MODULATION OF CIRCULATING CELLULAR ADHESION MOLECULES IN POSTMENOPAUSAL WOMEN WITH CORONARY-ARTERY DISEASE

Objectives. The present study examined the association of estrogen (E- 2) and the inflammatory response of endothelium in coronary artery dis ease (CAD) by measuring circulating cellular adhesion molecules (cCAMs ) in subjects with atherosclerosis. Background. Atherosclerotic plaque demonstrates features similar to inflammation. Endothelial cell activ ation by inflammatory cytokines induces expression of cellular adhesio n molecules (CAMs), thereby perhaps augmenting leukocyte adhesion and recruitment and subsequent development of atherosclerosis. The inciden ce of CAD is lower in women; this may be due to the cardioprotective e ffects of E-2. Methods. Consecutive eligible subjects with CAD admitte d for cardiac catheterization were studied. The groups evaluated were men, postmenopausal women receiving E-2 replacement therapy (ERT), pos tmenopausal women not receiving ERT and premenopausal women. Control g roups included men and women without CAD. Preprocedural blood samples were drawn from all groups. Measurements of cCAMs, E-selectin, vascula r cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecul e-1 were performed by enzyme-linked immunoabsorbant assay. E-2 levels were assessed by radioimmunoassay. Results. We observed a statisticall y significant increase in all cCAMs in men with CAD and postmenopausal women with CAD not receiving ERT compared with postmenopausal women w ith CAD receiving ERT. Premenopausal women with CAD and postmenopausal women with CAD receiving ERT had a significant increase in VCAM-1 alo ne compared with the female control group. Conclusions. A possible mec hanism by which E-2 exerts one of its cardioprotective effects is by l imiting the inflammatory response to injury by modulating the expressi on of CAMs from the endothelium. (C) 1998 by the American College of C ardiology.