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Delayed treatment effects of xanthine oxidase inhibition on systolic overload-induced left ventricular hypertrophy

X Xu1, L Zhao, X Hu

  • 1Cardiovascular Division, Department of Medicine, University of Minnesota, The Center of Vascular Biology, Minneapolis, Minnesota 55455, USA.

Nucleosides, Nucleotides & Nucleic Acids
|June 15, 2010
PubMed

Insights

Delayed treatment with febuxostat showed modest improvement in heart function after heart failure onset in mice. Allopurinol did not improve function and increased mortality, suggesting febuxostat may be a safer option for heart failure management.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Biochemistry

Background:

  • Xanthine oxidase (XO) inhibition is a therapeutic target for cardiovascular diseases.
  • Febuxostat, a nonpurine selective XO inhibitor, attenuates left ventricular (LV) hypertrophy and dysfunction when initiated early after transverse aortic constriction (TAC).
  • The efficacy of delayed XO inhibition initiation after heart failure (HF) onset remains unclear.

Purpose of the Study:

  • To investigate the effects of delayed treatment with XO inhibitors febuxostat and allopurinol on established TAC-induced heart failure in mice.
  • To determine if initiating treatment 7 days after TAC can reverse or improve cardiac dysfunction and hypertrophy.

Main Methods:

  • Mice underwent TAC to induce heart failure.
  • Treatment with febuxostat, allopurinol, or vehicle was initiated 7 days post-TAC.
  • LV hypertrophy, function (ejection fraction), and mortality were assessed.

Main Results:

  • Neither febuxostat nor allopurinol significantly affected TAC-induced LV hypertrophy.
  • Febuxostat treatment resulted in a modest improvement in LV ejection fraction (approximately 10%) compared to vehicle.
  • Allopurinol treatment showed a trend towards increased mortality in HF mice compared to vehicle or febuxostat.

Conclusions:

  • Delayed initiation of febuxostat treatment offers a modest benefit in LV function in established HF post-TAC.
  • Allopurinol is not effective in improving cardiac function in this model and may increase mortality.
  • These findings suggest a potential therapeutic window for febuxostat in managing heart failure, but caution is warranted with allopurinol.

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