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Uric Acid and Cardiovascular Disease: How to Solve Another Chicken or Egg Puzzle

Many cross-sectional, retrospective and most importantly prospective studies have found a graded and continuous association between SUA with subclinical and clinical atherosclerotic disease [3–6] . However, not all studies were able to separate the effect of SUA on clinical events from confounders, such as hypertension, diuretic use, the metabolic syndrome and especially renal failure [7] . In this issue of Cardiology , Brodov et al. [8] evaluated in a post hoc analysis the association of SUA and renal dysfunction (estimated glomerular filtration rate ! 60 ml/min) with myocardial infarction and sudden cardiac death in 2,796 subjects who had previously been enrolled in the Bezafibrate Infarction Prevention (BIP) study. The BIP study was a prospective trial that tested the effects of bezafibrate on the recurrence of coronary events and death in secondary prevention subjects. The authors found that SUA levels within the fifth quintile of distribution, e.g. 1 6.76 mg/dl, were associated with approximately a 50% greater chance of dying or having a myocardial infarction after adjustment for renal function and for the components that characterize the metabolic syndrome. This subanalysis of the BIP trial suggests that increased SUA is an independent marker of cardiovascular disease even for subjects at an already higher risk of event recurrence. Brodov et al. [8] add further evidence of the link between SUA and cardiovascular disease. However, Recently, a huge wave of new laboratory and imaging biomarkers for cardiovascular disease risk prediction has swamped preventive cardiology [1, 2] . There has been a lot of discussion on whether the use of tests such as C-reactive protein, lipoprotein-associated phospholipase 2 or coronary calcium scores determined by cardiac computerized tomography add prognostic value and show costeffectiveness in comparison to clinical risk stratification. The association of serum uric acid (SUA), a biomarker known since the 19th century, with gout, cardiovascular risk factors, and coronary disease is crystal clear [3] . Historically, this relationship evolved from the classic descriptions of gout attacks to the more recent definition of the metabolic syndrome. Despite recent genome-wide studies associating SUA concentration with a few single nucleotide polymorphisms in Caucasian and black individuals that affect renal tubular handling of uric acid [4] , increased SUA concentration is frequently associated with hypertension, atherogenic dyslipidemia, diabetes, diuretic use, alcohol consumption and renal failure [3] . All the conditions previously cited, maybe with the exception of diuretic use, predispose to atherosclerosis. On the other hand, SUA may be proatherogenic per se since studies have associated SUA concentrations with increased oxidative stress, endothelial dysfunction, inflammation and hyperinsulinemia. Received: July 10, 2009 Accepted: July 10, 2009 Published online: September 23, 2009