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Gout and the risk for incident heart failure and systolic dysfunction
  1. Eswar Krishnan
  1. Department of Medicine, Stanford University School of Medicine, Palo Alto, California, USA
  1. Correspondence to Dr Eswar Krishnan; e.krishnan{at}


Objective To test the hypothesis that gouty arthritis (gout) is a risk factor for incidence of heart failure and for echocardiographic measures signifying subclinical heart failure.

Design Post-hoc, longitudinal and cross-sectional analyses of a prospective cohort study where data were collected in 4-year intervals since 1971.

Settings The population-based Framingham Offspring Study.

Participants 4989 adults (mean age 36 years, 52% women) free of clinical heart failure at baseline.

Outcome measures Incident heart failure, echocardiographic measures of left ventricular systolic dysfunction, dilatation and hypertrophy.

Results Participants with gout (n=228) had two to three times higher incidence of clinical heart failure and echocardiographic measures of systolic dysfunction compared with those without. In Cox regression analyses, gout was associated with an adjusted HR of 1.74 (95% CI 1.03 to 2.93) for incident heart failure and RRs of 3.70 (95% CI 1.68 to 8.16) for abnormally low left ventricular ejection fraction and of 3.60 (95% CI 1.80 to 7.72) for global left ventricle systolic dysfunction. These risk relationships were consistently observed in all clinical subgroups. Overall, participants with gout had greater mortality than those without (adjusted HR 1.58, 95% CI 1.40 to 1.78). Mortality was elevated in subgroup of patients with gout and heart failure (adjusted HR 1.50, 95% CI 1.30 to 1.73) compared to those with heart failure but without gout.

Conclusion Gout is associated with increased risk for clinical heart failure, subclinical measures of systolic dysfunction and mortality.

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  • To cite: Krishnan E. Gout and the risk for incident heart failure and systolic dysfunction. BMJ Open 2012;2:e000282. doi:10.1136/bmjopen-2011-000282

  • Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests EK has received honoraria, research grants, ad-board fees or consulting fees from the following entities: Ardea Biosciences, UCB, Inc., Centocor OrthoBiotech, URL Pharma, Metabolex, Takeda Pharmaceuticals and Savient Pharmaceuticals. In the past 5 years, he has held common stocks of Savient Pharmaceuticals. This manuscript does not discuss any proprietary products manufactured by these companies.

  • Contributors This study was unsponsored. EK possesses raw data, analysis code and will be the guarantor of the scientific integrity of this work.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement I am unable to share data due to data sharing agreements in place with the National Heart, Lung and Blood Institute.

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