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Leukocyte count is associated with reduced endothelial reactivity

Leukocyte count has been associated with cardiovascular and cerebrovascular disease in several studies. We hypothesized that white blood cell count is associated with endothelial reactivity. Leukocyte count was measured in a sample of stroke-free community participants undergoing brachial artery tes...

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Published in:Atherosclerosis 2005-08, Vol.181 (2), p.329-338
Main Authors: Elkind, Mitchell S.V., Sciacca, Robert R., Boden-Albala, Bernadette, Tondella, Maria Lucia C., Feikin, Daniel R., Fields, Barry S., Sacco, Ralph L., Tullio, Marco R. Di, Homma, Shunichi
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Language:English
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Summary:Leukocyte count has been associated with cardiovascular and cerebrovascular disease in several studies. We hypothesized that white blood cell count is associated with endothelial reactivity. Leukocyte count was measured in a sample of stroke-free community participants undergoing brachial artery testing for endothelial reactivity. Flow-mediated dilation (FMD) during reactive hyperemia was assessed in each subject using high-resolution B-mode ultrasound. Multivariate linear regression was used to calculate the effect of leukocyte count on endothelial reactivity after adjusting for potential confounding factors. Mean age of the 868 participants was 66.7 ± 8.8 years; 57% were women. Mean leukocyte count was (6.1 ± 1.8) × 10 9/L. Each unit increase in leukocyte count was associated with a mean 0.18% decrease in FMD ( p = 0.01). After adjusting for other atherosclerosis risk factors, including age, sex, hypertension, diabetes, hyperlipidemia, and smoking, the relationship persisted (mean decrease in FMD per unit leukocyte count = 0.17%, p = 0.02). There was a linear decrease in FMD by quartile of leukocyte count ( p = 0.0014). The effect of leukocyte count on FMD was greater for women, those under age 70, and non-diabetics. Relative elevations in leukocyte count are associated with a reduction in brachial artery endothelial reactivity. These findings are consistent with current hypotheses regarding the inflammatory or infectious etiology of risk of atherosclerosis and stroke, but also suggest interactions with demographic and other risk factors.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2005.01.013