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Cardiol Clin. 2003 Aug;21(3):315-25.

C-reactive protein, inflammation, and coronary risk.

Author information

  • 1Center for Cardiovascular Disease in Women, Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Pmridker@bics.bwh.harvard.edu

Abstract

Advancements in understanding of the pathobiology of atherothrombosis have implicated inflammation as a central contributor to the progression of atherosclerotic vascular disease. Epidemiologic data demonstrate an association between the inflammatory marker hs-CRP and risk for future cardiovascular morbidity and mortality among those at high risk or with documented vascular disease. Moreover, a series of prospective studies provides consistent data documenting that mild elevation of baseline levels of hs-CRP among apparently healthy individuals is associated with higher long-term risk for future cardiovascular events. Among men and women, this predictive capacity of hs-CRP is independent of traditional cardiovascular risk factors and offers a prognostic advantage over measurement of lipids alone. Further, observations from the PHS and CARE trial suggest that the increased risk associated with systemic inflammation may be modified with certain preventive therapies and that inflammatory markers such as hs-CRP may help to identify those who would benefit most from these pharmacologic interventions. Given that high-throughput assays for inflammatory markers, including hs-CRP, are likely to become available for clinical use, carefully designed studies are needed to evaluate the clinical efficacy of hs-CRP as a new marker to stratify cardiovascular risk. Further, prospective, randomized trials are important to test directly the value of inflammatory markers in targeting specific preventive therapies. Finally, it is still undetermined as to whether elevation of these inflammatory markers reflects the degree of underlying atherosclerosis or plaque vulnerability or rather results from some other environmental or infectious stimulus or even has direct effects on platelet aggregation or coagulation [1]. Ongoing and future investigation will clarify the specific pathophysiologic relationships through which these markers correlate with adverse prognosis.

PMID:
14621448
[PubMed - indexed for MEDLINE]
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