Are C-Reactive Protein and Fibrinogen Risk Factors?

  • Frits Haverkate
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 197)


The function of haemostasis components in the cause and progression of atherosclerosis gained considerable interest since a study by de Wood et al.1 who showed the importance of coronary obstruction by thrombi and an epidemiological study by Meade et al.2 who found that fibrinogen and a few other haemostasis parameters indicated the risk of a coronary event in a healthy population. In the years which followed several haemostasis components in blood, including platelet, coagulation and fibrinolysis factors, were found to have a different concentration from normals in individuals at cardiovascular risk. As most, if not all, changes of levels pointed towards a hypercoagulable state in stroke, coronary disease or peripheral atherosclerosis, the rationale of the association between haemostasis and cardiovascular disease in prospective studies seems to be obvious: a change in levels of a haemostatic parameter triggers arterial thrombosis, a key factor in the etiology of cardiovascular disease. Out of all the haemostatic risk factors, fibrinogen has a dominant place. It has been repeatedly found to be a risk factor in stroke, coronary heart disease and peripheral atherosclerosis.3 Moreover, in contrast to other haemostatic risk factors, it is gradually correlated to the extent of the atherosclerosis as determined by coronary angiography4 or ultrasound techniques.5


Coronary Event Angina Pecteris Include Smoking Status Peripheral Atherosclerosis European Concert Action 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    De Wood MA Spores J, Notske R et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980;303:897-902.CrossRefGoogle Scholar
  2. 2.
    Meade TW, North WRS, Chakrabarti R, Stirling Y, Haines AP, Thompson SG. Haemostatic function and cardiovascular death: early results of a prospective study. Lancet 1 980;i: 1050-54.CrossRefGoogle Scholar
  3. 3.
    Koenig W, Ernst E. Fibrinogen and artherothrombogenesis. Current Opinion Lipidol 1993; 4:471–76.CrossRefGoogle Scholar
  4. 4.
    Bolibar I, Kienast J, Thompson SG, Matthias R, Niessner H, Fechtrup C on behalf of the ECAT Angina Pectoris Study Group. Relation of fibrinogen to presence and severity of coronary artery disease is independent of other coexisting heart disease. Am Heart J 1993;125:1601–1605.PubMedCrossRefGoogle Scholar
  5. 5.
    Folsom AR, Wu KK, Shakar E, Davis CE for the Atherosclerosis Risk in Communities (ARIC) Study Investigators. Arterioscler Thromb 1993;13:1829–36.PubMedCrossRefGoogle Scholar
  6. 6.
    Thompson SG, Kienast J, Pyke SDM, Haverkate F, Loo JCW van de, for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. IN Engl J Med 1995;332:635-41. PubMedCrossRefGoogle Scholar
  7. 7.
    Clauss von A. Gerinnungsphysiologische Schnellmethode zur Bestimmung des Fibrinogens. Acta Haematol 1957;17:237–46.PubMedCrossRefGoogle Scholar
  8. 8.
    Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997;349:462–66.PubMedCrossRefGoogle Scholar
  9. 9.
    Haverkate F. Low-grade acute-phase reactions in arteriosclerosis and the consequences for haemostatic risk factors. Fibrinolysis 1992;6(SuppI.3):17-18.CrossRefGoogle Scholar
  10. 10.
    Ridker PM, Cushman M. Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997:336:973–9.PubMedCrossRefGoogle Scholar
  11. 11.
    Kuller LH, Tracy RP, Shaten J, Meilahn EN, for the MIRFIT Research Group. Relation of C-reactive Protein and Coronary Heart Disease in the MRFIT nested case-control study. Am J Epidemiol 1996;144:537-47.PubMedGoogle Scholar
  12. 12.
    Liuzzo G, Biasucci LM, Gallimore JR et al. The prognostic value of C-Reactive Protein and Serum Amyloid A Protein in severe unstable angina. N Engl J Med 1994;331:417–24.PubMedCrossRefGoogle Scholar
  13. 13.
    Patel P, Mendall MA, Carrington D et al. Association of Helicobactor pylori and Chlamydia pneumoniae infections with coronary heart disease and cardiovascular risk factors. Br Med J 1995;311:711–4.Google Scholar
  14. 14.
    Jousilahti P, Vartiainen E, Tuomilehto J, Puska P. Symptoms of chronic bronchitis and risk of coronary disease. Lancet 1996;348:567–72.PubMedCrossRefGoogle Scholar
  15. 15.
    Cermak J, Key NS, Bach RR, Balla J, Jacob HS, Vercellotti GM. C-Reactive Protein induces human peripheral blood monocytes to synthesize tissue factor. Blood 1993;82:513–520.PubMedGoogle Scholar
  16. 16.
    Pepys MB, Rowe IF, Baltz ML. C-Reactive Protein: binding to lipids and lipoproteins. Int Rev Exp Pathol 1985;27:83-111. PubMedGoogle Scholar
  17. 17.
    Volanakis JE, Narkas AJ. Interaction of C-Reactive protein with artificial phosphatidyl-choline bilayers and complement. J Immunol 1981;126:1820–25.PubMedGoogle Scholar
  18. 18.
    Volanakis JE. Complement activation by C-Reactive Protein complexes. Ann N Y Acad Sci 1982;389:235–50.PubMedCrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1997

Authors and Affiliations

  • Frits Haverkate

There are no affiliations available

Personalised recommendations