C-reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

doi:10.1084/jem.190.12.1733

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© The Rockefeller University Press, 0022-1007/1999/12/1733/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 12, December 20, 1999 1733-1740

Original Article

C-reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

M. Griselli^a,b, J. Herbert^a, W.L. Hutchinson^a, K.M. Taylor^b, M. Sohail^c, T. Krausz^c, and M.B. Pepys^a
^a Immunological Medicine Unit, Division of Medicine,
^b Cardiothoracic Unit, Department of Surgery
^c Department of Histopathology, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom

Correspondence to: M.B. Pepys, Dept. of Medicine, Royal Free Campus, Royal Free and University College Medical School, Rowland Hill St., London NW3 2PF, UK. Tel:44-20-7472-2801 Fax:44-20-7472-2803 E-mail:m.pepys{at}rfc.ucl.ac.uk.

Myocardial infarction in humans provokes an acute phase response,and C-reactive protein (CRP), the classical acute phase plasmaprotein, is deposited together with complement within the infarct.The peak plasma CRP value is strongly associated with postinfarctmorbidity and mortality. Human CRP binds to damaged cells andactivates complement, but rat CRP does not activate complement.Here we show that injection of human CRP into rats after ligationof the coronary artery reproducibly enhanced infarct size by~40%. In vivo complement depletion, produced by cobra venomfactor, completely abrogated this effect. Complement depletionalso markedly reduced infarct size, even when initiated up to2 h after coronary ligation. These observations demonstratethat human CRP and complement activation are major mediatorsof ischemic myocardial injury and identify them as therapeutictargets in coronary heart disease.

Key Words: heart, ischemia, necrosis, inflammation, acute phase response

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