Temporal Changes in Symptomatic Intracranial Arterial Disease: A Longitudinal High-Resolution Vessel Wall Imaging Study

Dong-Wan Kang^1,2Jonguk Kim³Do Yeon Kim^1,4,5Sung Hyun Baik⁶Cheolkyu Jung⁶Bijoy K Menon⁷Jae Won Song⁸MOON-KU HAN¹Hee-Joon Bae¹Beom Joon Kim^1*

• ¹Department of Neurology, Seoul National University Bundang Hospital, Seongnam-si, Republic of Korea
• ²Department of Neurosurgery, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi, Republic of Korea
• ³Department of Neurology, Inha University Hospital, Incheon, Republic of Korea
• ⁴Department of Public Health, Seoul National University Bundang Hospital, Seongnam-si, Republic of Korea
• ⁵Department of Neurology, Gyeonggi Provincial Medical Center Icheon Hospital, Icheon-si, Gyeonggi, Republic of Korea
• ⁶Department of Radiology, Seoul National University Bundang Hospital, Seongnam-si, Republic of Korea
• ⁷Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
• ⁸Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA, United States

Introduction: The temporal dynamics of the vessel wall in intracranial arterial disease (ICAD) may differ depending on the etiology. We investigated temporal changes in narrowed intracranial arteries after ischemic stroke using serial high-resolution vessel wall imaging (HR-VWI).Methods: We retrospectively recruited patients with ICAD-related ischemic stroke who underwent two or more HR-VWI scans. The lumen area (LA), total vessel area (TVA), and enhancing area (EA) of the narrowest part of the culprit lesion were manually segmented. Degree of stenosis was estimated as [1-LA/TVA]×100(%), the enhancing proportion as EA/TVA×100(%), and enhancement ratio as (T1GDlesion/T1GDref)/(T1lesion/T1ref). Linear mixed models were used to investigate temporal changes in these parameters and whether such changes differed by etiologies.Results: Of a total of 208 patients, ICAD-related stroke was caused by atherosclerosis (69%), arterial dissection (24%), vasculitis (3%), moyamoya disease (1%), and other (2%). The median follow-up was 319 [IQR, days. HR-VWI imaging parameters, namely, degree of stenosis, enhancing proportion, and enhancement ratio showed a trend to decrease over time. Patients with intracranial dissection as a cause of intracranial narrowing showed a faster reduction in degree of stenosis and enhancing proportion vs. when such narrowing was identified as due to atherosclerosis (β [95% C.I.], -0.59%[-0.80%~-0.38%] and -0.81%[-1.23%~-0.39%], respectively, both P<0.01). The enhancement ratio did not change over time in dissection, while it decreased in atherosclerosis (-0.01[-0.02~0], P=0.04).Conclusions: Intracranial vessel narrowing in patients with ischemic stroke changes over time with different stroke etiologies having their own unique temporal patterns.