“Pumping Iron” to Improve Exercise Performance in Heart Failure
New Data and New Guidelines
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Article, see p 1374
Iron homeostasis in patients with heart failure (HF) is abnormal because of the effects of proinflammatory cytokines on the key liver-derived iron regulatory protein hepcidin.1,2 Increased hepcidin synthesis in response to proinflammatory signals induces a state of functional iron deficiency characterized by decreased dietary iron absorption, reduced bioavailability of stored iron for erythropoiesis in the bone marrow, and increased iron stores in the liver and other nonerythrocyte cell types.1 Functional iron deficiency is present in 50% of subjects with HF and is associated with exercise intolerance and greater mortality risk in patients with (hazard ratio (HR), 1.71; 95% confidence interval (CI), 1.24–2.36; P=0.001) or without (HR, 1.44; 95% CI, 1.11–1.87; P=0.006) concomitant anemia.3,4 Two previous multisite randomized double-blind placebo-controlled clinical trials have demonstrated that repletion of iron stores with intravenous ferric carboxymaltose is associated with improvement in measures of submaximal exercise capacity and functional capacity in subjects with HF with reduced ejection fraction (HFrEF) and biochemical markers consistent with functional iron deficiency.5 In this issue of Circulation, van Veldhuisen and colleagues6 report the findings of a well-designed and -executed prospective multisite open-label randomized clinical trial with blinded end point assessment to determine the effects of intravenous iron repletion with ferric carboxymaltose versus usual care (including optional oral iron supplementation) on peak aerobic capacity in symptomatic …