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Lookup NU author(s): Dr Claire WelshORCiD, Dr Carlos Celis Morales
This is the authors' accepted manuscript of an article that has been published in its final definitive form by Lippincott Williams and Wilkins, 2018.
For re-use rights please refer to the publisher's terms and conditions.
© 2018 American Heart Association, Inc. Objective-Elevated white blood cell count is associated with a higher risk of cardiovascular disease (CVD). We aimed to investigate whether specific leukocyte subpopulations, which may more closely indicate a specific inflammatory pathway, are specifically associated with CVD. Approach and Results-Participants (478 259) from UK Biobank with data for white blood cell count were included. Death because of CVD (n=1377) and non-CVD causes (n=8987) occurred during median follow-up time of 7.0 years (interquartile range, 6.3-7.6). In Cox models, deciles of leukocyte counts (lymphocytes, monocytes, neutrophils, eosinophils, and basophils) were examined using the fifth decile as the referent group. Models were stratified by sex and adjusted for a range of classical risk factors. A sensitivity analysis excluded participants with baseline comorbidites and the first 2 years of follow-up. Men (hazard ratio [HR], 1.59; 95% confidence interval, 1.22-2.08) and women (HR, 2.15; 95% confidence interval, 1.38-3.35) in the highest decile of neutrophil count were at higher risk of CVD mortality and nonfatal CVD (men HR, 1.28; 95% confidence interval, 1.16-1.42 and women HR, 1.21; 95% confidence interval, 1.06-1.38). In the sensitivity analysis, the power to investigate CVD mortality was limited, but for both sexes combined, the linear HRs for a 1×109/L cell count increase in white blood cell count and neutrophils, respectively, was 1.05 (1.03-1.07) and 1.07 (1.04-1.11). Conclusions-Among circulating leukocyte subpopulations, neutrophil count in men was most consistently associated with fatal and nonfatal CVD. Further studies of interventions that lower circulating neutrophils, such as canakinumab, are required to investigate causality.
Author(s): Welsh C, Welsh P, Mark PB, Celis-Morales CA, Lewsey J, Gray SR, Lyall DM, Iliodromiti S, Gill JMR, Pell J, Jhund PS, Sattar N
Publication type: Article
Publication status: Published
Journal: Arteriosclerosis, Thrombosis, and Vascular Biology
Year: 2018
Volume: 38
Issue: 6
Pages: 1415-1423
Print publication date: 01/06/2018
Online publication date: 01/06/2018
Acceptance date: 09/04/2018
Date deposited: 17/10/2019
ISSN (print): 1079-5642
ISSN (electronic): 1524-4636
Publisher: Lippincott Williams and Wilkins
URL: https://doi.org/10.1161/ATVBAHA.118.310945
DOI: 10.1161/ATVBAHA.118.310945
PubMed id: 29699973
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