I. ALCOHOL AND CORONARY HEART DISEASE
B. Alcohol Consumption and Hemostatic Factors
1. Analysis of the Framingham Offspring Cohort
Because cardioprotection is not fully explained by the modest increase in HDL cholesterol caused by alcohol, Mukamal et al. assessed the effects of alcohol on hemostatic factors.
Methods: There were 3223 adults from the Framing-ham offspring study done in 1971 used. These offspring were assessed 20 years later. Patients with coronary heart disease were excluded. Alcohol use was rated as none, <3, 3–7, 7–21, and more than 21 drinks per week.
Results: After allowing for variables of up to seven drinks per week, there were lower levels of fibrinogen, plasma viscosity, and von Willebrand factor. Seven to 21 drinks weekly were associated with impaired fibrinolytic potential and higher levels of type-1 plasminogen activator inhibitor (PAI-1) antigen and tissue plasminogen activator (t-PA) antigen.
Perspective: Light alcohol consumption is associated with lower levels of coagulation factors. Higher consump¬tion may impair fibrinolytic activity. These results may help explain the apparent protective effect of mild alcohol consumption not found in heavy drinkers. It is not known whether individuals at high risk for CHD may benefit, because this group was excluded from study.