Background and Objectives: Oxidative stress is recognized as an important contributor to heart failure (HF) pathophysiology, but the relationships of individual oxidative and antioxidant biomarkers with symptomatic severity and systolic dysfunction remain insufficiently defined. This study examined circulating oxidative and nitrosative stress markers across New York Heart Association (NYHA) classes and left ventricular ejection fraction (LVEF) categories in HF and their associations with HF severity. Materials and Methods: In this case–control study, 85 patients with HF and 33 healthy controls were included. Malondialdehyde (MDA), nitrates and nitrites (NOx), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), sulfhydryl (SH) groups, and NT-proBNP were measured. Group differences were analyzed using the Kruskal–Wallis test with post hoc comparisons. Adjusted ordinal logistic regression models examined associations with NYHA class and LVEF category, and receiver operating characteristic (ROC) analysis evaluated discriminatory performance. Results: Compared with controls, all biomarkers differed significantly across NYHA classes and LVEF categories (all p < 0.001). In separate adjusted models, higher NOx, MDA, and NT-proBNP were associated with worse NYHA class and more impaired LVEF, whereas higher antioxidant marker levels were associated with lower odds of severe HF. In combined models, NOx remained independently associated with worse NYHA class (OR 1.07, 95% CI 1.04–1.11; p < 0.001), while MDA remained independently associated with more impaired LVEF (OR 1.02, 95% CI 1.00–1.03; p = 0.022). NT-proBNP showed the best discrimination for NYHA III/IV versus I/II (AUC 0.966), while among oxidative biomarkers NOx performed best for symptomatic severity (AUC 0.782) and MDA for LVEF ≤ 40% (AUC 0.751). Conclusions: HF is characterized by increased oxidative and nitrosative stress together with reduced antioxidant defense. NOx appears more closely related to symptomatic severity, whereas MDA appears more closely related to systolic dysfunction. However, NT-proBNP remained the strongest overall discriminator. NOx and MDA may provide complementary mechanistic information on redox imbalance across HF severity categories.

Background/Objectives: Inflammatory indices are increasingly studied in heart failure (HF), but direct comparisons remain limited. We compared eight indices across New York Heart Association (NYHA) classes and assessed the leading indices against N-terminal pro-B-type natriuretic peptide (NT-proBNP). Methods: This analysis included 85 patients with established HF. The systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), neutrophil-to-lymphocyte ratio (NLR), neutrophil-to-HDL ratio (NHR), lymphocyte-to-HDL ratio (LHR), monocyte-to-HDL ratio (MHR), platelet-to-HDL ratio (PHR), and uric acid-to-HDL ratio (UHR) were evaluated using group comparisons, Spearman correlations, ordinal logistic regression, and multivariable models for NYHA III/IV versus I/II. Primary multivariable models used a parsimonious adjustment set comprising age, smoking status, and HF duration, while broader covariate adjustment was examined in sensitivity analyses. Internal validation used 1000 bootstrap resamples. Results: NHR and PHR differed across NYHA classes after FDR correction. In parsimoniously adjusted ordinal models, SII, SIRI, NLR, NHR, MHR, and PHR were associated with increasing NYHA class after FDR correction. In the NYHA III/IV versus I/II analysis, only NHR (OR per doubling 2.01, 95% CI 1.19–3.39) and MHR (OR 1.96, 95% CI 1.17–3.25) remained significant after FDR correction (q = 0.022 for both). AUCs were 0.688 for the reference model, 0.775 with NHR, 0.777 with MHR, and 0.978 with NT-proBNP. Bootstrap optimism-corrected AUCs were 0.739 for NHR, 0.739 for MHR, and 0.969 for NT-proBNP. Neither ratio improved model fit beyond NT-proBNP. Conclusions: NHR and MHR showed the most consistent adjusted associations with NYHA-defined symptomatic severity and remained robust across sensitivity analyses. They should be viewed as compact routine inflammatory-metabolic indices rather than independent biomarkers or replacements for NT-proBNP. External and prospective longitudinal validation is warranted.