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 4months. Left ventricular ejection fraction (LVEF) and infarct size were measured after 4months with cardiac MRI (CMR).
Results: In total, 247 patients had blood samples and CMR data available (mean age 57.7±11.6years; 79.8% male). Increased baseline galectin-3 (≥17.8ng/mL) identified patients with lower LVEF (50.3% (±9.1) vs. non-elevated galectin-3 55.0% (±8.0); P<0.001), and larger infarct size (13.8g. (±12.9) vs. 8.6g. (±8.7); P=0.002) after 4months. Elevated sST2 (≥35.0ng/mL) did not predict decreased LVEF or larger infarct size. Furthermore we showed that at baseline, galectin-3 was an independent predictor for LVEF (β=-0.18; P=0.005) and infarct size (β=0.18; P=0.004). We repeated the analyses using median values of galectin-3 (13.4ng/mL) and sST2 (30.3ng/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 4months. We hypothesize that galectin-3 may play a role in the pathophysiology of cardiac remodeling after acute MI.
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