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European Journal of Heart Failure Advance Access originally published online on April 4, 2009
European Journal of Heart Failure 2009 11(5):444-452; doi:10.1093/eurjhf/hfp042
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Oxidative stress and hyperuricaemia: pathophysiology, clinical relevance, and therapeutic implications in chronic heart failure

Corinna Bergamini, Mariantonietta Cicoira*, Andrea Rossi and Corrado Vassanelli

Department of Biomedical and Surgical Sciences, Division of Cardiology, Ospedale Civile Maggiore, University of Verona, Piazzale Stefani 1, 37126 Verona, Italy

* Corresponding author. Tel: +39 0458123706, Fax: +39 045914727, Email: mariantonietta.cicoira{at}univr.it


  Abstract

Heart failure (HF) is a state of chronic deterioration of oxidative mechanisms due to enhanced oxidative stress and consequent subcellular alterations. In this condition, oxidant-producing enzymes, in particular xanthine oxidase (XO), the major cardiovascular source of reactive oxygen species (ROS), are up-regulated. Growing evidence shows that this impaired oxidative metabolism due to enhanced ROS release is implicated in the development of cardiac hypertrophy, myocardial fibrosis, left ventricular remodelling, and contractility impairment responsible for worsening of cardiac function in CHF. Uric acid (UA) has long been linked with cardiovascular diseases, and hyperuricaemia is a common finding in patients with CHF. Hyperuricaemia is associated with impairment of peripheral blood flow and reduced vasodilator capacity, which relate closely to clinical status and reduced exercise capacity. Recent studies also suggest an association between UA levels and parameters of diastolic function; more importantly, UA has emerged as a strong independent prognostic factor in patients with CHF. In this review, we describe the up-to-date experimental and clinical studies that have begun to test whether the inhibition of XO translates into meaningful beneficial pathophysiological changes. This treatment gives evidence that myocardial energy, endothelial dysfunction, and vasodilator reactivity to exercise are improved by reducing markers of oxidative stress responsible for vascular dysfunction, so it represents an interesting therapeutic alternative for better outcome in CHF patients.

Key Words: Oxidative stress • Ventricular function • Treatment

Received September 11, 2008; Revised January 5, 2009; Accepted March 2, 2009


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