Postmenopausal Coronary Artery Disease Risk
Endothelial & Platelet Dysfunction with Possible Role of Glu298Asp eNOS Gene Polymorphism
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Menopause increases the risk for women independent of age. Prior to menopause, the risk of Coronary Artery Disease (CAD) for women lags behind the risk for men. After menopause, women have similar risks of CAD as men of the same age. The functional and morphological alteration in endothelial cells is critical to atherosclerotic process. After menopause, marked decline in Estrogen and Nitric Oxide (NO) levels takes place. Estrogen exerts its various CAD protective actions by arterial endothelium sex steroid receptors. Nitric oxide released from vascular endothelium is one of most known versatil...
Menopause increases the risk for women independent of age. Prior to menopause, the risk of Coronary Artery Disease (CAD) for women lags behind the risk for men. After menopause, women have similar risks of CAD as men of the same age. The functional and morphological alteration in endothelial cells is critical to atherosclerotic process. After menopause, marked decline in Estrogen and Nitric Oxide (NO) levels takes place. Estrogen exerts its various CAD protective actions by arterial endothelium sex steroid receptors. Nitric oxide released from vascular endothelium is one of most known versatile molecules and has a role in almost every biological system. Nitric oxide inhibits various key steps in development of atherosclerosis via inhibition of platelet activity and smooth muscle cell proliferation. Further presence of Endothelial Nitric Oxide Synthase (eNOS) gene polymorphism Glu298Asp may provide additional insult by decreasing NO levels adding to the CAD risk. Hence, postmenopausal women those who presents with eNOS Glu298Asp polymorphic gene may have higher CAD risk.
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