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.
