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(Circulation. 2003;107:1951.)
© 2003 American Heart Association, Inc.

Editorial

Uric Acid Predicts Clinical Outcomes in Heart Failure

Insights Regarding the Role of Xanthine Oxidase and Uric Acid in Disease Pathophysiology

Joshua M. Hare, MD; Richard J. Johnson, MD

From the Department of Medicine, Cardiology Division, Johns Hopkins Hospital, Baltimore, Md (J.M.H.); and the Nephrology Division, Baylor College of Medicine, Houston, Tex (R.J.J.).

Correspondence to Joshua M. Hare, MD, The Johns Hopkins Hospital School of Medicine, Cardiology Division, 600 N Wolfe St, Carnegie 568, Baltimore, MD 21287 (e-mail jhare@mail.jhmi.edu); or Richard J. Johnson, MD, Division of Nephrology, Baylor College of Medicine, 6550 Fannin, SM 1273, Houston, TX 77030 (e-mail rjohnson@bcm.tmc.edu).

Key Words: Editorials • antioxidants • nitric oxide • cardiovascular diseases • kidney

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In the current issue of Circulation, Anker and colleagues¹ report that elevated levels of uric acid (UA) predict mortality and the need for heart transplantation in patients with congestive heart failure (HF). Serum concentrations of UA added important prognostic information alone and when combined with measures of cardiac function (ejection fraction) and patient functional status (maximal oxygen consumption with exercise) and were independent of renal function, serum sodium, serum urea, diuretic usage, and patient age. Receiver operating curve analysis identified a cutoff of 585 µmol/L (9.8 mg/dL) as the best mortality predictor. This finding is not only potentially of value in patient management but also raises extremely interesting questions regarding the pathophysiological underpinnings of this finding.

See p 1991

A consideration of the mechanism of UA production and metabolism offers insight into the relationship between UA levels and HF outcomes. Indeed, accumulating data support the idea that UA, in addition to being a potentially valuable prognostic marker, possesses specific toxic or other properties that could contribute to HF pathophysiology. Moreover, UA levels may reflect xanthine oxidase (XO) pathway activity, which has the potential to contribute to the progression of left ventricular dysfunction by interfering with myocardial energetics² and myofilament calcium sensitivity.³

Potential Mechanisms for Increased Uric Acid in Heart Failure

UA is a metabolic byproduct of purine metabolism (Figure). Serum UA may increase in the failing circulation because of increased generation, decreased excretion, or a combination of the 2 factors. There are several possible contributors to increased UA production in HF, including increased abundance and activity . . . [Full Text of this Article]

Related Article:

Uric Acid and Survival in Chronic Heart Failure: Validation and Application in Metabolic, Functional, and Hemodynamic Staging

Stefan D. Anker, Wolfram Doehner, Mathias Rauchhaus, Rakesh Sharma, Darrel Francis, Christoph Knosalla, Constantinos H. Davos, Mariantonietta Cicoira, Waqar Shamim, Michel Kemp, Robert Segal, Karl Josef Osterziel, Francisco Leyva, Roland Hetzer, Piotr Ponikowski, and Andrew J.S. Coats
Circulation 2003 107: 1991-1997. [Abstract] [Full Text]

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