Background: Fibrosis is a pivotal event in infarct repair and progressive remodeling after myocardial infarction (MI). Biomarkers may be used to monitor fibrosis, and therefore we evaluated the predictive value of galectin-3 and sST2 for cardiac remodeling after MI.
Methods: Plasma galectin-3 and sST2 were measured in patients admitted with primary percutaneous coronary intervention (PCI) for acute MI, at baseline and at 4 months. Left ventricular ejection fraction (LVEF) and infarct size were measured after 4 months with cardiac MRI (CMR).
Results: In total, 247 patients had blood samples and CMR data available (mean age 57.7 +/- 11.6 years; 79.8% male). Increased baseline galectin-3 (>= 17.8 ng/mL) identified patients with lower LVEF (503% (+/- 9.1) vs. non elevated galectin-3 55.0% (+/- 8.0); P <0.001), and larger infarct size (13.8 g. (+/- 12.9) vs. 8.6 g. (+/- 8.7); P = 0.002) after 4 months. Elevated sST2 (>= 35.0 ng/mL) did not predict decreased LVEF or larger infarct size. Furthermore we showed that at baseline, galectin-3 was an independent predictor for LVEF (beta = -0.18; P = 0.005) and infarct size (beta = 0.18; P = 0.004). We repeated the analyses using median values of galectin-3 (13.4 ng/mL) and sST2 (303 ng/mL) as a cut point, and this validated our results.
Conclusion: The fibrosis biomarker galectin-3, but not sST2, taken immediately after MI, predicts LVEF and infarct size after 4 months. We hypothesize that galectin-3 may play a role in the pathophysiology of cardiac remodeling after acute MI. (C) 2015 Elsevier B.V. All rights reserved.