Article Text
Abstract
Objective The present study tested the hypothesis that arterial stiffness will be elevated across overall and specific inflammatory disorders compared with an inflammation-free comparison group.
Methods Adults (n=171 125) aged 40–70 years from the UK Biobank who were cardiovascular disease (CVD) free and who had their arterial stiffness assessed at the time of study recruitment between 2006 and 2010 were included. The main exposure was represented by a global measure of chronic inflammatory disorders. Two inflammatory biomarker measures (eg, leucocytes count, granulocytes count) were included as markers of inflammation severity. The arterial stiffness index assessed by a non-invasive technique represented the study primary outcome measure.
Results A total of 5976 (3%) participants diagnosed with inflammatory disorders and 165 149 participants without an inflammatory disorder had data on arterial stiffness. Adjusted linear regression analyses revealed a 14% increment in mean arterial stiffness for chronic inflammatory disorders (beta coefficient (β) 1.14, 95% CI 1.05 to 1.24, P=0.002) compared with no chronic inflammatory disorder. Arterial stiffness tended to increase (P value=0.031) with tertiles of leucocytes and granulocytes count. For instance, mean arterial stiffness values increased from 1.11 (95% CI 0.96 to 1.29) in the first tertile to 1.17 (95% CI 1.02 to 1.34) in the second tertile, and 1.21 (95% CI 1.05 to 1.39) in the third tertile of leucocytes count. There was evidence for similar associations with some of the most common individual inflammatory disorders, including psoriasis and rheumatoid arthritis.
Conclusion Arterial stiffness was associated with multiple chronic inflammatory disorders. An increasing trend in mean arterial stiffness was also documented with increasing tertiles of different inflammatory biomarkers. Future studies are needed to investigate the discriminant value of arterial stiffness to predict major CVD events within various inflammatory disorders.
- inflammatory markers
- systemic inflammatory diseases
- epidemiology
- aortic and arterial disease
- cardiac imaging and diagnostics
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Footnotes
Contributors The author is a single contributor to developing the study research question, data access, data analysis, and drafting the manuscript and write-up of the final version.
Funding This study has been conducted using the UK Biobank resource. UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwestern Regional Development Agency. It has also had funding from the Welsh Assembly and the British Heart Foundation. AD is supported by the National Institute for Health Research Biomedical Research Center at Guy’s and St Thomas’ National Health Service Foundation Trust and King’s College London.
Disclaimer The views expressed are those of the author and not necessarily those of the National Health Service, the National Institute of Health Research, or the Department of Health.
Competing interests None declared.
Ethics approval Ethical approval was obtained by the data holders from the National Health Service National Research Ethics Service (Ref: 11.NW/0382).
Provenance and peer review Not commissioned; externally peer reviewed.