Highlights
- •Vertebrobasilar artery dissection (VBD) have unknown mechanism.
- •More than 1/4 of VBD stroke have high leukocyte and neutrophil counts.
- •Higher leukocyte/neutrophil counts in VBD than large artery atherosclerosis stroke
Abstract
Introduction
Vertebrobasilar artery dissection(VBD) is a common etiology of posterior circulation
stroke(PCS). However, the etiology of VBD itself remains unclear. The present study
aimed to test whether inflammation is involved in the mechanism of VBD by evaluating
its relationship with total and differential leukocyte counts.
Methods
Patients with PCS caused by VBD or by large artery atherosclerosis(LAA) were recruited
between January 1, 2012 and December 31, 2014 from the Taipei Veterans General Hospital.
Age- and sex-matched non-stroke(NS) volunteers were also included. Univariate and
multivariate analyses were performed to compare total/differential leukocyte counts
among VBD, LAA, and NS groups.
Results
One-hundred-one patients with VBD [average age: 64.8(15.1) years; 77(76.2%) males],
70 with LAA [average age: 73.9(10.6) years; 44(62.9%) males], and 202 NS [average
age: 64.8(15.1) years; 77(76.2%) males] patients were included in the present study.
Compared with the NS and LAA groups, respectively, the VBD group had significantly
higher total leukocyte and neutrophil counts and frequency of high leukocyte (>10,000 × 106/L) and high neutrophil (>8000 × 106/L) counts. Multivariate analyses, adjusted for age, sex, and vascular risk factors,
showed that the VBD group, compared with the other groups, had an odds-ratio of 5.04
(95% confidence interval:2.43–10.43) and 5.90 (2.70–12.92) with respect to the prevalence
of high leukocyte and high neutrophil counts.
Conclusion
VBD was associated with high leukocyte and neutrophil counts. Our results support
that inflammation and neutrophil-related pathophysiology might be involved in the
mechanism of VBD; however, the causal relationship would need further investigations.
Keywords
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Article info
Publication history
Published online: July 18, 2019
Accepted:
July 17,
2019
Received in revised form:
June 21,
2019
Received:
April 13,
2019
Identification
Copyright
© 2019 Elsevier B.V. All rights reserved.
