Circulating Adhesion Molecules VCAM-1, ICAM-1, and E-selectin in Carotid Atherosclerosis and Incident Coronary Heart Disease Cases

Ovid Technologies (Wolters Kluwer Health) - Tập 96 Số 12 - Trang 4219-4225 - 1997
Shih‐Jen Hwang1, Christie M. Ballantyne1, A. Richey Sharrett1, Louis C. Smith1, C.E. Davis1, Antonio M. Gotto1, Eric Boerwinkle1
1From the Human Genetics Center (S.-J.H., E.B.) and Institute of Molecular Medicine (E.B.), University of Texas–Houston Health Science Center; the Department of Medicine, Baylor College of Medicine (C.M.B., L.C.S., A.M.G.), Houston, Tex; the Epidemiology and Biometry Program, National Heart, Lung, and Blood Institute, Bethesda, Md (A.R.S.); and the Department of Biostatistics, University of North Carolina School of Public Health, Chapel Hill (C.E.D.).

Tóm tắt

Background Recruitment of circulating leukocytes at sites of atherosclerosis is mediated through a family of adhesion molecules. The function of circulating forms of these adhesion molecules remains unknown, but their levels may serve as molecular markers of subclinical coronary heart disease (CHD). Methods and Results To determine the ability of circulating vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intercellular adhesion molecule-1 (ICAM-1) to serve as molecular markers of atherosclerosis and predictors of incident CHD, we studied 204 patients with incident CHD, 272 patients with carotid artery atherosclerosis (CAA), and 316 control subjects from the large, biracial Atherosclerosis Risk In Communities (ARIC) study. Levels of VCAM-1 were not significantly different among the patients with incident CHD, those with CAA, and control subjects. Higher levels of E-selectin and ICAM-1 were observed for the patients with CHD (means [ng/mL]: E-selectin, 38.4; ICAM-1, 288.7) and those with CAA (E-selectin, 41.5; ICAM-1, 283.6) compared with the control subjects (E-selectin, 32.8; ICAM-1, 244.2), but the distributions were not notably different between the patients with CHD and CAA. Results of logistic regression analyses indicated that the relationship of ICAM-1 and E-selectin with CHD and CAA was independent of other known CHD risk factors and was most pronounced in the highest quartile. The odds of CHD and CAA were 5.53 (95% CI, 2.51–12.21) and 2.64 (95% CI, 1.40–5.01), respectively, for those with levels of ICAM-1 in the highest quartile compared with those in the lowest quartile. Odds of CAA were 2.03 (95% CI, 1.14–3.62) for those with levels of E-selectin in the highest quartile compared with those in the lowest quartile. Conclusions These data indicate that plasma levels of ICAM-1 and E-selectin may serve as molecular markers for atherosclerosis and the development of CHD.

Từ khóa


Tài liệu tham khảo

Nicholls ES, Peruga A, Restrepo HE. Cardiovascular disease mortality in the Americas. World Health Stat Q. 1993;46:134–150.

Faggiotto A, Ross R, Harker L. Studies of hypercholesterolemia in the nonhuman primate, I: change that leads to fatty streak formation. Arteriosclerosis. 1990;4:323–340.

10.1161/res.46.4.6244120

Gerrity RG. The role of the monocyte in atherogenesis, I; transition of blood-borne monocytes into foam cells in fatty lesions. Am J Pathol. 1981;103:181–190.

Joris I, Zand T, Nunnari JJ, Krolikowski FJ, Majno G. Studies on the pathogenesis of atherosclerosis, I; adhesion and emigration of mononuclear cells in the aorta of hypercholesterolemic rats. Am J Pathol. 1983;113:341–358.

Munro JM, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest. 1988;58:249–261.

10.1161/circ.73.4.3948368

10.1016/0735-1097(88)90356-7

10.1161/circ.92.3.646

10.1016/S0033-0620(05)80009-X

10.1161/circ.93.11.1951

10.1161/circ.91.1.54

Hajjar DP, Nicholson AC. Atherosclerosis. Am Sci. 1995;83:460–467.

10.1096/fasebj.8.8.8181668

10.1016/0167-5699(93)90267-O

10.1096/fasebj.9.10.7542213

10.4049/jimmunol.155.7.3538

10.1096/fasebj.9.10.7542214

10.4049/jimmunol.137.1.245

10.1146/annurev.bi.64.070195.000553

10.1016/0092-8674(91)90393-D

Li H, Cybulsky MI, Gimbrone MA, Libby P. Inducible expression of vascular cell adhesion molecule-1 by vascular smooth muscle cells in vitro and within rabbit atheroma. Am J Pathol. 1993;143:1551–1559.

10.1002/path.1711710311

Poston RN, Haskard DO, Coucher JR, Gall NP, Johnson-Tidey RR. Expression of intercellular adhesion molecule-1 in atherosclerotic plaques. Am J Pathol. 1992;140:665–673.

van der Wal AC, Das PK, Tigges AJ, Becker AE. Adhesion molecules on the endothelium and mononuclear cells in human atherosclerotic lesions. Am J Pathol. 1992;141:1427–1433.

10.1111/j.1365-2559.1993.tb00157.x

10.1172/JCI116670

10.1161/circ.93.4.672

Ballantyne CM, Mainolfi EA, Young JB, Windsor NT, Cocanougher B, Lawrence EC, Pollack MS, Entman ML, Rothlein R. Relationship of increased levels of circulating intercellular adhesion molecule 1 after heart transplantation to rejection: human leukocyte antigen mismatch and survival. J Heart Lung Transplant. 1994;13:597–603.

Nakai K, Itoh C, Kawazoe K, Miura Y, Sotyanagi H, Hotta K, Itoh T, Kamata J, Hiramori K. Concentration of soluble vascular cell adhesion molecule-1 (VCAM-1) correlated with expression of VCAM-1 mRNA in the human atherosclerotic aorta. Coron Artery Dis. 1996;6:497–502.

10.4049/jimmunol.147.11.3788

10.1016/0006-291X(92)91234-H

10.1093/oxfordjournals.aje.a115184

10.1161/01.CIR.74.6.1399

10.1161/atv91.13.8.8343489

10.1016/1047-2797(92)90017-K

10.1161/atv91.13.12.8241104

SAS Institute. SAS User’s guide: Statistics. Cary NC: SAS Institute Inc; 1994.

Conover WJ. Practical Nonparametric Statistics. 2nd ed. New York NY: John Wiley & Sons Inc: 1980.

Cox DR Snell EJ. The Analysis of Binary Data. 2nd ed. London UK: Chapman and Hall; 1989.

10.1093/jnci/80.15.1198

10.1016/0091-7435(79)90328-1

10.1093/ajh/7.1.7

10.1055/s-0038-1648827

10.1007/BF02263499

10.1038/362801a0

10.1056/NEJM198602203140806

10.1161/atvb.15.11.1987

10.1161/circ.93.7.1334

10.1055/s-0038-1648993

10.1111/j.1749-6632.1992.tb51633.x

10.1161/atv91.14.5.7513552

10.1002/jcp.1041600118

10.1161/circ.91.4.941

10.1073/pnas.92.5.1505

10.1182/blood.V76.5.965.965

10.1161/atvb.15.1.2

10.2307/2530744

10.2337/diab.41.12.1668

10.1159/000246627

10.1159/000217946

Thông tin
Thông tin xuất bản

Ovid Technologies (Wolters Kluwer Health)

Tập 96 Số 12

4219-4225

Thông tin tác giả