Abstract

Purpose: To investigate the relationships among the degree of intracranial atherosclerotic stenosis (ICAS), plaque enhancement (PE), and ischemic stroke events (ISEs) using 3. 0 T high-resolution magnetic resonance imaging (HR-MRI).Materials and Methods: Fifty-two ICAS patients who underwent HR-MRI were retrospectively analyzed. The patients were divided into two groups according to the results of whole-brain digital subtraction angiography (DSA): the mild-moderate stenosis group (group MID) and the severe stenosis group (group SEV). According to the onset time of the ISEs, the plaques were divided into the acute/sub-acute phase culprit plaque group (group ACU, within 1 month), the chronic-phase culprit plaque group (group CHR, more than 1 month), and the non-culprit plaque group (group NON). Two neuroradiologists independently measured the signal intensity of PE and pituitary enhancement in the HR-MRI and calculated the ratio of the two indices. According to the ratio, the patients were divided into three groups: the marked enhancement group (group MA), the mild enhancement group (group ME), and the no enhancement plaque group (group NO). The relationships among the degree of ICAS, the degree of PE and ISEs were analyzed.Results: Seventy-two ICAS plaques were identified in 52 patients. The multiple independent samples Kruskal-Wallis H test showed that the differences among group ACU, CHR, and NON were significant in the degree of PE (P = 0.002). Group CHR and group NON were combined as the non-acute phase group (group non-ACU). Group NO and group ME were combined as the non-marked enhancement group (group non-MA). The comparison between group ACU and group non-ACU showed significant differences in the degree of both ICAS (P = 0.014) and PE (P = 0.006) according to the univariate logistic regression. The multivariate logistic regression model was used to analyze the impact of the degree of ICAS and PE on ISEs, and the results showed that severe stenosis (P = 0.036) and marked PE (P = 0.013) were independent risk factors for acute ISEs, respectively.Conclusion: Severe intracranial arterial stenosis and marked plaque enhancement are independent risk factors for acute ischemic stroke events, respectively. The study provides new ideas for further exploring the pathogenesis of stroke caused by intracranial atherosclerotic stenosis.

Highlights

  • Intracranial atherosclerotic disease (ICAD) is the leading cause of global ischemic stroke [1]

  • Certain autopsy results have shown that symptomatic intracranial atherosclerotic stenosis (ICAS) caused by atherosclerotic plaques, the percentage of lipid nuclear within plaques, and neovascularization were significantly related to the occurrence of ischemic stroke [12]

  • We retrospectively analyzed the clinical data of 268 consecutive patients who were admitted to the Department of Neurology, Provincial Hospital Affiliated to Shandong University and who underwent intracranial arterial high-resolution magnetic resonance imaging (HR-MRI) from January 01, 2015 to December 31, 2016

Read more

Summary

Introduction

Intracranial atherosclerotic disease (ICAD) is the leading cause of global ischemic stroke [1]. A study published in 2017 showed that, in patients with mild basal arterial stenosis, the plaques that caused symptomatic pontine infarctions were mostly distributed in the dorsal and bilateral walls of the basilar artery [11]. Certain autopsy results have shown that symptomatic intracranial atherosclerotic stenosis (ICAS) caused by atherosclerotic plaques, the percentage of lipid nuclear within plaques, and neovascularization were significantly related to the occurrence of ischemic stroke [12]. Studies have shown that the degree of PE in patients with moderate-severe intracranial arterial stenosis is significantly related to ischemic stroke [13, 14]. Patients with mild-moderate and severe ICAS were included to further investigate the relationships among the degree of ICAS, the degree of PE and acute ischemic stroke events (ISEs) respectively

Methods
Results
Discussion
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.