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World J Cardiol. Nov 26, 2010; 2(11): 365-369
Published online Nov 26, 2010. doi: 10.4330/wjc.v2.i11.365
Published online Nov 26, 2010. doi: 10.4330/wjc.v2.i11.365
Linking inflammation and thrombosis: Role of C-reactive protein
William P Fay, Department of Internal Medicine and Medical Pharmacology and Physiology, University of Missouri, School of Medicine, and the Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, MO 65212, United States
Author contributions: Fay WP contributed solely to this paper.
Supported by Merit Review Award from the Department of Veterans Affairs, research grants from the Missouri Life Sciences Research Board and NIH, No. HL57346
Correspondence to: William P Fay, MD, Department of Internal Medicine and Medical Pharmacology and Physiology, University of Missouri, School of Medicine, and the Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, 5 Hospital Drive, CE344-DC095.00, Columbia, MO 65212, United States. fayw@missouri.edu
Telephone: +1-573-8822296 Fax: +1-573-8847743
Received: August 2, 2010
Revised: September 18, 2010
Accepted: September 23, 2010
Published online: November 26, 2010
Revised: September 18, 2010
Accepted: September 23, 2010
Published online: November 26, 2010
Abstract
C-reactive protein (CRP) is a biomarker of inflammation. Increased plasma levels of CRP are associated with an increased risk of myocardial infarction. However, the correlation between plasma CRP concentration and atherosclerotic plaque burden is poor. Based on these observations, it has been hypothesized that CRP increases the risk of myocardial infarction by promoting thrombosis. This article reviews available data that link enhanced CRP expression to increased risk of thrombosis, with a focus on the effects of CRP on hemostasis, platelet function, and fibrinolysis. Overall, the available data support the hypothesis that CRP is an important mechanistic link between inflammation and thrombosis.
Keywords: C-reactive protein, Thrombosis, Inflammation, Tissue factor, Fibrinolysis, Plasminogen activator inhibitor-1