Potential Cardioprotective Effects of Estrogen Involving Ion Channels, Endothelium, and Coronary Artery Reactivity

Abstract

The protective effects of estrogen have been studied extensively in the cardiovascular system, where reproductive hormones are known to have major influence on morbidity and mortality. Epidemiological data indicate that women in their reproductive years have a much lower incidence of coronary disease than men of similar age, an advantage that diminishes rapidly with the onset of menopause (1,2). These studies demonstrate a direct correlation between plasma estrogen levels and coronary disease among these populations. A component of the cardioprotective effect of estrogen appears to be related to favorable effects on lipid profiles, which results in less atherosclerotic disease. Estrogen may also have antiproliferative effects by interfering with fibroblast activity that may account for part of the antiatherogenic activity of this hormone (3). Direct or indirect effects of estrogen may also lead to decreased platelet and monocyte adhesion, and a lower likelihood of thrombosis. A number of studies, however, suggest that effects on coronary artery contractility might also account for a substantial portion of the cardioprotective action of estrogen (1,2). Estrogen appears to reduce coronary vasoconstrictor activity, which may increase coronary blood flow, and/ or decrease the likelihood or severity of an ischemic event in the coronary circulation.