Pathophysiology of Anemia in Heart Failure

Inder Anand

Research output: Contribution to journalReview articlepeer-review

32 Scopus citations

Abstract

Renal dysfunction and neurohormonal and proinflammatory cytokine activation appear to contribute to anemia of chronic disease in most patients, resulting in inappropriate erythropoietin production and defective iron utilization. Under normal conditions, reduced tissue oxygenation caused by chronic anemia results in non-hemodynamic and hemodynamic compensatory responses to enhance oxygen carrying capacity. Erythropoiesis is the predominant non-hemodynamic response to hypoxia, but because erythropoiesis is defective in heart failure, hemodynamic mechanisms may predominate in chronic severe anemia. Hemodynamic responses are complex and involve a vasodilation-mediated high-output state with neurohormonal activation. The high output state initially helps to increase oxygen transport. However, the hemodynamic and neurohormonal alterations could potentially have deleterious long-term consequences and may contribute to anemia's role as an independent risk factor for adverse outcomes.

Original languageEnglish (US)
Pages (from-to)279-288
Number of pages10
JournalHeart Failure Clinics
Volume6
Issue number3
DOIs
StatePublished - Jul 1 2010

Keywords

  • Anemia
  • Chronic kidney
  • Erythropoietin
  • Heart failure
  • High output heart failure
  • Pathophysiology

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