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The role of serum uric acid as a risk factor for CV disease has been extensively debated for many years without reaching a final agreement among clinicians and researchers. In particular, most of the evidence about the pathogenetic role of uric acid in CV disease have been achieved in the population of patients with severe hyperuricemia or gout while its role in patients with mildly elevated serum levels of uric acid is only poorly recognized. Serum uric acid represents an important, independent risk factor for cardiovascular and renal disease in patients with hypertension, heart failure, or diabetes. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Although the mechanism(s) by which uric acid may play a pathogenetic role in cardiovascular disease is still unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Whether a reduction in uric acid impacts CV and renal disease remains to be determined. However, recent findings from LIFE suggest the possibility that a treatment-induced decrease in serum uric acid may indeed attenuate cardiovascular risk. Clearly, randomized clinical trials are needed to investigate further the long-term cardioprotective benefits issue of reducing hyperuricemia in hypertensive patients. The main purpose of the present symposium is twofold. First of all to reinforce the role of uric acid in the pathogenesis of gout and gout-related non-rheumatic diseases including renal involvement. Second to provide an updated review of the evidence supporting a possible and relevant role of (elevated) uric acid as a risk factor for cardiovascular diseases. To fullfil this goal we will present a series of comprehensive lectures mainly focused on the different aspects of the relationship between serum uric acid and cardiovascular diseases with the aim to define whether or not the increase in the amount of our knowledge about uric acid may improve the presenting of CV disease. 

Co-Presidents of the Meeting Claudio Borghi and Thomas Bardin

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