(Circulation. 2006;114:1557-1560.)
© 2006 American Heart Association, Inc.
Editorial |
From the Department of Medicine II, Johannes Gutenberg-University Mainz, Germany (S.B.), and the Population Health Research Institute, McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada (S.Y.).
Correspondence to Dr Salim Yusuf, McMaster University and Hamilton Health Sciences, 237 Barton St E, Hamilton, Ontario L8L 2X2, Canada. E-mail yusufs@mcmaster.ca
Key Words: Editorials cardiovascular diseases inflammation stroke
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Article p 1591
The hypothesis that inflammation is a central contributor to atherothrombosis has stimulated sustained efforts to characterize the specific molecules and pathways that may be involved and to identify biomarkers in humans that enable detection of underlying inflammatory activation to improve cardiovascular risk prediction. Ridker and coworkers1 reported that systemic low-grade inflammation assessed by measurements of the acute-phase reactant C-reactive protein (CRP) is associated with future cardiovascular events in apparently healthy individuals. This intriguing concept stimulated intense interest in further investigating the ability of inflammatory markers to add information for cardiovascular risk stratification beyond that obtained from traditional risk factors.
| CRP as Predictor for Cardiovascular Events |
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The utility of CRP for risk stratification has been proposed mainly in healthy individuals. Several large, prospective cohort studies have consistently reported that higher levels of CRP are associated with an increased risk for cardiovascular
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