Galectin-3 Outperforms N-Terminal Pro-B-type Natriuretic Peptide in Identifying Cardiac Dysfunction among Chronic Liver Disease Patients: Evidence from a Prospective Cohort

Abstract Introduction: Cirrhotic cardiomyopathy (CCM) is a prevalent yet underrecognized complication of chronic liver disease (CLD), characterized by diastolic dysfunction and subclinical myocardial impairment. While N-terminal pro-B-type natriuretic peptide (NT-proBNP) is commonly elevated in cirrhosis due to myocardial wall stress, its diagnostic utility is confounded by hyperdynamic circulation and impaired renal clearance. Galectin-3, a biomarker of myocardial fibrosis and inflammation, has emerged as a potentially superior marker. This study aimed to compare the diagnostic performance of Galectin-3 and NT-proBNP for identifying cardiac dysfunction in patients with CLD Materials and Methods: A present cross-sectional study included 280 adults with CLD who underwent comprehensive echocardiography and biomarker testing. Patients were categorized as cases or controls based on systolic or diastolic dysfunction. Diagnostic accuracy was assessed using receiver operating characteristic curves, sensitivity, specificity, predictive values, and multivariable logistic regression. Associations between biomarkers and echocardiographic parameters were evaluated using Spearman correlations Results: Galectin-3 levels were significantly higher in cases than controls (27.5 ± 9.9 vs. 14.1 ± 3.9 ng/mL, P 300 pg/mL; accuracy 79.8%). In multivariable models, Galectin-3, right ventricular systolic pressure (RVSP), and E/A ratio remained independent predictors (AUC 0.99). Galectin-3 showed strong correlations with ejection fraction (ρ = −0.88) and left atrial diameter (ρ = 0.43), whereas NT-proBNP correlated only weakly with RVSP Conclusions: Galectin-3 demonstrates superior diagnostic accuracy and stronger associations with echocardiographic dysfunction compared with NT-proBNP. Incorporating Galectin-3 into diagnostic pathways may enhance early detection and risk stratification of CCM in patients with CLD.