A Study of Prognostic Value of Hs-CRP and Fibrinogen in Patients of Unstable Angina


  • Government Medical College, Department of Medicine, Amritsar, Punjab, India


Background: Unstable angina constitutes a clinical syndrome that is usually caused by atherosclerotic coronary artery disease and is associated with an increased risk of cardiac death and myocardial infarction.

Material and Methods: An open, prospective, observational, comparative study was conducted. The study included 50 cases in age group 20-80 years admitted in Government Medical College, Amritsar diagnosed as unstable angina ruled out by Trop T and CPK-MB at admission. Hs-CRP and Fibrinogen levels were estimated at time of admission and repeated after 48 hours.

Results: There was significant difference in the mean value of Hs-CRP between favourable and unfavourable group at the time of admission (0.807±0.37mg/l v/s 3.57±1.70mg/l, p<0.001). A significant difference in the mean value of Hs-CRP was found between favourable and unfavourable group after 48 hours (0.51±0.22mg/l v/s 4.03±1.84mg/l, p<0.001) There was significant difference in the mean value of fibrinogen between favourable and unfavourable group at the time of admission (356.94±72.50mg/dl v/s 588.60±94.89mg/dl, p<0.001). A significant difference in the mean value of fibrinogen was found between favourable and unfavourable group after 48 hours (309.11±75.25mg/dl v/s 622.60±133.42mg/dl, p<0.001).

Conclusion: It is concluded that in patients with unstable angina, elevated levels of Hs-CRP and Fibrinogen at admission indicate an adverse hospital outcome.


Hs-CRP, Unstable Angina, Fibrinogen, Myocardial Infarction, Coronary Artery Disease.

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Hamm CW, Ravkilde J, Gerhardt W, Jørgensen P, Peheim E, Ljungdahl L, et al. The prognostic value of serum troponin T in unstable angina. New England Journal of Medicine 1992;327(3):146-50.

Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Harrison’s Principles of Internal Medicine. 2015;19(2):1594.

Greenland P, Knoll MD, Stamler J, Neaton JD, Dyer AR, Garside DB, et al. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA. 2003;290(7):891-7.

Danesh J, Wheeler JG, Hirschfield GM, Eda S, Eiriksdottir G, Rumley A, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. New England Journal of Medicine 2004;350(14):1387-97.

Ridker PM, Rifai N, Rose L, Buring JE, Cook NR. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. New England journal of medicine 2002;347(20):1557-65.

Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000;102(18):2165-8.

Pasceri V, Chang J, Willerson JT, Yeh ET. Modulation of C-reactive protein–mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation 2001;103(21):2531-4.

Venugopal SK, Devaraj S, Yuhanna I, Shaul P, Jialal I. Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 2002;106(12):1439-41.

Wang CH, Li SH, Weisel RD, Fedak PW, Dumont AS, Szmitko P, et al. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle. Circulation 2003;107(13):1783-90.

Han KH, Hong KH, Park JH, Ko J, Kang DH, Choi KJ, et al. C-reactive protein promotes monocyte chemoattractant protein-1-mediated chemotaxis through upregulating CC chemokine receptor 2 expression in human monocytes. Circulation 2004;109(21):2566-71.

Torzewski J, Torzewski M, Bowyer DE, Fröhlich M, Koenig W, Waltenberger J, et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arteriosclerosis, thrombosis, and vascular biology 1998;18(9):1386-92.

Roberts WL. CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease. Circulation 2004;110(25):e572-6.

Hicks RC, Golledge J, Mir-Hasseine R, Powell JT. Vasoactive effects of fibrinogen on saphenous vein. Nature 1996;379(6568):818-20.

Schneider DJ, Taatjes DJ, Howard DB, Sobel BE. Increased reactivity of platelets induced by fibrinogen independent of its binding to the IIb-IIIa surface glycoprotein. Journal of the American College of Cardiology 1999;33(1):261-6.

Fatah KA, Hamsten A, Blombäck B, Blombäck M. Fibrin gel network characteristics and coronary heart disease: relations to plasma fibrinogen concentration, acute phase protein, serum lipoproteins and coronary atherosclerosis. Thrombosis and hemostasis 1992;68(2):130-5.

McDonagh J, Lee MH. How does hyperfibrinogenemia lead to thrombosis.? Fibrinolysis and Proteolysis 1997;11:13-7.

Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. New England Journal of Medicine 1995;332(10):635-41.

Gil M, Zarȩbinski M, Adamus J. Plasma fibrinogen and troponin I in acute coronary syndrome and stable angina. International journal of cardiology 2002;83(1):43-6.

Koenig W, Löwel H, Baumert J, Meisinger C. C-reactive protein modulates risk prediction based on the Framingham score. Circulation 2004;109(11):1349-53.

Kumar A, Sivakanesan R. Does plasma fibrinogens and c-reactive protein predicts the incidence of myocardial infarction in patients with normal lipids profile.? Pakistan Journal of Medical Sciences 2008;24(2):336.

Rana JS, Cote M, Despres JP, Sandhu MS, Talmud PJ, Ninio E, et al. Inflammatory biomarkers and the prediction of coronary events among people at intermediate risk: the EPIC-Norfolk prospective population study. Heart 2009;95(20):1682-7.


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