An examination of the relationship between serum uric acid level, a clinical history of gout, and cardiovascular outcomes among patients with acute coronary syndrome - 27/09/17
, Connie N. Hess, MD, MHS b, Robert M. Clare, MS a, Axel Akerblom, MD, PhD c, Pierluigi Tricoci, MD, PhD, MHS a, Daniel Wojdyla, MSc a, Robert T. Keenan, MD, MPH d, Stefan James, MD c, Claes Held, MD, PhD c, Kenneth W. Mahaffey, MD e, Alyssa B. Klein, MPH f, Lars Wallentin, MD, PhD c, Matthew T. Roe, MD, MHS aAbstract |
Background |
Studies have suggested a relationship between higher baseline serum uric acid (sUA) levels and an elevated risk of subsequent ischemic cardiovascular outcomes among acute coronary syndrome (ACS) patients; this relationship may be modified by a clinical history of gout and has not been studied in large patient cohorts. We sought to understand the effect of sUA and gout on ACS outcomes.
Methods |
Using PLATO and TRACER data on 27,959 ACS patients, we evaluated baseline sUA levels in relation to a composite of cardiovascular death, myocardial infarction (MI), or stroke. We assessed interaction terms to determine if a baseline clinical diagnosis of gout modified this putative relationship; 46% (n=12,882) had sUA levels elevated >6.0 mg/dL.
Results |
Patients with elevated levels were more often male with a history of prior MI, diabetes, and heart failure compared with those with sUA <6.0 mg/dL. The unadjusted risk of the composite endpoint increased with corresponding elevations in sUA levels (per 1 mg/dL increase) (HR=1.23 [95% CI: 1.20–1.26]) above the statistical inflection point of 5.0 mg/dL. After adjustment, the association between sUA level and the composite outcome remained significant (HR=1.07 [95% CI: 1.04–1.10]), and baseline gout did not modify this relationship.
Conclusions |
In patients with ACS, increasing levels of sUA are associated with an elevated risk of cardiovascular events, regardless of a clinical diagnosis of gout. Further investigation is warranted to determine the mechanism behind this relationship and to delineate whether sUA is an appropriate therapeutic target to reduce cardiovascular risk.
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| Paul W. Armstrong, MD served as guest editor for this article. |
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| Source of funding: This study was funded by Astra Zeneca. |
Vol 187
P. 53-61 - mai 2017 Retour au numéro
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