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. |
