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Cardiovascular disease remains a major cause of mortality among postmenopausal women. After menopause, atherogenesis is promoted by a number of metabolic and vascular changes. A multitude of observational clinical studies have come to the conclusion that estrogen replacement therapy (ERT) reduces cardiovascular risk by approximately 50% and that estrogen's favorable effects on the lipid profile can explain only 25-50% of the overall observed reduction. Estrogens are now known to have potent anti-atherogenic properties through lipid and non-lipid mechanisms; both will be highlighted in view of the recent literature. Estrogens induce favorable changes on lipids and lipoproteins, partly by increasing HDL-cholesterol and decreasing both LDL-cholesterol and lipoprotein (a). Non-lipid mechanisms of estrogen action include decreasing insulin resistance, serum fibrinogen, factor VII and plasminogen activator inhibitor-1 (PAI-1). Moreover, estrogens maintain endothelial cell integrity, decrease expression of adhesion molecules, lower systemic blood pressure, promote vasodilatation, decrease platelet aggregability, inhibit vascular smooth muscle cell proliferation, possess potent antioxidant and calcium antagonist activities, inhibit adrenergic responses and downregulate platelet and monocyte reactivity. Also mentioned are recent reports linking estrogen to the renin-angiotensin system, relaxin, serotonin and homocysteine. What was once thought of as a simple action is now being increasingly appreciated as a complex, multifaceted mechanism, which serves to prove that estrogen is a powerful cardiovascular agent.
Nasr et al. (Thu,) studied this question.