Functional iron deficiency is present in about half of heart failure patients and is associated with poorer effort tolerance and higher mortality. Abnormal iron hemostasis in heart failure is mediated by the effect of proinflammatory cytokines on hepcidin, an important iron regulatory protein. Increase in hepcidin is responsible for the functional iron defiency due to decreased iron absorption, reduced bioavailability of iron for erythropoiesis and increased iron stores in non erythrocyte cell types . Veldhuisen and colleagues in an article published in Circulation  with acronym EFFECT-HF study evaluated the effect of ferric carboxymaltose on peak oxygen consumption (VO2) in heart failure.
They evaluated 172 patients with mild – moderate symptoms despite optimal medical treatment for heart failure with reduced ejection fraction (HFrEF). 1:1 open label randomization was between ferric carboxymaltose and standard of care. Primary end point of the study was the change in peak VO2 from baseline to 24 weeks. Effect on hematinic parameters, biomarkers, quality of life and safety were the secondary endpoints. At 24 weeks, VO2 was maintained in the study group while it decreased in the control group. Paient’s global assessment and NYHA (New York Heart Association) functional class also improved in the active treatment group. As expected, treatment with ferric carboxymaltose caused repletion of iron stores. It was noted that decline in VO2 in the control group was driven by deaths.
- Katz SD. “Pumping Iron” to Improve Exercise Performance in Heart Failure: New Data and New Guidelines. Circulation. 2017 Oct 10;136(15):1384-1386.
- van Veldhuisen DJ et al. Effect of Ferric Carboxymaltose on Exercise Capacity in Patients With Chronic Heart Failure and Iron Deficiency. Circulation. 2017;136:1374-1383.