Galectin-3 predicts left ventricular remodelling after anterior-wall myocardial infarction treated by primary percutaneous coronary intervention.

Abstract

Despite modern reperfusion therapies, left ventricular remodelling (LVR) occurs frequently after an ST-elevated myocardial infarction (STEMI) and represents a strong predictor of mortality and heart failure. Galectin-3 (Gal-3), a novel biomarker involved in inflammation, tissue repair and fibrogenesis, might be a valuable predictor of LVR. We enrolled consecutively admitted patients with a first anterior STEMI and left anterior descending artery occlusion treated by primary percutaneous coronary intervention (pPCI). Gal-3, N-terminal pro-B-type natriuretic peptide (NT-proBNP), echocardiography and cardiovascular events were evaluated 48 hours after admission, at 1 and 6 months. LVR was defined as a ≥15% increase in LV end-systolic volume. We recruited 103 patients (28% women, aged 64.6±12 years, LV ejection fraction 47±11%). Median baseline Gal-3 and NT-proBNP levels were 13.2 ng/mL (10.8-17.1 ng/mL) and 2132 pg/mL (1019-4860 pg/mL) respectively. During 6 months of follow-up, 4 patients dropped out, 7 died and 26 (28.3%) of the 92 survivors developed LVR (LVR+). LVR+ patients had higher Gal-3 levels at baseline, 1 and 6 months than LVR- (p<0.0001). By univariable logistic regression, age, female gender, higher baseline Gal-3 and NT-proBNP, smaller LV end-diastolic volume (LVEDV) were associated to an increased risk of LVR. By multivariable analysis, only LVEDV (OR 0.96, 95% CI 0.93 to 0.99/1 mL change) and Gal-3 levels (OR 1.22, 95% CI 1.06 to 1.42/1 ng/mL change) independently predicted LVR (C-statistics 0.84, 95% CI 0.75 to 0.93). Gal-3 serum levels measured during hospitalisation could be clinically useful in predicting LVR among patients admitted with anterior STEMI treated by pPCI.