Abstract 11986: Erythropoietic Response After Intravenous Iron in Heart Failure With Reduced Ejection Fraction With or Without Background Treatment With Sodium-Glucose Co-Transporter 2 Inhibitors

Abstract

Introduction: Intravenous (IV) iron increases hemoglobin/hematocrit and improve outcomes in patients with heart failure with reduced ejection fraction (HFrEF) and iron deficiency. Sodium glucose co-transporter 2 inhibitors (SGLT2i) also increase hemoglobin/hematocrit and improve outcomes in HF by mechanisms linked to nutrient deprivation signaling, and inflammation/oxidative stress reduction. The effect of IV iron among patients using SGLT2i has not yet been studied. Hypothesis: We hypothesize that HFrEF patients with iron deficiency treated with IV iron with a background treatment including a SGLT2i will have an increase erythropoietic response comparing to SGLT2i non users. Methods: Retrospective, single-center analysis of HFrEF patients with iron deficiency treated with IV iron using (n=60) and not using (n=60) SGLT2i, matched for age and sex. The primary outcome was the difference in absolute hemoglobin change (before vs after IV iron administration) between SGLT2i users and nonusers. The main secondary outcomes were the difference in hematocrit and iron biomarkers (total iron, ferritin and trasnferrin saturation) changes between SGLT2i users and nonusers. Results: Mean age was 73±12 years, 48% were men, with more than 65% of patients having chronic kidney disease and anemia. After adjustment for all baseline differences, SGLT2i users experienced a greater increase in hemoglobin and hematocrit compared to SGLT2i nonusers: hemoglobin +0.57 g/dL (95%CI 0.04-1.10, p=0.036) and hematocrit +1.64% (95%CI 0.18-3.11, p=0.029). No significant differences were noted for iron biomarkers or any of the secondary outcomes. Conclusion: Combined treatment with IV iron and background SGLT2i was associated with a greater increase in hemoglobin and hematocrit than IV iron without background SGLT2i. These results suggest that in HFrEF patients treated with IV iron, SGLT2i may increase the erythropoietic response.