Independent prognostic value of elevated C-reactive protein in unstable angina.

BACKGROUND There is growing evidence of the prognostic importance of C-reactive protein (CRP) in unstable angina. However, the independent value of CRP relative to other conventional markers at different stages of treatment has not been established. Therefore, we assessed the in-hospital and 90-day prognostic values of serum CRP in unstable angina. We also compared the relation of CRP at admission and discharge with 90-day outcome. METHODS AND RESULTS One hundred ninety-four consecutive patients were included in a derivation (n = 105) and a validation set (n = 89). Serum CRP was measured at admission, at 48 hours, and at hospital discharge. A cutoff point of 1.5 mg/dL for CRP provided optimum sensitivity and specificity for adverse outcome, based on the receiver operator curves. No association was found between CRP on admission and in-hospital outcome. CRP at admission, adjusted for age, ECG findings on admission, silent ischemia, left ventricular wall motion score, and high-risk clinical presentation, was related to the combined end point of refractory angina, myocardial infarction, or death at 90 days (hazard ratio [HR] 1.9, 95% CI 1.2 to 8.3, P = 0.002). CRP at hospital discharge was the strongest independent marker of an adverse outcome (HR 3.16, 95% CI 2.0 to 5.2, P = 0.0001). These results were confirmed in the validation set (CRP at discharge: HR 3. 3, 95% CI 2.0 to 7.69, P = 0.0001). CONCLUSIONS In unstable angina, CRP is a strong independent marker of increased 90-day risk. Compared with CRP at admission, CRP at discharge is better related to later outcome and could be of great utility for risk stratification.

[1]  R. Diaz,et al.  Clinical predictors of in-hospital prognosis in unstable angina: ECLA 3. The ECLA Collaborative Group. , 1999, American heart journal.

[2]  M. Lauer Noninvasive risk stratification after myocardial infarction: which test is best? , 1998, American heart journal.

[3]  E. Vicaut,et al.  Early increase of von Willebrand factor predicts adverse outcome in unstable coronary artery disease: beneficial effects of enoxaparin. French Investigators of the ESSENCE Trial. , 1998, Circulation.

[4]  E. Antman,et al.  C-Reactive Protein Is a Potent Predictor of Mortality Independently of and in Combination With Troponin T in Acute Coronary Syndromes: A TIMI 11A Substudy , 1998 .

[5]  A. Siegbahn,et al.  Prognostic influence of increased fibrinogen and C-reactive protein levels in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. , 1997, Circulation.

[6]  P. Ridker,et al.  Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. , 1997, The New England journal of medicine.

[7]  S. Thompson,et al.  Production of C-reactive protein and risk of coronary events in stable and unstable angina , 1997, The Lancet.

[8]  A. Rebuzzi,et al.  Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia. , 1996, Journal of the American College of Cardiology.

[9]  V. Fuster,et al.  Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. , 1995, Circulation.

[10]  A. Rebuzzi,et al.  The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. , 1994, The New England journal of medicine.

[11]  V. Fuster,et al.  Macrophage Infiltration in Acute Coronary Syndromes: Implications for Plaque Rupture , 1994, Circulation.

[12]  E. Braunwald Unstable angina : diagnosis and management , 1994 .

[13]  A. Becker,et al.  Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. , 1994, Circulation.

[14]  G. Specchia,et al.  Increased Expression of Neutrophil and Monocyte Adhesion Molecules in Unstable Coronary Artery Disease , 1993, Circulation.

[15]  J. Fleiss,et al.  Detection and Significance of Myocardial Ischemia in Stable Patients after Recovery from an Acute Coronary Event , 1993 .

[16]  N. Coplan,et al.  The role of exercise testing for evaluating patients with unstable angina. , 1992, American heart journal.

[17]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.

[18]  M. Field,et al.  Guidelines for Clinical Practice: From Development to Use , 1992 .

[19]  W. Weintraub,et al.  Elevation of C-reactive protein in "active" coronary artery disease. , 1990, The American journal of cardiology.

[20]  N. Reichek,et al.  Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. , 1989, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[21]  E. Braunwald,et al.  Unstable angina. A classification. , 1989, Circulation.

[22]  E. Falk Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. , 1985, Circulation.

[23]  M J Davies,et al.  Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. , 1984, The New England journal of medicine.

[24]  P. Constantinides,et al.  Plaque fissures in human coronary thrombosis , 1966 .