Iron deficiency in heart failure: Efficacy and safety of intravenous iron therapy.

Abstract

To discuss the pathophysiology of iron metabolism in chronic heart failure (CHF) and the current knowledge of the efficacy of intravenous (IV) iron therapy in patients with CHF and identify points of controversy as well as highlight areas for future research. Iron deficiency is a recognized complication of many chronic conditions. Numerous studies have reported that iron deficiency is highly prevalent in patients with CHF and is associated with exercise intolerance, reduced quality of life, and increased risk of hospitalization and mortality. Several small studies have demonstrated IV iron to be associated with improvements in symptoms, exercise capacity, quality of life, renal function, New York Heart Association (NYHA) functional class and left ventricular ejection fraction (LVEF), and reduction in NT-pro-brain natriuretic peptide (NT-proBNP) in patients with CHF and iron deficiency. Two larger-scale trials confirming these results (FAIR-HF and CONFIRM-HF) have led to guideline recommendations that IV iron therapy should be considered in patients with CHF with reduced ejection fraction and iron deficiency (serum ferritin <100μg/L, or ferritin between 100 and 299μg/L with transferrin saturation <20%) to provide symptomatic relief and improve exercise capacity and quality of life. Intravenous iron therapy improves symptoms, exercise capacity, and quality of life, at least in the short-to-intermediate time. However, there are still currently no standardized criteria used to define iron deficiency and the underlying mechanism of iron deficiency in CHF remains incompletely understood. Further work is required to improve the ability to identify iron deficiency in patients with CHF and evaluate the effect of iron repletion on hard endpoints including hospitalization and mortality.