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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 …
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.
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