Restoring iron deficiency with IV ferric carboxymaltose improves exercise capacity in HF patients
Effect of Ferric Carboxymaltose on Exercise Capacity in Patients with Iron Deficiency and
Chronic Heart Failure (EFFECT-HF): A Randomized, controlled studyPresented on AHA Scientific Sessions 2016 by: D.J. van Veldhuisen, University Medical Center Groningen, Groningen, Netherlands
Restoring iron deficiency with IV ferric carboxymaltose (FCM) improves exercise capacity in patients with heart failure (HF).
Iron deficiency is a frequent comorbidity in patients with stable HF and in patients that are admitted to the hospital due to worsening HF. This is associated with impaired functional capacity, a poor quality of life and increased mortality. Iron deficiency can result from reduced oxygen delivery due to a hemoglobulin (Hb) decrease or from impaired O2 utilization through the reduction of aerobic enzymes. Both a reduction in O2 delivery and utilization results in reduced peak oxygen consumption (pVO2). pVO2 is an important prognostic factor in HF patients and even a modest increase has been associated with a more favourable outcome. Prior studies including FAIR-HF and CONFIRM-HF already confirmed benefit of FCM in iron deficient HF patients.
To validate this, the multicentre, open label, randomized, assessor-blinded and standard of care-controlled EFFECT-HF trial assessed whether restoring iron deficiency using IV FCM would improve cardiopulmonary exercise tolerance in symptomatic HF patients. Therefore, the maximum pVO2 was measured in 174 patients with HF NYHA class II/III and a left-ventricular ejection fraction (LVEF) ≤45%, a pVO2 of 10-20 mL/kg/min, BNP > 100 pg/mL and/or NT-proBNP >400 pg/mL, a Hb <15 g/dL and iron deficiency (serum ferritin <100 ug/L or 100-300 ug/L if TSAT <20%). Patients were randomized to FCM, which was administered at day 0, week 6 and week 12 or standard of care (SoC). At week 24, the pVO2 was measured.
The results showed that the iron-related parameters ferritin, TSAT and Hb were all enhanced from baseline in FCM-treated patients, whereas sTfR was reduced in these patients. These differences were significantly different from differences observed in SoC patients. Moreover, the primary endpoint pVO2 was improved in FCM-treated patient compared to SoC patients; the adjusted changes from baseline were approximately -0,2 mL/kg/min for treated patients and -1,2 mL/kg/min for SoC patients (p=0.02). Furthermore, the carbon dioxide production relationships (VE/VCO2 slope) were comparable between both groups. On the other hand, the numbers of hospitalizations slightly increased from 15.3 to 30.7%, whereas the mortality was 0% for FCM-treated patients and 4.7% for SoC patients. Also the frequency of adverse events (AEs) was higher in FCM-treated patients. This concerned any AE (60% vs. 48.2% for SoC), severe AE (14.8% vs. 9.4% for SoC), serious AE (31.8 vs. 18.8% for SoC), treatment-related event (9.1% vs. none for SoC) and severe treatment-related AE (3.4% vs. non for SoC). In contrast, AEs leading to study drug withdrawal (2.3% vs. 5.9% for SoC) or death (none vs. 5.9%) were lower in FCM-treated patients.
Overall, there was as significant improvement in peak VO2 for patients treated with FCM compared to SoC patients. This shows that FCM improves exercise capacity and symptoms and confirm and extend the findings of previous FCM study results.
- Our reporting is based on the information provided during the AHA congress –