Association between Serum Galectin-3 Levels and Left Ventricular Remodeling in Heart Failure with Reduced Ejection Fraction

Background: Heart failure with reduced ejection fraction (HFrEF) is characterized by progressive left ventricular (LV) remodeling driven by maladaptive fibrotic and inflammatory processes. Galectin-3 (Gal-3), a β-galactoside-binding lectin implicated in myocardial fibrosis and inflammation, has emerged as a promising biomarker for risk stratification in heart failure. However, the precise relationship between circulating Gal-3 concentrations and echocardiographic parameters of LV remodeling across varying HFrEF severities remains insufficiently characterized. Methods: This cross-sectional analytical study enrolled 286 patients with established HFrEF (left ventricular ejection fraction [LVEF] ≤40%) at a tertiary cardiac center. Serum Gal-3 levels were quantified using enzymelinked immunosorbent assay (ELISA). Comprehensive transthoracic echocardiography was performed to assess LV end-diastolic volume index (LVEDVi), LV end-systolic volume index (LVESVi), LV mass index (LVMi), LVEF, left atrial volume index (LAVi), and global longitudinal strain (GLS). Correlation and multivariable regression analyses were performed to evaluate associations between Gal-3 and remodeling parameters. Results: The median serum Gal-3 level was 21.4 ng/mL (IQR: 15.8–29.6). Patients in the highest Gal-3 tertile (>26.2 ng/mL) demonstrated significantly greater LVEDVi (118.4 ± 32.6 vs. 86.2 ± 24.8 mL/m²; p < 0.001), LVMi (148.6 ± 38.4 vs. 112.8 ± 28.6 g/m²; p < 0.001), and worse GLS (−8.2 ± 2.4% vs. −12.6 ± 3.1%; p < 0.001) compared to the lowest tertile. In multivariable analysis, Gal-3 remained independently associated with LVEDVi (β = 0.34; p < 0.001), LVMi (β = 0.31; p < 0.001), and GLS (β = 0.28; p = 0.001) after adjustment for age, NT-proBNP, estimated glomerular filtration rate, and NYHA functional class. Conclusion: Elevated serum Gal-3 levels are independently associated with adverse LV remodeling parameters in HFrEF patients, suggesting that Gal-3 may serve as a clinically informative biomarker reflecting the degree of myocardial structural deterioration beyond conventional markers.