| AimSerum uric acid (SUA) formed from xanthine oxidase (XO). Apoptosis and tissue hypoxia causes increased purine catabolism, which, finally, increases XO activity and leading increased SUA levels. This Meta-analysis was performed as a meta-analysis to evaluate the evidence supporting SUA as a predictor of all-cause mortality in patients with heart failure (HF).MethodsSearch Strategy. We accessed MEDLINE through PubMed, the Internet access site provided by the National Library of Medicine. MEDLINE includes articles from2002until March2013. As a first step in the review process, two members of the study team independently reviewed the abstracts identified by the search to exclude those did not meet our eligibility criteria. When there was no abstract or when the reviewers could not determine from the abstract whether the article met the eligibility criteria, a third member of our team will make the decision.The key exposure variable was the SUA measurement at baseline in mg/dL. One study reported SUA in μmol/L, and we converted those values using the following conversion equivalence:1mg/dL=59.48μmol/L. All studies measured SUA using the uricase-peroxidase enzymatic method.The study team developed article review forms that were pilot tested and have been validated in prior projects. The quality assessment forms included items about study quality in the following categories:representativeness of study population, bias and confounding; statistical quality and interpretation, and conflict of interest.Statistical Analysis. We reported relevant baseline characteristics as median values with the range of observations. To assess for heterogeneity across studies we used the Cochran Q chi-square statistic (significance level of P<.10). Publication bias was assessed using a visual inspection of the Begg’s funnel plot and tested using the Egger’s weighted regression method. ResultsSix studies were enrolled in our research. All studies were single-center, prospective cohorts that included1456HF patients and evaluated mortality in a median follow-up of40months (range,12-51months). Four studies reported results on patients with acute HF hospitalizations. The median ejection fraction (EF) in the studies was32%(range,26%-40%), with a median serum creatinine of1.3mg/dL (range,1.0-1.3mg/dL). The studies included patients with ischemic cardiomyopathy in a median of58%(range,25%-71%).ConclusionOur study found that high SUA levels increase all-cause mortality in patients with HF, that this increase is consistent in patients with both acute and chronic HF, and that this increase in risk seems to start at an SUA level of7mg/dL. The strengths of this analysis are the inclusion of studies from different countries, the lack of heterogeneity and publication bias, and large sample size, permitting an analysis of dose-dependence.This prospective, long-term study is the largest single investigation undertaken to date to assess the association between baseline SUA concentration in men and their risk of subsequent mortality from CHF, CHD, and stroke. As expected, our findings suggests SUA values>398.81μmol/L have about a50%greater risk for fatal CHF and stroke and about a40%greater risk for mortality from other cardiovascular events than do men with SUA concentrations≤273.81μmol/L. That our results were stable after exclusion of participants>75years old accented the prognostic significance of SUA for mortality from CHF and stroke, although not necessarily as a causal risk factor. |
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