Cardiovascular disease remains a major cause of death among postmenopausal women. After menopause, atherogenesis is promoted by a number of metabolic and vascular changes.
Atherogenesis is the formation of fatty deposits in the artery. These fatty deposits can become inflammed, and enlarged which then creates blockages in the coronary & cerebral arteries. Occluded (blocked) arteries reduce the ability of the heart and brain to receive oxygen and nutrients (ischemia). As such, heart and brain cells are not functioning at full capacity.
A multitude of observational clinical studies concluded that estrogen replacement therapy (ERT) reduces cardiovascular risk by approximately 50%. Yet, estrogen's favorable effects on the lipid profile explains only 30-50% of the overall observed risk reduction. It is now understood that estrogen has anti-atherogenic properties through both lipid (fat/cholesterol)and non-lipid mechanisms.
Estrogens induce favorable changes on lipids and lipoproteins, partly by increasing HDL-cholesterol and decreasing both LDL-cholesterol and lipoprotein (a). HDL is the cholesterol that transports fats away from the arteries to the liver for removal. HDL also helps protect LDL cholesterol from becoming oxidized (rancid). A high HDL concentration is cardio-protective.
Non-lipid mechanisms of estrogens cardio-protective actions include decreasing insulin resistance, serum fibrinogen, factor VII and plasminogen activator inhibitor-1 (PAI-1).
Studies indicate estrogen helps maintain endothelial cell integrity, decreases expression of adhesion molecules, lowers systemic blood pressure, promotes vasodilatation, decreases platelet aggregability, inhibits vascular smooth muscle cell proliferation, possesses potent antioxidant and calcium antagonist activities, inhibits adrenergic responses and downregulate (lessen) platelet and monocyte reactivity.
More recent reports are linking estrogen to the renin-angiotensin system, relaxin, serotonin and homocysteine.
Keep in mind, the vascular effects of estrogen replacement (17B-estradiol) depends on the timing, initiation, type and mode of administration (oral or transdermal).
Source:
Gynecol-Endocrinol. 1998 Feb; 12(1): 43-59
Author: Nasr, A : Breckwoldt, M
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