Objective. To assess the value of C-reactive protein (CRP) in predicting postinfarct left ventricular remodelling (LVR). Methods. We measured in-hospital plasma CRP concentrations in patients with a first ST-segment elevation myocardial infarction (STEMI). Results. LVR was present at 6 months in 27.8% of 198 patients. CRP concentration rose during the first 24？h, mainly in LVR group. The prevalence of LVR was higher in patients from the highest quartile of CRP concentrations at 24？h as compared to those from any other quartile (odds ratio (OR) 3.48, 95% confidence interval (95% CI) 1.76–6.88). Multivariate analysis identified CRP concentration at 24？h (OR for a 10？mg/L increase 1.29, 95% CI？1.04–1.60), B-type natriuretic peptide at discharge (OR for a 100？pg/mL increase 1.21, 95% CI？1.05–1.39), body mass index (OR for a 1？kg/m2 increase 1.10, 95% CI？1.01–1.21), and left ventricular end-diastolic volume (OR for a 1？mL increase 0.98, 95% CI？0.96-0.99) as independent predictors of LVR. The ROC analysis revealed a limited discriminative value of CRP (area under the curve 0.61; 95% CI？0.54–0.68) in terms of LVR prediction. Conclusions. Measurement of CRP concentration at 24？h after admission possesses a significant but modest value in predicting LVR after a first STEMI. 1. Introduction Left ventricular remodelling (LVR) often complicates acute ST-segment elevation myocardial infarction (STEMI) [1, 2]. The acute loss of myocardium results in an abrupt increase in loading conditions that induces LVR, the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors [3]. Postinfarct LVR leads to a progressive rise in systolic and diastolic left ventricular volumes, distortion of ventricular shape and mural hypertrophy, in the weeks and months after STEMI [3]. It has been identified as an important marker of poor prognosis, linked with excessive cardiovascular mortality and risk of heart failure [1–4]. The major determinants of LVR after STEMI include infarct size, anterior location of infarction, and late or unsuccessful reperfusion therapy both at the epicardial artery level and at the microvascular level, transmurality of the infarct and extent of myocardial stunning [3–7]. Acute myocardial infarction (MI) is associated with a systemic inflammatory response with augmented production of nonspecific plasma acute-phase proteins, including C-reactive protein (CRP) [8]. The increase in plasma CRP concentration in the course of acute MI takes place in the first hours since the onset of symptoms and peaks
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