EFFECT OF ESTROGEN REPLACEMENT THERAPY ON VASCULCAR CELL ADHESION MOLECULE- 1 AND E-SELECTIN IN POSTMENOPAUSAL WOMEN WITH CORONARY ARTERY DISEASE
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present work was designed to study the effect of estrogen replacement therapy (ETR) in postmenopausal women with coronary artery disease (cAp)„ on cell adhesion molecules (vascular cell adhesion molecule-1 "VACAM-1" and E-selectin ) which are markers of the inflammatory response of endothelium in CAD. The groups evaluated were 15 postmenopausal women without CAD not receiving ER-T (group Ia), 15 postmenopausal women with CAD not receiving ERT (group Ib), 15 postmenopausal women without CAD receiving ERT (group IIa) and 15 postmenopausal women with CAD receiving ERT (group II b). Control group included 10 healthy premenopausal women. Exclusion• criteria included acute myocardial infarction, use of progesterone, ERT by topical application, recent viral illness, diabetes mellitus, smoking, active inflammatory or connective tissue disease and clinically significant systemic illness. Detailed history, clinical examination, and the following laboratory investigations were performed to every subject: fasting plasma glucose, serum cholesterol, serum triglycerides, serum LDL, serum HDL, serum estradiol and serum levels of cell adhesion molecules (sEselectin and 5VCAM-1), ECG and stress test (when indicated). Diagnosis of CAD was documented by coronary angiography. We observed a statistically significant increase in the serum level of cell adhesion molecules in all postmenopausal women versus premenopausal controls. ERT is associated with singificant reduction in the serum level of cell adhesion molecules in postmenopausal women with and without CAD. However, ERT had no significant influence on other cardiac risk factors (cholesterol, triglycerides, LDL and HDL). Serum levels of cell adhesion molecules were significantly elevated in patients with CAD compared to women without CAD. However no difference existed in other cardiac risk factors between patients with CAD and women without CAD. So, we can conclude that E-selectin and VCAM-1 are implicated in the pathogenesis of coronary atherosclerosis and they can be considered as independent risk factors of coronary artery disease. Also we can conclude that one of the possible mechanisms by which ERT exerts one of its cardioprotective effect is by limting the inflammatory response to injury by modulating the expression of E-selectin and VCAM-1 from vascular endothelium.