Clinical Chemistry
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Clinical Chemistry 54: 273-284, 2008. First published November 26, 2007; 10.1373/clinchem.2007.094425
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Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 2008;54:273-284.)
© 2008 American Association for Clinical Chemistry, Inc.


Lipids, Lipoproteins, and Cardiovascular Risk Factors

Serum Uric Acid and Risk of Cardiovascular Mortality: A Prospective Long-Term Study of 83 683 Austrian Men

Alexander Strasak1,a, Elfriede Ruttmann2, Larry Brant3, Cecily Kelleher4, Jochen Klenk5, Hans Concin6, Günter Diem6, Karl Pfeiffer1, Hanno Ulmer1,6 and the VHM&PP Study Group

1 Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria;
2 Department of Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria;
3 Gerontology Research Center, National Institute on Aging, Baltimore, MD, USA;
4 School of Public Health and Population Sciences, University College Dublin, Dublin, Ireland;
5 Department of Epidemiology, University of Ulm, Ulm, Germany;
6 Agency for Preventive and Social Medicine, Bregenz, Austria.

aAddress correspondence to this author at: Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Schoepfstrasse 41, 6020 Innsbruck, Austria. Fax 43 (512) 9003-73922; e-mail alexander.strasak{at}i-med.ac.at.

Background: The role of serum uric acid (SUA) as an independent risk factor for cardiovascular disease (CVD) remains controversial, and little is known about its prognostic importance for mortality from congestive heart failure (CHF) and stroke. Few large-scale epidemiologic studies with sufficient follow-up have addressed the association of SUA and CVD mortality in apparently healthy men across a wide age range.

Methods: A cohort of 83 683 Austrian men (mean age, 41.6 years) was prospectively followed for a median of 13.6 years. We used Cox proportional hazards models adjusted for established risk factors to evaluate SUA as an independent predictor for CVD mortality.

Results: The highest quintile of SUA concentration (>398.81 µmol/L) was significantly related to mortality from CHF (P = 0.03) and stroke (P <0.0001); adjusted hazard ratios (95% confidence interval) for the highest vs lowest quintiles of SUA were 1.51 (1.03–2.22) and 1.59 (1.23–2.04), respectively. SUA was not associated, however, with mortality from acute, subacute, or chronic forms of coronary heart disease (CHD) after adjustment for potential confounding factors (P = 0.12). Age was a significant effect modifier for the relation of SUA to fatal CHF (P = 0.05), with markedly stronger associations found in younger individuals.

Conclusions: Our study demonstrates for the first time in a large prospective male cohort that SUA is independently related to mortality from CHF and stroke. Although increased SUA is not necessarily a causal risk factor, our results suggest the clinical importance of monitoring and intervention based on the presence of an increased SUA concentration, especially because SUA is routinely measured.




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