Mechanisms and Treatment of Anemia in Chronic Heart Failure

Stuart D. Katz, MD

Disclosures

CHF. 2004;10(5) 

In This Article

Abstract and Introduction

Anemia is highly prevalent in patients with chronic heart failure (HF) and is associated with poor clinical outcomes. Multiple mechanisms contribute to anemia in chronic HF, and subnormal compensatory rise in endogenous erythropoietin levels in response to anemia is one contributory factor. Randomized trials with recombinant human erythropoietin therapy in anemic patients with chronic kidney disease and concomitant heart disease have demonstrated a reduction in left ventricular hypertrophy but variable effects on clinical outcome. Preliminary clinical trials in anemic patients with chronic HF demonstrate that erythropoietin therapy is well tolerated and associated with short-term clinical improvement. The optimum target hemoglobin, erythropoietic agent, and dosing regimen, and the role of iron supplementation in patients with chronic HF, are not known. Additional studies are needed to determine the safety and efficacy of long-term erythropoietic therapy in chronic HF patients.

Anemia is highly prevalent in patients with chronic heart failure (HF) and is independently associated with increased mortality risk in this patient population.[1,2] This report will review the mechanisms that contribute to anemia in chronic HF, physiology and pharmacology of erythropoietin, and findings of the published clinical experience with erythropoietic therapy for anemic patients with chronic HF with and without concomitant chronic kidney disease (CKD).

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