Background Inflammation may be important in the pathogenesisof atherothrombosis. We studied whether inflammation increasesthe risk of a first thrombotic event and whether treatment withaspirin decreases the risk.
Methods We measured plasma C-reactive protein, a marker forsystemic inflammation, in 543 apparently healthy men participatingin the Physicians' Health Study in whom myocardial infarction,stroke, or venous thrombosis subsequently developed, and in543 study participants who did not report vascular disease duringa follow-up period exceeding eight years. Subjects were randomlyassigned to receive aspirin or placebo at the beginning of thetrial.
Results Base-line plasma C-reactive protein concentrations werehigher among men who went on to have myocardial infarction (1.51vs. 1.13 mg per liter, P<0.001) or ischemic stroke (1.38vs. 1.13 mg per liter, P = 0.02), but not venous thrombosis(1.26 vs. 1.13 mg per liter, P = 0.34), than among men withoutvascular events. The men in the quartile with the highest C-reactiveprotein values had three times the risk of myocardial infarction(relative risk, 2.9; P<0.001) and two times the risk of ischemicstroke (relative risk, 1.9; P = 0.02) of the men in the lowestquartile. Risks were stable over long periods, were not modifiedby smoking, and were independent of other lipid-related andnon–lipid-related risk factors. The use of aspirin wasassociated with significant reductions in the risk of myocardialinfarction (55.7 percent reduction, P = 0.02) among men in thehighest quartile but with only small, nonsignificant reductionsamong those in the lowest quartile (13.9 percent, P = 0.77).
Conclusions The base-line plasma concentration of C-reactiveprotein predicts the risk of future myocardial infarction andstroke. Moreover, the reduction associated with the use of aspirinin the risk of a first myocardial infarction appears to be directlyrelated to the level of C-reactive protein, raising the possibilitythat antiinflammatory agents may have clinical benefits in preventingcardiovascular disease.
Source Information
From the Divisions of Preventive Medicine (P.M.R., C.H.H.) and Cardiovascular Disease (P.M.R.) and the Channing Laboratory (M.J.S.), Department of Medicine, Brigham and Women's Hospital; the Department of Ambulatory Care and Prevention, Harvard Medical School (C.H.H.); and the Departments of Epidemiology (M.J.S., C.H.H.) and Nutrition (M.J.S.), Harvard School of Public Health — all in Boston; and the Laboratory for Clinical Biochemistry Research, University of Vermont, Burlington (M.C., R.P.T.).
Address reprint requests to Dr. Ridker at the Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave. E., Boston, MA 02215-1204.
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A correction has been published: N Engl J Med 1997;337(5):356.
