Association between the degree of vertebrobasilar stenosis, location, infarction pattern, and QMRA flow state

医学 狭窄 椎动脉 冲程(发动机) 放射科 椎基底动脉供血不足 心脏病学 闭塞 磁共振成像 磁共振血管造影 内科学 机械工程 工程类
作者
Ahmad A. Ballout,Brendan Huang,Seok Yoon Oh,Karen Black,Panagiotis Sideras,Rohan Arora,Shadi Yaghi,Jeffrey M. Katz,Richard Libman
出处
期刊:Journal of Neuroimaging [Wiley]
卷期号:33 (4): 598-605
标识
DOI:10.1111/jon.13112
摘要

Abstract Background and Purpose We aimed to investigate the relationship between the degree and location of vertebrobasilar stenosis and quantitative magnetic resonance angiography (QMRA) distal flow. Methods We retrospectively reviewed patients who presented with acute ischemic stroke with ≥50% stenosis of the extracranial or intracranial vertebral or basilar arteries, and QMRA performed within 1 year of stroke. Standardized techniques were used to measure stenosis and to dichotomize vertebrobasilar distal flow status. Patients were grouped based on the involved artery and the severity of disease. All p ‐values were calculated using chi‐squared analysis and Fisher exact test with statistical significance defined as p < .05. Results Sixty‐nine patients met study inclusion, consisting of 31 with low distal flow and 38 with normal distal flow. The presence of severe stenosis or occlusion was 100% sensitive, but only 47% predictive and 26% specific of a low distal flow state. Bilateral vertebral disease was only 55% sensitive but was 71% predictive and 82% specific of a low‐flow state and was five times and nearly three times more likely to result in a low‐flow state compared to unilateral vertebral disease (14%) and isolated basilar disease (28%), respectively. Conclusions Severe stenosis of ≥70% may mark the minimal threshold required to cause hemodynamic insufficiency in the posterior circulation, but nearly half of these patients may remain hemodynamically sufficient. Bilateral vertebral stenosis resulted in a fivefold increase in QMRA low distal flow status compared to unilateral vertebral disease. These results may have implications in the design of future treatment trials of intracranial atherosclerotic disease.
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