Hyperuricemia: a novel old disorder-relationship and potential mechanisms in heart failure

Heart Fail Rev. 2020 Jan;25(1):43-51. doi: 10.1007/s10741-019-09869-z.

Abstract

Uric acid, the metabolic mediator of gout and urate renal stones, is associated with increased cardiovascular risk burden. Hyperuricemia is an old emerging metabolic disorder, and interaction among uric acid and cardiovascular diseases has been clearly described. Several illness including hypertension, myocardial infarction, metabolic syndrome, and heart failure, are related with uric acid levels increase. In this review, we will discuss the pathophysiology of hyperuricemia and describe the biological plausibility for this metabolite to participate in the pathogenesis of cardiovascular disorders. In particular, we will focus on the implications of hyperuricemia in the onset and progression of heart failure, paying special attention to the pathophysiology and the possible clinical implications. We will conclude by discussing the effects of lowering plasma uric acid concentration on the prognosis of heart failure by reviewing most of available data on the different classes of drugs directly or indirectly involved in the hyperuricemia management.

Keywords: Cardiovascular diseases; Heart failure; Uric acid; Xanthine oxidase.

Publication types

  • Review

MeSH terms

  • Angiotensin II Type 1 Receptor Blockers / therapeutic use
  • Cardiovascular Diseases / drug therapy*
  • Cardiovascular Diseases / etiology
  • Disease Progression
  • Gout / drug therapy
  • Gout / etiology
  • Gout Suppressants / therapeutic use
  • Heart Failure / drug therapy*
  • Heart Failure / etiology
  • Humans
  • Hyperuricemia / drug therapy*
  • Hyperuricemia / physiopathology
  • Protease Inhibitors / therapeutic use
  • Randomized Controlled Trials as Topic
  • Sodium-Glucose Transporter 2 Inhibitors
  • Uric Acid / blood*
  • Xanthine Oxidase / antagonists & inhibitors*

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Gout Suppressants
  • Protease Inhibitors
  • Sodium-Glucose Transporter 2 Inhibitors
  • Uric Acid
  • Xanthine Oxidase