Published: 23 April 2021
Author(s): Giuseppe Ambrosio, Marisa G. Crespo Leiro, Lars H. Lund, Stefano Coiro, Andrea Cardona, Gerasimos Filippatos, Roberto Ferrari, Massimo F. Piepoli, Andrew J.S. Coats, Stefan D. Anker, Cécile Laroche, Luis Almenar-Bonet, Pentti Poder, David Bierge Valero, Anna Frisinghelli, Aldo P. Maggioni
Issue: July 2021
Section: Original article

Heart failure (HF) is a heterogeneous clinical syndrome, associated with a spectrum of metabolic disorders. Serum uric acid (sUA), the end-product of purine degradation, has shown prognostic value in the general population and in patients with various cardiovascular disorders [1–3]. Exploring the prognostic role of sUA is of particular interest in the case of HF, as sUA is frequently increased in this condition [4]. Interestingly, high sUA in HF may reflect a specific metabolic alteration, since the UA-forming enzyme xanthine-oxidase (XO) is overexpressed in HF patients [5–7], thus providing a mechanistic explanation for elevated sUA levels.


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