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Modulation of circulating cellular adhesion molecules in postmenopausal women with coronary artery disease
T Caulin-Glaser1, W J Farrell, S E Pfau
1Division of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8017, USA. teresa.caulin-glaser@yale.edu
Insights
Estrogen (E2) may protect the heart by reducing inflammation in coronary artery disease (CAD). E2 replacement therapy (ERT) in postmenopausal women with CAD lowered inflammatory markers (cCAMs) compared to those not on ERT.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Immunology
Background:
- Atherosclerosis involves inflammation, with endothelial cell activation promoting leukocyte adhesion and potentially contributing to disease development.
- Coronary artery disease (CAD) incidence is lower in women, suggesting a potential cardioprotective role for estrogen (E2).
Purpose of the Study:
- To investigate the association between estrogen (E2) levels and endothelial inflammatory response in coronary artery disease (CAD).
- To measure circulating cellular adhesion molecules (cCAMs) as indicators of endothelial inflammation in subjects with atherosclerosis.
Main Methods:
- Study included men, premenopausal women, and postmenopausal women (with and without estrogen replacement therapy [ERT]) with CAD, alongside control groups without CAD.
- Blood samples were analyzed for cCAMs (E-selectin, VCAM-1, ICAM-1) using ELISA and for E2 levels via radioimmunoassay.
Main Results:
- Men with CAD and postmenopausal women with CAD not on ERT showed significantly higher cCAMs compared to postmenopausal women with CAD on ERT.
- Premenopausal women with CAD and postmenopausal women with CAD on ERT had elevated vascular cell adhesion molecule-1 (VCAM-1) compared to female controls.
Conclusions:
- Estrogen (E2) may exert cardioprotective effects by mitigating the endothelial inflammatory response.
- Modulation of cellular adhesion molecules (CAMs) expression by E2 is a potential mechanism underlying its protective role in CAD.
Objectives:
The present study examined the association of estrogen (E2) and the inflammatory response of endothelium in coronary artery disease (CAD) by measuring circulating cellular adhesion molecules (cCAMs) in subjects with atherosclerosis.
Background:
Atherosclerotic plaque demonstrates features similar to inflammation. Endothelial cell activation by inflammatory cytokines induces expression of cellular adhesion molecules (CAMs), thereby perhaps augmenting leukocyte adhesion and recruitment and subsequent development of atherosclerosis. The incidence of CAD is lower in women; this may be due to the cardioprotective effects of E2.
Methods:
Consecutive eligible subjects with CAD admitted for cardiac catheterization were studied. The groups evaluated were men, postmenopausal women receiving E2 replacement therapy (ERT), postmenopausal women not receiving ERT and premenopausal women. Control groups included men and women without CAD. Preprocedural blood samples were drawn from all groups. Measurements of cCAMs, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 were performed by enzyme-linked immunoabsorbant assay. E2 levels were assessed by radioimmunoassay.
Results:
We observed a statistically significant increase in all cCAMs in men with CAD and postmenopausal women with CAD not receiving ERT compared with postmenopausal women with CAD receiving ERT. Premenopausal women with CAD and postmenopausal women with CAD receiving ERT had a significant increase in VCAM-1 alone compared with the female control group.
Conclusions:
A possible mechanism by which E2 exerts one of its cardioprotective effects is by limiting the inflammatory response to injury by modulating the expression of CAMs from the endothelium.