Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy

Background: Left ventricular (LV) fibrosis, aßeßed by late gadolinium enhancement (LGE) at cardiac magnetic resonance imaging (MRI), is a marker of LV remodeling, and holds prognostic value in nonischemic dilated cardiomyopathy (NICM). Galectin-3 has been shown to participate in tißue fibrogenesis and to be a prognosticator in heart failure. Our aimwas to investigate the relationships between galectin-3 circulating level andmyocardial fibrosis at MRI in patients with NICM. Methods and results: One-hundred-fifty patients were enrolled (males 73%; age 58, SD 14 years), with a NICM diagnosis according to theWorld Health Organization criteria. All patients underwent a comprehensive clinical aßeßment and biohumoral characterization, including galectin-3 aßay, and cardiac MRI, with LGE aßeßment of fibrosis. Median galectin-3 value was 14.4 ng/mL (IQR 11.7-19.0 ng/mL), and LGE was detected in 106 (71%) patients. Patients with LGE had higher galectin-3 than those without (15.4, 11.8-21.0, vs 13.1, 11.7- 16.4 ng/mL, p = 0.006). Among univariate predictors of LGE presence (galectin-3, male sex, disease duration, arterial hypertension, left and right ventricular ejection fraction, left ventricular stroke volume), galectin-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At receiver operating characteristic analysis the optimal galectin-3 cut-off for LGE prediction was 14.6 ng/mL (AUC 0.651, sensitivity 57%, specificity 73%). Conclusions: Galectin-3 is aßociated with LGE-aßeßed myocardial replacement fibrosis in patients with NICM. These results support the hypothesis that galectin-3 is involved in cardiac fibrosis and remodeling in NICM, and that its aßay may help to select subgroups at higher risk.