Uric acid, heart failure survival, and the impact of xanthine oxidase inhibition

Congest Heart Fail. May-Jun 2012;18(3):179-82. doi: 10.1111/j.1751-7133.2011.00262.x. Epub 2011 Nov 9.

Abstract

Increasing evidence suggests that serum uric acid (UA), a product of xanthine oxidase (XO), may be a useful marker for metabolic, hemodynamic, and functional staging in heart failure (HF) and a valid predictor of survival in HF patients. Recent data support an expanded role for UA and the XO pathway in the pathogenesis of HF, as studies have shown that an elevation in the enzymatic activity of XO can lead to increases in oxidative stress, endothelial dysfunction, and reduced myocardial function. Numerous population studies have previously reported that elevated UA levels are an independent predictor of cardiovascular mortality, and recent evidence suggests that lowering serum levels of UA may lead to improved outcomes in HF patients. The question of whether UA is only a marker rather than a causal factor in the pathogenesis of HF remains. Regardless of whether UA levels are ready for routine clinical use, either as a prognostic factor or novel therapeutic target, further prospective studies are necessary to demonstrate that routine measurement or reduction of UA levels improves outcomes in HF patients.

Publication types

  • Review

MeSH terms

  • Allopurinol / therapeutic use*
  • Biomarkers
  • Enzyme Inhibitors / therapeutic use*
  • Heart Failure / blood
  • Heart Failure / drug therapy*
  • Heart Failure / metabolism
  • Humans
  • Hyperuricemia / complications*
  • Hyperuricemia / metabolism
  • Uric Acid / blood
  • Uric Acid / metabolism*
  • Xanthine Oxidase / antagonists & inhibitors*
  • Xanthine Oxidase / metabolism

Substances

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