Chronic heart failure (CHF) is a multi-organ syndrome with changes in the periphery affecting muscle and blood vessels, neurohormonal activation and metabolic and hormonal changes. It is now recognised that anaemia is also frequently part of this syndrome.
Epidemiology and pathophysiology
If we define anaemia as a haemoglobin (Hb), less than 12.0 g/dl anaemia affects between 10-25% of CHF patients with more in the sicker patients’ population. The cause of anaemia in chronic heart failure is not known.
In many cases anaemia in chronic failure shows similarities to the anaemia of chronic disorders, in which there is a defect in iron utilisation. The commonly recognised causes of anaemia in a general population such as iron, folate or B12 deficiency can exist in CHF and should be looked for. Blood loss can also be excessive in patients on anti-platelet and/or anticoagulant regimes for their primary cardiovascular disorder. In most CHF cases with anaemia, however, there is no identifiable cause. Aetiological factors are thought to include bone marrow dysfunction secondary to poor perfusion, impaired renal function and the effects of cytokine activation -especially TNF-alpha- which can induce both reduced erythropoietin production and increased resistance to its effects. In severe heart failure immune activation and pro-inflammatory cytokines correlate strongly with the severity of anaemia.
Anaemia has an independent effect on exercise intolerance by further reducing an already impaired oxygen delivery to the exercising muscle groups. Studies in large heart failure populations including cohorts from several of the large outcome trials in CHF have shown an independent detrimental effect of anaemia on the risk of death or admission to hospital for worsening heart failure. These findings suggest that treatment of anaemia might have the potential to improve outcomes.
Where an identifiable cause of anaemia in chronic heart failure is found it should be treated appropriately. We know that both erythropoietin or IV Iron treatment can increase haemoglobin levels in CHF and in early reports this has been associated with improved well-being and exercise tolerance. Whether this is with an acceptable safety profile and indeed whether it reduces the risk of mortality and morbidity is presently unknown. This exciting new treatment option awaits proper randomised outcome trials in the next few years.
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