Iron Deficiency in Heart Failure

Stockholm, Sweden, 29 August: Iron plays a key role in human homeostasis.  It is essential for growth and survival, and is a vital ingredient in numerous processes including erythropoiesis, oxygen transport and storage, oxidative metabolism in the skeletal and heart muscle, synthesis and degradation of lipids, carbohydrates, DNA and RNA. Important though it is, iron metabolism must be precisely controlled because iron is insoluble and excess levels can be toxic.

Iron deficiency is a relatively common nutritional disorder that affects more than one third of the general population, and is often associated with chronic diseases such as inflammatory bowel disease, Parkinson’s disease, rheumatoid diseases and renal failure. Until recently, there has been little interest in the linkage between iron deficiency and the natural course of chronic heart failure (CHF) syndrome. Traditionally iron deficiency has been linked with a presence of anaemia in CHF, and its reported prevalence varies from 20 percent to 70 percent. Recent research carried out at the Military Hospital, Medical University of Wroclaw has now demonstrated that iron deficiency must be viewed in a much broader clinical context, as it also affects at least one-third of non-anaemic CHF patients.

The research was led by Doctor Piotr Ponikowski, who said, “Iron deficiency appears to be independent of the severity of CHF symptoms, and occurs irrespective of anaemia. It also seems to be associated with exercise intolerance and leads to a reduced quality of life. Our research shows that it probably constitutes an ominous sign of a poor outcome, independently of the other well-established prognosticators. In light of its high prevalence and clinical consequences, iron deficiency may well be perceived as an attractive therapeutic target in CHF.”

Several earlier reports have already shown that, in iron deficient CHF patients, iron repletion can safely improve functional capacity, exercise tolerance and quality of life. Cardiologists should become more aware of the importance of iron deficiency in CHF patients, and be able to evaluate iron status using a combination of simple, clinically relevant parameters of iron metabolism. More studies are needed to evaluate whether correction of iron deficiency in CHF would translate into clinical benefits. 

ENDS