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

Serum C-reactive protein rises in acute myocardial infarction,correlating positively with infarct size if thrombolytic treatmentis not given. This correlation disappears if thrombolytic treatmentis given, although the serum C-reactive protein concentrationis still associated with the clinical outcome of the patient. We studied the effect of early coronary recanalization inducedby thrombolytic treatment alone or combined with coronary angioplastyon the infarct related rise in serum C-reactive protein concentration. The C-reactive protein response caused by the myocardial infarctwas lower in patients with an open infarct-related coronaryartery than in patients with a closed infarct-related coronaryartery, or in control patients who did not receive thrombolytictherapy. In control patients we found the expected strong positivecorrelation between infarct size and serum C-reactive protein(r = 0.58; P <0.001, n = 48), which was similar to that inpatients with a closed infarct-related coronary artery (r =0.62; P <0.001, n = 17). In patients with an open infarct-relatedcoronary artery the correlation between infarct size and serumC-reactive protein was much weaker (r = 30; P < 0.00l, n=91).Consequently infarct size explained approximately 35% of thevariation in serum C-reactive protein values in the controlpatients and 36% in the patients with a closed infarct-relatedcoronary artery, but only 9% of the variation in the patientswith an open infarct-related artery. Ejection fraction correlatednegatively with serum C-reactive protein in both control andrecanalized patients. The association was again much strongerin the control patients. Ejection fraction explained 27% (28%if only first infarctions were considered) of the variationin serum C-reactive protein in the control patients and 8% (6%)in the recanalized patients. The present results show that coronary recanalization variablyreduces the infarct-associated rise in serum C-reactive protein.This explains the weaker association between serum C-reactiveprotein and infarct size in the patients receiving thrombolytictreatment when compared to those treated without thrombolyticdrugs and may have clinical implications.