Although chronic heart failure can be successfully managed, the clinical outcome for many patients is still poor. This indicates the importance of identifying and treating co-morbid factors that independently accelerate disease progression. Iron deficiency is linked to both disease severity and mortality in patients with chronic heart disease, and its correction has been shown to elicit a significant improvement in cognitive, symptomatic and exercise performance1,2. Despite common expectations to the contrary, iron deficiency has been shown to be a greater influence of overall prognosis than anaemia in this patient population2–4.
Figure 2. Cumulative survival in patients with and without iron deficiency (ID)4
Copyright permission obtained from Jankowska et al, 2010. Available here. By permission of Oxford University Press on behalf of the European Society of Cardiology.
© Not to be included under a Creative Commons license, or any other open-access license allowing onward reuse.
Iron deficiency is a particular problem in cardiac patients due to the central role iron plays in oxidative metabolism. Iron atoms bind oxygen directly and are therefore vital at all stages of oxidative metabolism5,6. Haemoglobin (oxygen transport), myoglobin (oxygen storage) and electron transport enzymes (oxidative metabolism) all require iron for normal functioning and both cardiac and skeletal muscles rely heavily on cellular oxidative metabolism for energy production.
Impairment of oxidative metabolism results in reduced cellular energy production, which has significant consequences for cells with a high energy demand, such as cardiomyocytes. Therefore, patients with chronic heart failure and iron deficiency often demonstrate reduced aerobic activity performances and poor physical conditioning, as observed using measures, such as the 6-minute walking test. This, in turn, can have a detrimental effect on overall clinical outcome by limiting the patient’s ability to exercise – a common recommendation in the management of heart disease7.
Figure 3. The role of iron deficiency in the pathogenesis of exercise intolerance7,8