In over 30 years of surveillance of 2873 women, 574 developed initial clinical manifestations of CHD. A number of antecedent metabolic risk factors proved atherogenic, including blood lipids, glucose tolerance, uric acid, and menopause. Serum total cholesterol predicts as strongly in women as in men. The predictive power of cholesterol is strengthened when the total cholesterol is partitioned into its atherogenic LDL and protective HDL fractions. Contrary to the case in men, triglyceride may be a contributor to risk in older women. A total-to-HDL cholesterol ratio exceeding 7.5 equalizes the risk in men and women. Impaired glucose tolerance also eliminates the female CHD risk advantage over men, conferring a three-fold increased risk. Serum uric acid, although lower in women than in men, is equally predictive in the sexes. Central obesity confers an increased CHD risk in women and predisposes to diabetes, hyperuricemia, hypertension, and an unfavorable LDL/HDL cholesterol ratio. A combination of obesity, low HDL cholesterol, and impaired glucose tolerance predisposes especially. Age-adjusted risk of CHD is increased two- to threefold compared to pre menopausal women, even when induced surgically without removing the ovaries. It is not clear whether post menopausal estrogen replacement eliminates this excess risk. Fibrinogen is higher in women than in men, and is increased with hypertension, diabetes, hypercholesterolemia, high hematocrit, and cigarette smoking. At any level of multivariate risk, fibrinogen added to the CHD risk in women.