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      Serum Uric Acid Independently Predicts Mortality in Patients with Significant, Angiographically Defined Coronary Disease

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          Abstract

          Background: Uric acid is a nontraditional risk factor implicated in the development of coronary artery disease (CAD). This study prospectively evaluated the predictive value of serum uric acid (SUA) levels for mortality after angiographic diagnosis of CAD. Methods: Blood samples were collected from 1,595 consecutive, consenting patients with significant, angiographically defined CAD (stenosis 70%). Baseline and procedural variables were recorded and levels of SUA were measured. Patients were followed to death or to the time of contact (mean 2.6 years, range 1.8–5.0 years). Results: Patients averaged 65 ± 11 years of age, 78% were male and 170 subjects died during the follow-up period. In univariate analysis of prospectively defined quintiles, SUA predicted all-cause mortality (fifth quintile vs. first four quintiles: hazard ratio 1.9, p < 0.001). In multivariable Cox regression controlling for 20 covariables, independent predictive value for mortality was retained by SUA (hazard ratio 1.5, confidence interval 1.02–2.1, p = 0.04). In subgroup analysis based on diuretic use status, SUA independently predicted mortality among patients not using diuretics, while SUA was not a significant predictor of mortality among those who used diuretics. Conclusions: In patients with significant, angiographically defined CAD, SUA predicted mortality independent of traditional risk factors. This suggests that elevated SUA may be a risk factor for mortality in patients with significant cardiovascular disease and may be a stronger secondary than primary risk factor in CAD.

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          Most cited references 13

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          Serum Uric Acid and Cardiovascular Mortality

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            Sex differences in uric acid and risk factors for coronary artery disease.

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              Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: a subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study.

              Little is known about the effect of dyslipidemia on serum uric acid (SUA) levels, and less is known about the effect of statin treatment on them. The GREek Atorvastatin and Coronary-heart-disease Evaluation study suggested that a mean atorvastatin dose of 24 mg/d achieves the National Cholesterol Educational Program treatment goals and significantly reduces morbidity and mortality in patients with coronary heart disease (CHD) in comparison to the usual care. Here, we report the time course of SUA levels in usual-care patients undertreated for their dyslipidemia (12% were administered statins) in comparison to structured-care patients treated with atorvastatin in the vast majority (98%). Mean on-study SUA levels (up to 48 months) were compared with those at baseline by using analyses of variance to assess differences over time within and between treatment groups. Cox multivariate analysis was used to investigate whether changes in SUA levels during the study were clinically relevant. All patients had normal renal function at baseline; serum creatinine (SCr) levels less than 1.3 mg/dL (<115 micromol/L) and moderately elevated SUA levels (mean, 7.1 +/- 0.9 [SD] mg/dL [425 +/- 52 micromol/L]; upper normal limit, 7.0 mg/dL [415 micromol/L]). Usual-care patients (n = 800) showed an increase in SUA levels by 3.3% ( P < 0.0001). Structured-care patients (n = 800) had an 8.2% reduction in SUA levels ( P < 0.0001). In all patients not administered diuretics (n = 1,407), SUA level changes showed a positive correlation with changes in SCr levels ( r = 0.82; P < 0.0001) and an inverse correlation with estimated glomerular filtration rate ( r = -0.77; P < 0.0001). After adjustment for 19 predictors of all CHD-related events, Cox multivariate analysis involving backward stepwise logistic regression showed a hazard ratio (HR) of 0.89 (95% confidence interval [CI], 0.78 to 0.96; P = 0.03) with every 0.5-mg (30-micromol/L) reduction in SUA level, an HR of 0.76 (95% CI, 0.62 to 0.89; P = 0.001) with every 1-mg (60-micromol/L) reduction, an HR of 1.14 (95% CI, 1.03 to 1.27; P = 0.02) with every 0.5-mg increase, and an HR of 1.29 (95% CI, 1.17 to 1.43; P = 0.001) with every 1-mg increase in SUA levels. Data suggest that SUA level is an independent predictor of CHD recurrent events. Atorvastatin treatment significantly reduces SUA levels in patients with CHD, thus offsetting an additional factor associated with CHD risk.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2005
                February 2005
                22 March 2005
                : 25
                : 1
                : 45-49
                Affiliations
                aOhio State University Medical Center, Columbus, Ohio, bLDS Hospital and cUniversity of Utah, Salt Lake City, Utah, USA
                Article
                84085 Am J Nephrol 2005;25:45–49
                10.1159/000084085
                15724082
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 3, References: 25, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/84085
                Categories
                Original Report: Patient-Oriented, Translational Research

                Cardiovascular Medicine, Nephrology

                Serum uric acid, Defined coronary disease

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