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Previous Volume 332:635-641 March 9, 1995 Number 10 Next

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ABSTRACT

Background Increased levels of certain hemostatic factors may play a part in the development of acute coronary syndromes and may be associated with an increased risk of coronary events in patients with angina pectoris.

Methods We conducted a prospective multicenter study of 3043 patients with angina pectoris who underwent coronary angiography and were followed for two years. Base-line measurements included the concentrations of selected hemostatic factors indicative of a thrombophilic state or endothelial injury. The results were analyzed in relation to the subsequent incidence of myocardial infarction or sudden coronary death.

Results After adjustment for the extent of coronary artery disease and other risk factors, an increased incidence of myocardial infarction or sudden death was associated with higher base-line concentrations of fibrinogen (mean ±SD, 3.28±0.74 g per liter in patients who subsequently had coronary events, as compared with 3.00±0.71 g per liter in those who did not; P = 0.01), von Willebrand factor antigen (138±49 percent vs. 125±49 percent, P = 0.05), and tissue plasminogen activator (t-PA) antigen (11.9±4.7 ng per milliliter vs. 10.0±4.2 ng per milliliter, P = 0.02). The concentration of C-reactive protein was also directly correlated with the incidence of coronary events (P = 0.05), except when we adjusted for the fibrinogen concentration. In patients with high serum cholesterol levels, the risk of coronary events rose with increasing levels of fibrinogen and C-reactive protein, but the risk remained low even given high serum cholesterol levels in the presence of low fibrinogen concentrations.

Conclusions In patients with angina pectoris, the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent acute coronary syndromes. In addition, low fibrinogen concentrations characterize patients at low risk for coronary events despite increased serum cholesterol levels. Our data are consistent with a pathogenetic role of impaired fibrinolysis, endothelial-cell injury, and inflammatory activity in the progression of coronary artery disease.

Source Information

From the Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London (S.G.T., S.D.M.P.); the Department of Internal Medicine, University of Münster, Münster, Germany (J.K., J.C.W.L.); and the Gaubius Laboratory, Leiden, the Netherlands (F.H.).

Address reprint requests to Dr. van de Loo at the Department of Internal Medicine, University of Münster, Albert-Schweitzer-Str. 33, D-48129 Münster, Germany.

Full Text of this Article

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Hemostatic Factors and the Risk of Myocardial Infarction
Otto C., Richter W. O., Ridker P. M., Vaughan D. E., van de Loo J. C.W., Haverkate F., Thompson S. G.
Extract | Full Text  
N Engl J Med 1995; 333:389-390, Aug 10, 1995. Correspondence

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