Abstract
There is a sexual dimorphism in the development of atherosclerotic cardiovascular disease in humans (1). The incidence of cardiovascular disease is much lower in premenopausal women than in age matched men, but rises steadily in women after the menopause (2). Epidemiologic and observational clinical studies have shown that postmenopausal women on estrogen replacement therapy have less severe coronary artery disease and a lower risk of cardiovascular mortality than women without hormone treatment (3). Thus, ovarian hormones, principally estrogens, appear to inhibit the development of atherosclerotic cardiovascular disease in women (4). Large-scale clinical studies, including the Women’s Health Initiative (WHI) and the Heart Estrogen-Progestin Replacement Study (HERS), are currently evaluating the role of estrogen in the prevention of cardiovascular morbidity and mortality. Emerging evidence from these and other studies suggests that estrogen may be cardioprotective through a combination of mechanisms. For example, estrogen replacement therapy results in decreased plasma low-density lipoprotein (LDL) and increased high-density lipoprotein (HDL) concentrations (5-7). Other benefits of estrogen replacement therapy, including the improvement of systemic hemodynamic parameters, appear to be unrelated to changes in plasma lipoprotein profiles (8). It has been clearly shown that endothelial cells and vascular smooth muscle cells (VSMCs) possess estrogen receptors (ER) and are thus physiological targets for estrogen action (9,10).
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Chen, YF., Oparil, S. (1998). Effects of Sex Steroids in Vascular Injury. In: Levin, E.R., Nadler, J.L. (eds) Endocrinology of Cardiovascular Function. Endocrine Updates, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5569-8_3
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