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The European Journal of Heart Failure 5 (2003) 3–4

Anaemia in heart failure: its diagnosis and management

Chronic heart failure (CHF) is a common syndrome w1x 9. A rightward shift of the oxyhemoglobin dissociation
affecting more than 20 million people world-wide and curve on exercise has been shown in patients with
approximately 7 million people in the European com- CHF w8x. Erythropoietin treatment can further

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munity. The incidence and prevalence of CHF have been increase 2,3 DPG levels with a further increase in
shown to increase sharply with age w2x. Prognosis is oxygen extraction w9,10x.
poor; 12 week mortality was 14% in the recently report- 10. Renal failure, hypercirculation due to therapeutic
ed Euroheart survey w3x. arterio-venous shunts and anaemia, hypertension as
Anaemia as a cofactor in CHF has not been well eval- well as left ventricular hypertrophy interact in vari-
uated and its contribution is ill defined w4,5x. ous ways and contribute further to heart failure and
The following factors have to be considered: vice versa to renal failure.
1. There may be reduced intestinal iron uptake associ-
ated with cardiac cachexia and malabsorption.
Taking into consideration all of the above mentioned
2. Tumour necrosis factor alpha, which is increased in
factors, anaemia favours the progression of heart failure.
patients with CHF, can lead to depression of bone
marrow and interferes with the action and utilisation Anaemia has been recognised to exacerbate pre-exist-
of erythropoietin and iron. ing heart failure w11x. Furthermore recent literature sug-
3. CHF activates the renin–angiotensin–aldosterone- gests a far more important role of anaemia in the natural
system and vasopressin, resulting in sodium and course of CHF. In addition, a vicious cycle between
water retention and dilutional anaemia. anaemia, chronic renal failure and exacerbation of heart
4. CHF can lead to renal dysfunction due to renal vaso- failure can be assumed.
constriction and ischemia resulting in an increase in Thus it seems logical, that Silverberg et al. w12,13x
erythropoietin. Usually renal anaemia develops in suggested treatment with a combination of erythropoietin
chronic renal dysfunction with serum creatinine over and intravenous iron. This combination has been shown
3.5 mgydl or a creatinine clearance below 30 mly to be safe and effective in patients with CHF before
min. starting dialysis as well as in patients on dialysis. Intra-
5. Diabetes as well as arterial hypertension can con- venous iron administration seems to be more effective
tribute to heart failure and are frequent concomitant than oral administration, possibly because of iron
diseases. Both can also cause further renal absorption disturbances in CHF patients. Intravenous
dysfunction. iron therapy can reduce the need for high erythropoietin
6. High doses of ACE-inhibitors can impair the doses, which it might be preferable to avoid since this
response to erythropoietin treatment in hemodialysis can lead to an increase in arterial pressure, which may
patients w6x. not be desirable. Improvement of symptoms of CHF and
7. Chronic anaemia contributes to CHF because an exercise capacity has also been observed w12–14x.
increased cardiac output is required to deliver oxy- These benefits might be more pronounced in the early
gen to the tissues. This leads to an increase in myo- stages of CHF, than in patients with end stage CHF
cardial oxygen demands and stimulates volume under dialysis and recombinant erythropoietin therapy
overload hypertrophy w7x. w15x.
8. Treatment of the disease underlying CHF, principally If treatment with erythropoietin and iron is preceded
coronary artery disease, with agents such as aspirin by exclusion of other causes of anaemia, for example
and warfarin can contribute to blood loss and anae- intestinal blood loss or fluid overload, it might be quite
mia due to gastrointestinal bleeding. effective for improvement of symptoms and reduction of

1388-9842/03/$30.00 䊚 2002 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
PII: S 1 3 8 8 - 9 8 4 2 Ž 0 2 . 0 0 1 6 1 - 7
4 Editorial

left ventricular size w5x. Prognostic benefits are unprov- w8x Agostoni P, Wasserman K, Perego GB, et al. Oxygen transport
en, but cannot be excluded. to muscle during exercise in chronic congestive heart failure
secondary to idiopathic dilated cardiomyopathy. Am. J. Car-
Recent studies have investigated a novel erythropoi- diol. 1997;79:1120 –4.
esis stimulating protein (NESP) which has a three-times w9x Metevier F, Marchais SJ, Guerin AP, Pannier B, London GM.
longer half-life due to addition of two extra carbohydrate Pathophysiology of anaemia: focus on the heart and blood ves-
chains w16x. NESP is a hyperglycosylated analogue of sels. Nephrol. Dial. Transplant 2000;15(Suppl 3):14 –8.
recombinant human erythropoietin that was used in 1500 w10x Birgegard G, Sandhagen B. Erythropoetin treatment can
patients for stimulation of erythropoiesis. increase 2,3-diphospho-glycerate levels in red blood cells.
In conclusion, moderate and severe anaemia of any Scand. J. Clin. Lab. Invest. 2001;61:337 –40.
w11x Task Force for the Diagnosis and Treatment of Chronic Heart
origin can exacerbate CHF. Patients with heart failure
Failure, European Society of Cardiology: Remme WJ, Swed-
may benefit from therapy of anaemia. Favourable influ- berg K. Task Force Report Guidelines for the diagnosis and
ences on the long-term course are possible but so far treatment of chronic heart failure. Eur Heart J 2001;22:1527–
unproven. Further studies are needed. 60.
w12x Silverberg DS, Wexler D, Blum M, et al. The use of subcuta-
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