Iron Deficiency and Anaemia in Heart Failure: Understanding the FAIR-HF Trial

José González-Costello; Josep Comín-Colet


Eur J Heart Fail. 2010;12(11):1159-1162. 

In This Article

Abstract and Introduction


Treatment of anaemia in patients with chronic heart failure (CHF) and reduced left ventricular ejection fraction has traditionally focused on erythropoietin-stimulating agents. However, recent studies have shown that treatment with intravenous (IV) iron can improve the symptoms and quality of life in patients with CHF and iron deficiency (ID), with or without anaemia. The management of ID is becoming an important therapeutic target in patients with CHF, and in this article, we will review iron metabolism in the context of anaemia and heart failure. We will also focus on the importance of diagnosing and treating ID, preferably with IV iron preparations, in patients with CHF.


Chronic heart failure (CHF) is increasingly viewed as a multi-system disease which, beyond the impairment of cardiac function, also affects the functional capacity of other organs such as the kidneys and skeletal muscle. Anaemia and chronic kidney disease (CKD) are the most prevalent comorbidities in CHF and they both confer an independent worse prognosis.[1] The diagnosis and treatment of these comorbidities by cardiologists will most likely increase over the years as mechanisms unrelated to haemodynamic dysfunction, such as inadequate tissue oxygen supply and impaired oxygen use by the skeletal muscle, may underlie impaired exercise tolerance.[2] Anaemia in CHF can be the consequence of reduced glomerular filtration rate, reduced plasma flow, impaired erythropoietin (EPO) production, and haemodilution.[3] In up to 53% of out-patients with anaemia and CHF due to systolic dysfunction, some sort of haematinic deficiency can be found, although up to 27% of patients with CHF and without anaemia can also have a haematinic deficiency.[1] In another study of 148 patients with anaemia and CHF, most patients (57%) presented anaemia of chronic disease, which was indicated by an inadequate production of EPO relative to the degree of anaemia and/or a defective iron supply for erythropoiesis. Both these findings seem to be associated with elevated levels of inflammatory cytokines.[4]