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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.
William P. Fay (Fri,) studied this question.