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(Circulation. 2005;112:1681-1683.)
© 2005 American Heart Association, Inc.

Editorial

Anemia and Chronic Heart Failure

Are We Asking the Right Questions?

Andrew L. Clark, MD; John G.F. Cleland, MD

From the Castle Hill Hospital, Hull, United Kingdom.

Correspondence to Dr Andrew L. Clark, Castle Hill Hospital, Castle Rd, Cottingham, Hull HU16 5JQ, UK. E-mail a.l.clark@hull.ac.uk

Key Words: Editorials • anemia • heart failure • angiotensin

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The treatment of patients with chronic heart failure is one of the great successes of modern medical therapy. Good medical management can approximately double life expectancy for patients with significant left ventricular systolic dysfunction,¹ and for some patients at least, induce a state of remission.² Mortality remains high, however, and many patients remain symptom limited.

See p 1743

The neurohormonal model has been the stimulus for many new treatment targets, but recent failures with novel neurohormonal antagonists^3,4 have prompted a successful reevaluation of mechanical means to improve cardiac function,⁵ and the hunt is on for the next target for medical management.

Anemia is common in patients with heart failure, usually normochromic and normocytic and often unrelated to deficiency of classic hematinic factors.^6,7 The cause of this "anemia of chronic disease" remains obscure, but it is associated with poorer cardiac and renal function, worse symptoms, and an adverse prognosis. In small-scale studies, treatment of anemia with erythropoeisis-stimulating proteins has improved symptoms and exercise capacity.^8,9 At first sight, it is somewhat surprising to find that treatments that improve heart failure, including angiotensin-converting enzyme (ACE) inhibitors and carvedilol,¹⁰ can exacerbate anemia.

The study by van der Meer et al in this issue⁷ offers insight into the mechanism of anemia in heart failure in patients without obvious hematinic deficiency. These investigators studied a small group of patients with heart failure and found anemia in 17%. Of these, 59% had anemia unexplained by hematinic deficiency or renal impairment. The tetrapeptide, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), an inhibitor . . . [Full Text of this Article]

Related Article:

Levels of Hematopoiesis Inhibitor N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Partially Explain the Occurrence of Anemia in Heart Failure

Peter van der Meer, Erik Lipsic, B. Daan Westenbrink, Ruud M.A. van de Wal, Regien G. Schoemaker, Edo Vellenga, Dirk J. van Veldhuisen, Adriaan A. Voors, and Wiek H. van Gilst
Circulation 2005 112: 1743-1747. [Abstract] [Full Text]

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