Objective: Given the emerging role of growth differentiation factor 15 (GDF-15) as a biomarker reflecting myocardial stress and fibrosis and the relevance of iron metabolism in heart failure (HF) prognosis, this study aimed to investigate the association between GDF-15 and biochemical and hematological parameters related to iron metabolism in HF overall, as well as in HF with preserved ejection fraction (HFpEF) and HF with non-preserved ejection fraction (HFnpEF), and to evaluate differences in GDF-15 levels between ejection fraction subtypes. Design and method: The study included a sample of 161 individuals with HF, with a median age of 83 years. GDF-15 was determined using an electrochemiluminescence immunoassay. The hematological and biochemical parameters studied hemoglobin (Hb), mean corpuscular volume (MCV), Red Cell Distribution Width (RDW), serum iron, ferritin, transferrin saturation, and total iron-binding capacity (TIBC) were collected from patients’ hospital records. Statistical analysis was performed using SPSS 28.0, with a significance level of p<0.05. Results: In the general HF population, GDF-15 levels showed a significant negative correlation with Hb and with TIBC. A significant positive correlation was also observed between GDF-15 and RDW, as well as with ferritin levels. In the analysis stratified by ejection fraction, no significant correlations were found between GDF-15 and iron metabolism parameters in patients with HFpEF. On the other hand, in patients with HFnpEF, and similarly to the general HF population, GDF-15 showed a significant negative correlation with Hb and with TIBC, and a significant positive correlation with RDW and with ferritin. No significant differences were observed in GDF-15 levels between ejection fraction subtypes. Conclusions: This study demonstrated significant associations between GDF-15 and parameters of iron metabolism in patients with heart failure, particularly in those with HFnpEF. The observed differences between phenotypes highlight the pathophysiological heterogeneity of heart failure and suggest a closer interplay between myocardial fibrosis and iron metabolism dysfunction in HFnpEF. These findings may contribute to improved understanding and support more personalized approaches to risk stratification and treatment.
Bicho et al. (Fri,) studied this question.