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Brief communication
QRISK3 improves detection of cardiovascular disease risk in patients with systemic lupus erythematosus
  1. Nicola Edwards1,
  2. Alexander W W Langford-Smith1,
  3. Benjamin J Parker2,3,
  4. Ian N Bruce2,3,
  5. John A Reynolds2,3,
  6. M Yvonne Alexander1,
  7. Eoghan M McCarthy2 and
  8. Fiona L Wilkinson1
  1. 1 Translational Cardiovascular Science, The Centre for Bioscience, Manchester Metropolitan University, Manchester, UK
  2. 2 NIHR Manchester Musculoskeletal Biomedical Research Centre, Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
  3. 3 Centre for Musculoskeletal Research, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK
  1. Correspondence to Dr Fiona L Wilkinson; F.Wilkinson{at}mmu.ac.uk

Abstract

Objective 10-year cardiovascular disease (CVD) risk scores are calculated using algorithms, including Framingham (worldwide) and QRISK2 (UK). Recently, an updated QRISK3 model was introduced, which considers new variables including SLE and steroid prescription, not included in QRISK2 and Framingham algorithms. We sought to determine the extent to which QRISK3 improves identification of high-risk patients with SLE and whether the score relates to standard and novel markers of SLE-specific endothelial dysfunction.

Methods Framingham and QRISK2/3 scores were calculated in patients with SLE (n=109) and healthy controls (n=29) using clinical measures. In a smaller cohort (n=58), markers of inflammation and endothelial dysfunction, including CD144+ endothelial microvesicles (EMVs), triglycerides, vascular cell adhesion molecule (VCAM) and high-sensitivity C reactive protein (hsCRP) were quantified by flow cytometry and ELISA, respectively.

Results Patients with SLE demonstrated significantly higher QRISK3 scores than controls (5.0%vs0.3%, p<0.001). 21/109 patients with SLE (19%) and 24/109(22%) were newly identified as being at high risk of a CV event when using QRISK3 versus QRISK2 (29vs8patients) and QRISK3 versus Framingham (29vs5patients; p<0.001), respectively. These ‘new QRISK3’ patients with SLE were more likely to have lupus nephritis, be anticardiolipin antibody positive, currently prescribed corticosteroids, had a higher Body Mass Index and systolic blood pressure (BP) than low-risk patients with SLE. Rates of antiplatelet (8/21) and statin use (5/21) were low in the new QRISK3 group. EMVs, hsCRP and triglyceride levels were significantly higher in new QRISK3 patientscompared with low-risk patients with SLE (p<0.05). Furthermore, pulse wave velocity and VCAM were significantly elevated in all high versus low QRISK3 patients.

Conclusions QRISK3 captures significantly more patients with SLE with an elevated 10-year risk of developing CVD, which is associated with measures of endothelial dysfunction; EMVs and systolic BP. The adoption of QRISK3 will enhance management of CVD risk in patients with SLE for improved outcome.

  • Cardiovascular risk
  • SLE
  • EMVs
  • QRISK2
  • QRISK3
  • Framingham

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/lupus-2018-000272

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    Footnotes

    • NE and AWWL-S contributed equally.

    • Contributors All authors included on this paper fulfil the criteria of authorship.

    • Funding IB is an NIHR Senior Investigator and is funded by Arthritis Research UK, the National Institute for Health Research Manchester Biomedical Research Centre and the NIHR/Wellcome Trust Manchester Clinical Research Facility. The views expressed in this publication are those of the authors and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health. BP is supported by National Institute for Health Research Manchester Biomedical Research Centre and the NIHR/Wellcome Trust Manchester Clinical Research Facility. This work was also supported by Lupus UK grant funding.

    • Competing interests None declared.

    • Patient consent Obtained.

    • Ethics approval North West Reference numbers 11/NW/0090 and 13/NW/0564.

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