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European Heart Journal 1993 14(7):915-919;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The European Society of Cardiology

Serum C-reactive protein and infarct size in myocardial infarct patients with a closed versus an open infarct-related coronary artery after thrombolytic therapy

K. PIETILÄ, A. HARMOINEN, W. HERMENS, M. L. SIMOONS, F. VAN DE WERF and M. VERSTRAETE

Clinic of Medicine and Department of Clinical Sciences, University of Tampere, Tampere Finland and Cardiovascular Research Institute Maastricht (CARIM) Maastricht, The Netherlands

Received 28 September 1992; revised 21 January 1992; .

Correspondence: Karl Pietilä, MD, Clinic of Medicine, Tampere University Hospital and Department of Clinical Sciences, University of Tampere, PO Box 607, SF 33101 Tampere, Finland

Abstract

Serum C-reactive protein rises in acute myocardial infarction, correlating positively with infarct size if thrombolytic treatment is not given. This correlation disappears if thrombolytic treatment is given, although the serum C-reactive protein concentration is still associated with the clinical outcome of the patient.

We studied the effect of early coronary recanalization induced by thrombolytic treatment alone or combined with coronary angioplasty on the infarct related rise in serum C-reactive protein concentration.

The C-reactive protein response caused by the myocardial infarct was lower in patients with an open infarct-related coronary artery than in patients with a closed infarct-related coronary artery, or in control patients who did not receive thrombolytic therapy. In control patients we found the expected strong positive correlation between infarct size and serum C-reactive protein (r = 0.58; P <0.001, n = 48), which was similar to that in patients with a closed infarct-related coronary artery (r = 0.62; P <0.001, n = 17). In patients with an open infarct-related coronary artery the correlation between infarct size and serum C-reactive protein was much weaker (r = 30; P < 0.00l, n=91). Consequently infarct size explained approximately 35% of the variation in serum C-reactive protein values in the control patients and 36% in the patients with a closed infarct-related coronary artery, but only 9% of the variation in the patients with an open infarct-related artery. Ejection fraction correlated negatively with serum C-reactive protein in both control and recanalized patients. The association was again much stronger in the control patients. Ejection fraction explained 27% (28% if only first infarctions were considered) of the variation in serum C-reactive protein in the control patients and 8% (6%) in the recanalized patients.

The present results show that coronary recanalization variably reduces the infarct-associated rise in serum C-reactive protein. This explains the weaker association between serum C-reactive protein and infarct size in the patients receiving thrombolytic treatment when compared to those treated without thrombolytic drugs and may have clinical implications.

Key Words: Myocardial infarction • thrombolytic treatment • reperfusion • C-reactive protein


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