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Extended report
Explaining the cardiovascular risk associated with rheumatoid arthritis: traditional risk factors versus markers of rheumatoid arthritis severity
  1. Daniel H Solomon1,
  2. Joel Kremer2,
  3. Jeffrey R Curtis3,
  4. Marc C Hochberg4,
  5. George Reed5,
  6. Peter Tsao6,
  7. Michael E Farkouh7,
  8. Soko Setoguchi6,
  9. Jeffrey D Greenberg8
  1. 1Division of Rheumatology, Brigham and Women's Hospital, 75 Francis Street, Boston, USA
  2. 2Division of Rheumatology, Albany Medical College (JK), USA
  3. 3Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham (JRC), USA
  4. 4Division of Rheumatology and Clinical Immunology, Department of Medicine and Division of Gerontology, Department of Epidemiology and Preventive Medicine, University of Maryland School of Medicine (MCH), Baltimore, USA
  5. 5University of Massachusetts, USA
  6. 6Brigham and Women's Hospital (DHS and PT), USA
  7. 7Clinical Trials Unit, Mount Sinai Heart (MEF), One Gustave L Levy Place, New York, USA
  8. 8Division of Rheumatology, New York University School of Medicine (JDG), NYU Hospital for Joint Diseases, New York, USA
  1. Correspondence to Daniel H Solomon, Division of Rheumatology, Brigham and Women's Hospital, 75 Francis Street, Boston Massachusetts 02115, USA; dhsolomon{at}partners.org

Abstract

Background Cardiovascular (CV) disease has a major impact on patients with rheumatoid arthritis (RA), however, the relative contributions of traditional CV risk factors and markers of RA severity are unclear. The authors examined the relative importance of traditional CV risk factors and RA markers in predicting CV events.

Methods A prospective longitudinal cohort study was conducted in the setting of the CORRONA registry in the USA. Baseline data from subjects with RA enrolled in the CORRONA registry were examined to determine predictors of CV outcomes, including myocardial infarction, stroke or transient ischemic attack. Possible predictors were of two types: traditional CV risk factors and markers of RA severity. The discriminatory value of these variables was assessed by calculating the area under the receiver operating characteristic curve (c-statistic) in logistic regression. The authors then assessed the incidence rate for CV events among subjects with an increasing number of traditional CV risk factors and/or RA severity markers.

Results The cohort consisted of 10 156 patients with RA followed for a median of 22 months. The authors observed 76 primary CV events during follow-up for a composite event rate of 3.98 (95% CI 3.08 to 4.88) per 1000 patient-years. The c-statistic improved from 0.57 for models with only CV risk factors to 0.67 for models with CV risk factors plus age and gender. The c-statistic improved further to 0.71 when markers of RA severity were also added. The incidence rate for CV events was 0 (95% CI 0 to 5.98) for persons without any CV risk factors or markers of RA severity, while in the group with two or more CV risk factors and three or more markers of RA severity the incidence was 7.47 (95% CI 4.21 to 10.73) per 1000 person-years.

Conclusions Traditional CV risk factors and markers of RA severity both contribute to models predicting CV events. Increasing numbers of both types of factors are associated with greater risk.

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Footnotes

  • Support: There was no specific support for these analyses. CORRONA has received general support in the last two years from Abbott, Amgen, BMS, Centocor, Genentech, Lilly and Roche. Dr. Solomon receives salary support from research grants from the NIH (AR AR055989 and AR 047782), AHRQ, the Arthritis Foundation, Abbott and Amgen. Jeffrey Curtis receives salary support from NIH (AR053351). Dr. Farkouh receives salary support from the NIH (HL071988 and HL092989). Dr Greenberg receives salary support from the NIH (K23AR054412) and the Arthritis Foundation.

  • Funding Other Funders: Abbott, Amgen, BMS, Centocor, Genentech, Lilly and Roche.

  • Competing interest CORRONA has received general support in the last two years from Abbott, Amgen, BMS, Centocor, Genentech, Lilly and Roche. Dr. Solomon receives salary support from research grants from the NIH (AR AR055989 and AR 047782), AHRQ, the Arthritis Foundation, Abbott and Amgen. Jeffrey Curtis receives salary support from NIH (AR053351). Dr Greenberg receives salary support from the NIH (K23AR054412) and the Arthritis Foundation.

  • Patient consent Obtained.

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

  • Ethics approval This study was conducted with the approval of the CORRONA.