Different mechanisms have been identified to contribute to the development of HF including endothelial dysfunction, oxidative stress and inflammatory factors.1,2 Some studies have shown increased activation and expression of xanthine oxidase (XO) in failing myocardial tissue.2 XO catalyzes the production of large amounts of reactive oxygen species (ROS) which have been found to mediate myocardial dilation and hypertrophy and to increase endothelial dysfunction. This evidence concerns the gene XDH and hydrops fetalis.