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Circulation. 1999;100:96-102

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*Substance via MeSH

(Circulation. 1999;100:96-102.)
© 1999 American Heart Association, Inc.


Current Perspective

C-Reactive Protein as a Cardiovascular Risk Factor

More Than an Epiphenomenon?

Wim K. Lagrand, MD; Cees A. Visser, MD, PhD; Willem T. Hermens, PhD; Hans W. M. Niessen, MD, PhD; Freek W. A. Verheugt, MD, PhD; Gert-Jan Wolbink, MD, PhD; C. Erik Hack, MD, PhD

From the Departments of Cardiology (W.K.L., C.A.V.), Pathology (H.W.M.N.), and Internal Medicine (C.E.H.), Free University Hospital, Amsterdam; Cardiovascular Research Institute Maastricht (CARIM) (W.T.H.), University of Maastricht; the Department of Cardiology (F.W.A.V.), University Hospital Sint Radboud, Nijmegen; and CLB (G.-J.W., C.E.H.), Sanquin Blood Supply Foundation, Amsterdam, The Netherlands.

Correspondence to Wim K. Lagrand, Free University Hospital, Department of Cardiology, PO Box 7057, NL 1007 MB Amsterdam, The Netherlands. E-mail cardiol{at}azvu.nl

Background—Circulating levels of C-reactive protein (CRP) may constitute an independent risk factor for cardiovascular disease. How CRP as a risk factor is involved in cardiovascular disease is still unclear.

Methods and Results—By reviewing available studies, we discuss explanations for the associations between CRP and cardiovascular disease. CRP levels within the upper quartile/quintile of the normal range constitute an increased risk for cardiovascular events, both in apparently healthy persons and in persons with preexisting angina pectoris. High CRP responses after acute myocardial infarction indicate an unfavorable outcome, even after correction for other risk factors. This link between CRP and cardiovascular disease has been considered to reflect the response of the body to the inflammatory reactions in the atherosclerotic (coronary) vessels and adjacent myocardium. However, because CRP localizes in infarcted myocardium (with colocalization of activated complement), we hypothesize that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis.

Conclusions—CRP constitutes an independent cardiovascular risk factor. Unraveling the molecular background of this association may provide new directions for prevention of cardiovascular events.


Key Words: cardiovascular diseases • myocardial infarction • inflammation • risk factors • physiology




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