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An examination of the relationship between serum uric acid level, a clinical history of gout, and cardiovascular outcomes among patients with acute coronary syndrome
Duke Univ Hlth Syst, Duke Clin Res Inst, Durham, NC USA..
Univ Colorado, Sch Med, Aurora, CO USA..
Duke Univ Hlth Syst, Duke Clin Res Inst, Durham, NC USA..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
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2017 (English)In: American Heart Journal, ISSN 0002-8703, E-ISSN 1097-6744, Vol. 187, p. 53-61Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
MOSBY-ELSEVIER , 2017. Vol. 187, p. 53-61
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Cardiac and Cardiovascular Systems
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URN: urn:nbn:se:uu:diva-327059DOI: 10.1016/j.ahj.2017.02.023ISI: 000401053600007PubMedID: 28454808OAI: oai:DiVA.org:uu-327059DiVA, id: diva2:1129380
Available from: 2017-08-02 Created: 2017-08-02 Last updated: 2017-08-02Bibliographically approved

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Akerblom, AxelJames, StefanHeld, ClaesWallentin, Lars

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