Abstract
The association between congestive heart failure and hyperuricemia is well known [1]. Furthermore, hyperuricemia has also shown to be independently predictive of poor long term outcomes in heart failure, although the exact mechanism of this contribution is unclear [2,3]. A leading hypothesis is that activation of the xanthine oxidase pathway causes an increase in free radical burden, which has been shown to mediate endothelial dysfunction.[4] It has therefore been proposed that xanthine oxidase inhibitors could function therapeutically, though results from these studies have been mixed [5,6].
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