Abstract

Atherosclerosis, lipoprotein structure, lipoprotein metabolism and role in atherogenesis, epidemiology of lipoproteins and coronary artery disease, and current public health guidelines for cholesterol control are described. Low density lipoprotein cholesterol levels rise with age in both men and women. High density lipoprotein (HDL) levels decline after menopause. Special aspects of coronary risk in women include the stronger role of diabetes, hypertriglyceridemia and HDL. In addition, the effects of exogenous hormone therapy, both in the form or oral contraceptives and post menopausal hormone replacement should be considered. Careful attention to these issues may reduce cardiovascular morbidity in adult women.

PIP:

Reduction of cardiovascular mortality in women requires that physicians be alert to associated risk factors. In women, the most significant of these include diabetes, hypertriglyceridemia, and high density lipoprotein (HDL) levels. Both epidemiologic and prospective studies have found high levels of HDL to lower the risk of coronary heart disease, while high levels of low density lipoprotein (LDL) are associated with an increased risk. Thus, the focus of medical intervention is to reduce LDL cholesterol levels to at least 160 mg/dl, and ideally to below 130 mg/dl, either through dietary changes or cholesterol lowering drugs such as niacin. It is important to note that LDL cholesterol levels increase with age and, after age 55 years, LDL cholesterol levels in women exceed those in men. Other sex-related differences in cardiovascular risk factors are the stronger role of diabetes, triglyceride levels, and changes in HDL in women versus men. Endogenous and exogenous sex hormones represent another potentially major factor in cardiovascular disease in women. The lower incidence of cardiovascular disease in premenopausal women and the finding that unopposed estrogen replacement therapy exerts a protective effect reflect estrogen's tendency to lower LDL cholesterol and increase both total HDL cholesterol and HDL2. Progestin, on the other hand, has the opposite effect and can negate the protective effect of estrogen. Researchers are seeking to identify a regimen that maintains the positive impact of the estrogen-progestin combination on uterine mucosa while preserving the beneficial effects of estrogen in circulating lipoproteins. The impact of oral contraceptive use remains unclear, although it appears that, in young nonsmokers, the estrogen component mediates the potentially atherogenic effect of progestins.