Uric acid in chronic heart failure

Semin Nephrol. 2005 Jan;25(1):61-6. doi: 10.1016/j.semnephrol.2004.09.010.

Abstract

The pathophysiologic understanding of chronic heart failure (CHF) has shifted from a mere hemodynamic disorder to a much more complex approach including changes and imbalances in neurohormonal, immune, and metabolic functions. Among metabolic abnormalities, hyperuricemia is a constant finding in CHF. The xanthine oxidase metabolic pathway increasingly is appreciated as an important contributor to both symptoms of CHF as well as progression of the disease. Recent data suggest hyperuricemia to be an independent marker of impaired prognosis in CHF. In this article, the significance of the xanthine oxidase metabolic pathway in CHF is discussed. Data on xanthine oxidase inhibition are reviewed, which suggest a beneficial effect of therapeutically targeting this enzymatic pathway.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Allopurinol / therapeutic use
  • Animals
  • Biomarkers / blood
  • Blood Flow Velocity / physiology
  • Blood Vessels / metabolism
  • Blood Vessels / physiopathology
  • Chronic Disease
  • Disease Progression
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / physiopathology
  • Enzyme Inhibitors / therapeutic use
  • Heart Failure / blood
  • Heart Failure / drug therapy
  • Heart Failure / etiology*
  • Heart Failure / physiopathology
  • Humans
  • Hyperuricemia / blood
  • Hyperuricemia / complications
  • Hyperuricemia / physiopathology
  • Prognosis
  • Uric Acid / blood*
  • Xanthine Oxidase / antagonists & inhibitors
  • Xanthine Oxidase / blood

Substances

  • Biomarkers
  • Enzyme Inhibitors
  • Uric Acid
  • Allopurinol
  • Xanthine Oxidase