Iron Therapy in Patients With Heart Failure and Iron Deficiency

Review of Iron Preparations for Practitioners

Marcin Drozd; Ewa A. Jankowska; Waldemar Banasiak; Piotr Ponikowski

Disclosures

Am J Cardiovasc Drugs. 2017;17(3):183-201. 

In This Article

Mechanisms of Iron Deficiency (ID) in Heart Failure (HF)

The pathophysiology of ID in HF is presumably multifactorial, and potential mechanisms include reduced intake and increased loss of iron, and re-distribution of this microelement to tissue compartments where it is not available for metabolic processes (for example, entrapment in the reticuloendothelial system), to name a few. It needs to be acknowledged that iron is not actively excreted from the body; however, a certain amount of iron is lost through shedding epidermal skin cells and intestinal lining cells.

It is considered that ID in HF partially results from inadequate iron intake in the diet,[19,20] low bioavailability of iron in the diet (more frequent in developing countries), and handicapped gastrointestinal absorption. The latter results from intestinal interstitial oedema, the use of medications increasing gastric pH (such as proton pump inhibitors or H2 receptor antagonists), and the ingestion of food reducing iron absorption (calcium, tannins, oxalates, phytate, phosphates, antiacids).[21,22] Increased iron loss is associated with several gastrointestinal disorders (peptic ulceration, esophagitis, gastritis, duodenitis), menstrual blood loss, and also frequent blood sampling. Importantly, there is no correlation between the prevalence of ID and the use of anticoagulants or antiplatelet drugs in patients with HF.[23,24]

Although the inflammatory state characterizing several chronic diseases (including HF) is considered responsible for impaired iron absorption, recycling and release from body stores,[16,26–29] in two studies, one recruiting patients with stable HF, the second performed among acute HF patients, ID was found in both anaemic and non-anaemic subjects, without the major involvement of measured inflammatory biomarkers.[16,26–29] Moreover, we would like to emphasise that although postulated, circulating hepcidin has been shown to be low (but not high) in patients with HF. First of all, in patients with chronic stable heart failure with reduced ejection fraction (HFrEF), we have demonstrated that patients with ID have low hepcidin.[25] Even more worthy of note is that 46% of patients with acute HF have very low hepcidin, not high, and low hepcidin predicted the worse outcome in these patients.[25,26]

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