Abstract
Objective Hyperuricemia is often observed in patients with chronic heart failure (CHF), and it is predictive of poor exercise capacity, inflammation and increased mortality. The uric acid (UA)-generating enzyme xanthine oxidase (XO) is a major source of reactive oxygen species (ROS) generation, and increased ROS has been accounted for multiple adverse effects in CHF pathophysiology. Therapeutic inhibition of XO with allopurinol reduced serum UA (SUA) levels and showed a range of beneficial effects in CHF with left ventricular (LV) systolic dysfunction. However, it is unclear if UA-lowering therapy by XO inhibition is beneficial in patients with LV diastolic dysfunction. Therefore, we evaluated the effects of the specific XO inhibitor febuxostat on LV diastolic function compared with the uricosuric agent benzbromarone. Methods and Results The effects of febuxostat and benzbromarone (24 weeks each) were tested in 20 hyperuricemic patients (SUA > 7.0mg/dL) with LV diastolic dysfunction in a double-blind, randomized crossover study design. Both febuxostat and benzbromarone significantly decreased SUA levels (-35% and -41%, respectively, both p Conclusions XO inhibition with febuxostat might improve LV diastolic function, especially in patients with high SUA levels. This effect may be related to the decreased oxidative stress by febuxostat.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
