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(Stroke. 2003;34:1956.)
© 2003 American Heart Association, Inc.
Original Contributions |
Section of Nephrology, Baylor College of Medicine, Houston, Texas
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hyperuricemia was first associated with hypertension and cardiovascular disease in 1879.1 Since that time, many have attributed this association to a simple clustering of hyperuricemia with well-established cardiovascular risk factors, and an elevated serum uric acid level by itself has generally been regarded as insignificant or incidental. A recent reanalysis of the Framingham study concluded that hyperuricemia was not an independent risk factor for cardiovascular events after controlling for these other associated factors.2 Nevertheless, other studies have found an elevated serum uric acid level to be an independent risk factor for cardiovascular and renal disease (reviewed elsewhere3). In particular, several studies have reported that hyperuricemia is an independent predictor of stroke in diabetic subjects,4 individuals with isolated systolic hypertension,5,6 and the general population.7 A new study reported in this issue of Stroke8 examining 2498 subjects admitted with acute stroke found that the admission serum uric acid also independently predicted worse outcome and a higher rate of repeated stroke or other cardiovascular event. Others have also reported that a higher uric acid level in patients with acute stroke is associated with poorer outcome.9 These studies suggest that uric acid may be a true risk factor for stroke and for a poor outcome after stroke.
Experimental evidence could provide a mechanism to explain how uric acid may have a pathogenetic role in stroke. Hypertension remains the most common cause of stroke, and there is increasing evidence that an elevation in uric acid may cause primary hypertension. Elevated serum uric acid is
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