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Background and Objectives: Previous studies showed that, paradoxically, obese patients with heart failure (HF) have better clinical outcomes compared to overweight, normal, or underweight patients. Scientific societies emphasize the importance of integrating quality of life (QoL) assessment in cardiovascular care. However, the association between QoL and weight remains understudied. Given the significant correlation between HF survival and QoL, it is essential to assess how obesity impacts patient-reported outcomes in this clinical setting. Methods: This cross-sectional multicenter study in 1028 HF patients with reduced ejection fraction (HFrEF) aims to evaluate the association between obesity and QoL, and whether the obesity paradox holds for HF patients regarding QoL. Specific and generic QoL questionnaires were administered alongside clinical parameters like body mass index (BMI) and body adiposity estimator (BAE). Results: Obese compared to non-obese reported worse QoL. In the adjusted linear regression models, neither BMI nor obesity were associated with QoL. Generalized additive models confirmed a strong non-parametric association between BMI, subdomain scores from Kansas City Cardiomyopathy Questionnaire (KCCQ) (OSS p = 0.004, CSS p = 0.006, TSS p = 0.02), and summary measurements of EQ-5D (EQ-5D index p = 0.003, visual analogue scale (VAS) p = 0.01). In contrast, BAE showed a statistically significant linear relation among QoL (OSS p ≤ 0.001, CSS p ≤ 0.001, TSS p ≤ 0.001) and EQ-5D summary measurements (EQ-5D index p ≤ 0.001, VAS p ≤ 0.001). Conclusions : Overall, obese patients have worse QoL; therefore, obesity cannot be considered a protective factor in terms of QoL in established HF.

Background . Iron deficiency (ID) is a significant, high-prevalence comorbidity in chronic heart failure (HF) that represents an independent predictor of a worse prognosis. However, a clear-cut diagnosis of ID in HF patients is not assured. The soluble transferrin receptor (sTfR) is a marker that reflects tissue-level iron demand and may be an early marker of ID. However, the impact of sTfR levels on clinical outcomes in non-anemic HF patients with a normal systemic iron status has never been evaluated. Methods . This is a post hoc analysis of an observational, prospective cohort study of 1236 patients with chronic HF of which only those with normal hemoglobin levels and a normal systemic iron status were studied. The final cohort consisted of 215 patients. Tissue ID was defined as levels of sTfR > 75th percentile (1.65 mg/L). Our aim was to describe the association between sTfR and clinical outcomes (all-cause death and HF hospitalization) and to explore its association with a wide array of serum biomarkers. Results . The sTfR level (HR 1.48, 95% CI 1.13-1.96, p = 0.005) and tissue ID (HR 2.14, 95% CI 1.22-3.75, p = 0.008) was associated with all-cause death. However, we found no association between sTfR levels and the risk of HF hospitalization. Furthermore, high sTfR levels were associated with a worse biomarker profile indicating myocardial damage (troponin and NT-proBNP), systemic inflammation (CRP and albumin), and impaired erythropoiesis (erythropoietin). Conclusions. In this cohort, the presence of tissue ID defined by sTfR levels is an independent factor for all-cause death in patients with normal systemic iron parameters.