Estrogen Effect upon Coronary Vasculature

Abstract

Death from cardiovascular disease is rare in women before menopause while it represents the leading cause of death after either natural or surgically induced menopause [1]. The fact that the increased incidence of cardiovascular disease after menopause is not simply due to aging, but is strictly dependent upon estrogen deficiency and that, therefore, menopausal status influences the development of coronary artery disease independently from age, is demonstrated by the fact that, at any age, menopausal women have a significantly higher incidence of cardiovascular disease than premenopausal ones. Several large-scale trials have shown that estrogen replacement therapy reduces the occurrence of coronary disease and perhaps of cerebrovascular disease by nearly 50% in treated women compared to nonusers. These findings are supported by the evidence that estrogens have a beneficial effect on cholesterol metabolism and deposition, contributing to the inhibition of atherosclerotic plaque formation in arterial walls [2-3]. Early reports suggested that up to 60% of the protective effect of estrogens on coronary artery disease was attributable to favorable changes in plasma lipids. Reanalysis of the data indicated that the lipid changes probably account for approximately 20% of the cardioprotective effect of estrogen, and that other effects are therefore likely to be important [4]. Therefore, the favorable effect of estrogen replacement therapy on plasma lipids cannot fully explain the beneficial effects of estrogens upon cardiovascular disease. The influence of estrogens upon carbohydrate metabolism, atheroma formation, and cardiovascular hemodynamics may also play an integral role in the overall beneficial effect of the hormones.