TY - JOUR
T1 - Plasma concentration of soluble vascular cell adhesion molecule-1 and subsequent cardiovascular risk
AU - de Lemos, James A
AU - Hennekens, Charles H.
AU - Ridker, Paul M.
N1 - Funding Information:
This study was supported by Grant HL-58755 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland. Dr. Ridker is also supported by an Established Investigator Award, American Heart Association, Dallas, Texas.
PY - 2000
Y1 - 2000
N2 - Objectives. The purpose of this study was to evaluate whether soluble vascular cell adhesion molecule-1 (sVCAM-1) is a marker for increased cardiovascular risk. Background. Soluble forms of cellular adhesion molecules (CAMs) may be useful markers of endothelial activation and local or systemic inflammation. Recent studies indicate that plasma concentration of soluble intercellular adhesion molecule-1 (sICAM-1) is elevated many years before a first myocardial infarction (MI) occurs. However, only a few prospective studies have evaluated whether sVCAM-1 is also a marker for increased cardiovascular risk. Methods. Baseline plasma samples were obtained prospectively from 14,916 healthy participants in the Physicians' Health Study. In a nested, case-control study design, the plasma concentration of sVCAM-1 was measured in 474 men with confirmed MI during the nine-year follow-up period, and in an equal number of control subjects who remained free of reported cardiovascular disease and who were matched for age, smoking status and length of follow-up. Results. No significant difference in the median baseline sVCAM-1 concentration was found between case and control subjects (638 vs. 634 ng/ml; p = NS). Cardiovascular risk was similar between patients with sVCAM-1 levels in the highest quartile and those in the lowest quartile, in both crude (relative risk [RR] 1.28, 95% confidence interval [CI] 0.85 to 1.92) and adjusted (RR 1.17, 95% CI 0.71 to 1.91) matched-pairs analyses. Conclusions. In contrast to previous data on sICAM-1, we found no evidence of an association between sVCAM-1 levels and the risk of future MI in a large cohort of apparently healthy men. These data suggest important pathophysiologic differences between sVCAM-1 and sICAM-1 in the genesis of atherothrombosis. (C) 2000 by the American College of Cardiology.
AB - Objectives. The purpose of this study was to evaluate whether soluble vascular cell adhesion molecule-1 (sVCAM-1) is a marker for increased cardiovascular risk. Background. Soluble forms of cellular adhesion molecules (CAMs) may be useful markers of endothelial activation and local or systemic inflammation. Recent studies indicate that plasma concentration of soluble intercellular adhesion molecule-1 (sICAM-1) is elevated many years before a first myocardial infarction (MI) occurs. However, only a few prospective studies have evaluated whether sVCAM-1 is also a marker for increased cardiovascular risk. Methods. Baseline plasma samples were obtained prospectively from 14,916 healthy participants in the Physicians' Health Study. In a nested, case-control study design, the plasma concentration of sVCAM-1 was measured in 474 men with confirmed MI during the nine-year follow-up period, and in an equal number of control subjects who remained free of reported cardiovascular disease and who were matched for age, smoking status and length of follow-up. Results. No significant difference in the median baseline sVCAM-1 concentration was found between case and control subjects (638 vs. 634 ng/ml; p = NS). Cardiovascular risk was similar between patients with sVCAM-1 levels in the highest quartile and those in the lowest quartile, in both crude (relative risk [RR] 1.28, 95% confidence interval [CI] 0.85 to 1.92) and adjusted (RR 1.17, 95% CI 0.71 to 1.91) matched-pairs analyses. Conclusions. In contrast to previous data on sICAM-1, we found no evidence of an association between sVCAM-1 levels and the risk of future MI in a large cohort of apparently healthy men. These data suggest important pathophysiologic differences between sVCAM-1 and sICAM-1 in the genesis of atherothrombosis. (C) 2000 by the American College of Cardiology.
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U2 - 10.1016/S0735-1097(00)00742-7
DO - 10.1016/S0735-1097(00)00742-7
M3 - Article
C2 - 10933352
AN - SCOPUS:0033866896
SN - 0735-1097
VL - 36
SP - 423
EP - 426
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -