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Open Access Research article

Hyperuricemia and untreated gout are poor prognostic markers among those with a recent acute myocardial infarction

Eswar Krishnan1*, Bhavik J Pandya2, Bharathi Lingala1, Ali Hariri3 and Omar Dabbous2

Author affiliations

1 Department of Medicine, Stanford University School of Medicine, 1000 Welch Rd, Suite 203, Palo Alto, CA 94304, USA

2 Takeda Pharmaceuticals International, Inc. One Takeda Parkway, Deerfield, IL 60015, USA

3 Takeda Pharmaceuticals North America, Inc. One Takeda Parkway, Deerfield, IL 60015, USA

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Citation and License

Arthritis Research & Therapy 2012, 14:R10  doi:10.1186/ar3684

Published: 17 January 2012

Abstract

Introduction

Patients with a history of myocardial infarction (MI) are often at risk for complications, including subsequent MI and death. Use of prognostic markers may aid in preventing these poor outcomes. Hyperuricemia is associated with increased risk for coronary heart disease (CHD) and/or mortality; however, it is unknown if serum urate (sUA) levels predict outcomes in patients with previous MI. The purpose of this study was to assess hyperuricemia as a biomarker of CHD outcomes in such patients.

Methods

These were post hoc analyses of datasets from the Aspirin Myocardial Infarction Study, a 1:1 randomized, double-blind clinical trial, conducted from 1975 to 1979, that examined mortality rates following daily aspirin administration over three years in individuals with documented MI. The primary outcome measures were all-cause death, CHD mortality, coronary incidence, and stroke by quartile of baseline sUA. A sub-analysis of all outcome measures in the presence or absence of gouty arthritis was also performed.

Results

Of 4,524 enrolled participants, data on 4,352 were analyzed here. All outcomes were greatest for patients in the fourth sUA quartile. In multivariate regression models, the hazard ratios (HR) for patients in the highest quartile were 1.88 for all-cause mortality (95% confidence interval (CI), 1.45 to 2.46), 1.99 for CHD mortality (95% CI, 1.49 to 2.66), and 1.36 for coronary incidence (95% CI, 1.08 to 1.70). Participants with untreated gout had an adjusted hazard ratio ranging from 1.5 to 2.0 (all P < 0.01) for these outcomes. Participants with gout who were receiving treatment did not exhibit this additional risk.

Conclusions

sUA and untreated gout may be independent prognostic markers for poor all-cause and CHD mortality in patients with recent acute MI.