Editorials |
From the Department of Medicine (N.M.), University of North Carolina at Chapel Hill, NC; and the Aab Cardiovascular Research Institute, Department of Medicine (M.B.T.), University of Rochester, NY.
Correspondance to Nigel Mackman, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. E-mail nmackman@med.unc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
C-reactive protein (CRP) is an acute-phase protein that participates in host defense against bacterial pathogens (reviewed in1,2). It has been used as a biomarker of inflammation, and several studies have shown that it has predictive value for cardiovascular events (reviewed in3). Based on these studies, blood CRP levels are being used increasingly by clinicians to help assess cardiovascular risk and to guide decisions on preventive therapies. CRP levels are also being used as secondary end points in numerous atherosclerosis trials, such as those involving statins. Statins were shown to reduce levels of both low-density lipoprotein (LDL) and CRP in individuals at risk for cardiovascular disease (CVD). This led to a clinical trial that examined the effect of statin therapy on primary prevention in healthy individuals with low LDL cholesterol but elevated CRP levels.4 The results suggested that the ability of statin therapy to reduce inflammation may be as important as its effects on LDL cholesterol in preventing CVD. Despite its value as a predictor of cardiovascular events, it is unclear whether CRP directly contributes to the development and progression of atherosclerotic disease or is simply a marker of the vascular inflammatory process that accompanies atherogenesis.
See accompanying article on page 698
Tissue factor (TF) is the primary cellular initiator of the blood coagulation cascade, which generates various proteases, including thrombin, and ultimately leads to fibrin deposition.5,6 TF also localizes factor VIIa to the cell membrane where it can cleave protease activated receptor 2 (PAR-2) and activate cells.7 Inhibition
Related Article:
Arterioscler Thromb Vasc Biol 2008 28: 698-704.
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