Serum Peroxides and Galectin-3 in Chronic Heart Failure: Cross-Sectional Associations with NT-proBNP and Cardiac Structure

Background/Objectives: Oxidative stress and galectin-3-related fibro-inflammatory processes contribute to heart failure pathophysiology, but their concurrent relationships with natriuretic peptides and structural/cardiorenal parameters remain incompletely characterized. We evaluated baseline associations of serum peroxide burden and galectin-3 with N-terminal pro-B-type natriuretic peptide (NT-proBNP) and related phenotypic parameters in chronic heart failure. Methods: This cross-sectional analysis included 57 patients from a prospective single-center cohort. Serum peroxides were quantified using the ferrous oxidation–xylenol orange assay and expressed as nmol H2O2 equivalents/mL. Associations were assessed using Spearman correlation and linear regression with ln-transformed NT-proBNP. Benjamini–Hochberg correction was applied to eight secondary/exploratory correlations. Results: Serum peroxide burden correlated with NT-proBNP (ρ = 0.387, p = 0.0095; n = 44) and remained significantly associated after adjustment for age, sex, and left ventricular ejection fraction (B = 0.1756, p = 0.0420; n = 43). After additional estimated glomerular filtration rate (eGFR) adjustment, the effect estimate remained similar, although statistical significance was not reached (B = 0.1646, p = 0.0525; n = 39). Galectin-3 correlated with NT-proBNP, left ventricular end-diastolic volume index (LVEDVi), and serum uric acid; all associations remained significant after false-discovery-rate correction. Serum peroxide burden and galectin-3 were not significantly correlated. In an exploratory joint model (n = 29), both biomarkers remained significantly associated with ln(NT-proBNP) (adjusted R2 = 0.4294). Conclusions: Serum peroxide burden and galectin-3 showed different cross-sectional association patterns with NT-proBNP and selected structural/cardiorenal parameters. Given the limited sample size, missing data, and exploratory nature of the joint model, these findings should be considered hypothesis-generating and do not establish biological independence or incremental clinical value.