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EFFECT-HF study

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 deficiency due to decreased iron absorption, reduced bioavailability of iron for erythropoiesis in the bone marrow and increased iron stores in in the liver and other 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 in heart failure. They evaluated 172 patients with mild - moderate symptoms despite optimal medical treatment for heart failure with reduced ejection fraction. 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. Patient's global assessment and NYHA 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. Web: https://johnsonfrancis.org/profession...