changes in hemostatic factors, resulting in decreased platelet aggregation (Demrow et al, 1995;Rubin and Rand, 1994). In addition, a positive association between moderate alcohol consumption and fibrinolysis has also been demonstrated (Veenstra et al, 1995). In a cohort study of 87,526 moderate-drinking nurses, alcohol drinkers were found to have a lower risk of both acute coronary events and ischemic stroke but an increased risk of hemorrhagic stroke, suggesting that alcohol consumption may result in perturbation of fibrinolytic components (Stampfer et al, 1988).…”