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First cardiovascular MRI study in individuals at risk of rheumatoid arthritis detects abnormal aortic stiffness suggesting an anti-citrullinated peptide antibody-mediated role for accelerated atherosclerosis
  1. Graham Fent1,
  2. Kulveer Mankia2,3,
  3. Bara Erhayiem1,
  4. Laura Hunt2,3,
  5. Jacqueline Leong Nam2,3,
  6. Lesley-Anne Bissell3,
  7. James RJ Foley1,
  8. Pei G Chew1,
  9. Louise E Brown1,
  10. John P Greenwood1,
  11. Paul Emery2,3,
  12. Sven Plein1,
  13. Maya H Buch2,3
  1. 1 Multidisciplinary Cardiovascular Research Centre (MCRC) & Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK
  2. 2 University of Leeds, Leeds Institute of Rheumatic and Musculoskeletal Medicine, Leeds, UK
  3. 3 NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK
  1. Correspondence to Professor Maya H Buch, Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds LS2 9JT, UK; m.buch{at}

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Patients with rheumatoid arthritis (RA) are at greater risk of major cardiovascular (CV) events, predominantly due to accelerated atherosclerosis, underpinned by inflammation and RA disease factors and also heart failure.1 Overall, modest event rate has necessitated the use of surrogate CV abnormalities of increased CV risk including arterial stiffness. Increased arterial stiffness is well recognised in established RA,2 with early, similar reports using comprehensive and reliable cardiac MRI (CMRI) in our treatment-naïve, early onset RA cohort.3 Autopsy, histopathological and clinical studies in general population and RA cohorts with and without CV disease (CVD) suggest citrullinated proteins as a mechanism for atherosclerosis, including presence of citrullination within the atherosclerotic plaque of subjects without RA.4 5 We hypothesised that individuals with circulating anti-cyclic citrullinated peptide (CCP) but no systemic inflammation (of RA typically associated with increased CV risk) also demonstrate …

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  • Handling editor Josef S Smolen

  • Contributors Not applicable.

  • Funding GF is funded by a National Institute of Health Research grant (number: 11/117/27). SP is funded by a British Heart Foundation Personal Chair (CH/16/2/32089). The research is supported by the National Institute for Health Research (NIHR) infrastructure at Leeds.

  • Disclaimer The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.

  • Competing interests None declared.

  • Patient consent for publication Not required.

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