Published: 21 January 2020
Author(s): Claudio Borghi, Eugenio Cosentino, Alessio Bragagni
Issue: January 2020

The prevalence of heart failure (HF) is increasing worldwide and in particular in the industrialized countries [1,2]. This is associated with a parallel increase in the rate of hyperuricemia and gout [3,4] that occurs with a high rate of hypertension, chronic kidney disease, atrial fibrillation, metabolic syndrome, diabetes, dyslipidemia, and obesity [5], leading to an overall increase in urate mediated cardiovascular risk. The close correlation between uric acid and HF is based on a complex pathophysiological mechanism that, probably, does not reflect a direct effect of elevated uric acid on left ventricular function, but rather involves the extensive activation of the enzyme xanthine-oxidase (XO) that is responsible for urate production and increased levels of oxidative stress [6].


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