Evolution of intracranial atherosclerotic disease under modern medical therapy. Issue 3 (29th January 2015)

• Record Type: Journal Article
• Authors: Leung, Thomas W.; Wang, Lily; Soo, Yannie O. Y.; Ip, Vincent H. L.; Chan, Anne Y. Y.; Au, Lisa W. C.; Fan, Florence S. Y.; Lau, Alex Y. L.; Leung, Howan; Abrigo, Jill; Wong, Adrian; Mok, Vincent C. T.; Ng, Ping Wing; Tsoi, Tak Hong; Li, Siu Hung; Man, Celeste B. L.; Fong, Wing Chi; Wong, Ka Sing; Yu, Simon C. H.
• Is Part Of: Annals of neurology. Volume 77:Issue 3(2015:Mar.)
• Page Start: 478
• Page End: 486
• Publication Date: 2015-01-29
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.24340
• Languages: English
• ISSNs: 0364-5134

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="ana24340-sec-0001" sec-type="section"> <title>Objective</title> <p>Understanding how symptomatic intracranial atherosclerotic disease (ICAD) evolves with current medical therapy may inform secondary stroke prevention.</p> </sec> <sec id="ana24340-sec-0002" sec-type="section"> <title>Methods</title> <p>In a prospective academic‐initiated study, we recruited 50 patients (mean age = 63.4 ± 9.0 years) with acute strokes attributed to high‐grade (≥70%) intracranial atherosclerotic stenosis for 3‐dimensional rotational angiograms before and after intensive medical therapy for 12 months. Treatment targets included low‐density lipoprotein ≤ 70mg/dl, glycosylated hemoglobin (HbA1c) ≤ 6.5%, and systolic blood pressure ≤ 140 mmHg. We analyzed infarct topography and monitored microembolic signal in recurrent strokes. The reference group was a published cohort of 143 ICAD patients.</p> </sec> <sec id="ana24340-sec-0003" sec-type="section"> <title>Results</title> <p>Overall, the stenoses regressed from 79% at baseline (interquartile range [IQR] = 71–87%) to 63% (IQR = 54–74%) in 1 year (<italic>p</italic> < 0.001). Specifically, the qualifying lesions (n = 49) regressed (stenosis reduced >10%) in 24 patients (49%), remained quiescent (stenosis same or ±10%) in 21 patients (43%), and progressed (stenosis increased >10%) in 4 patients (8%). There was no difference in intensity of risk factor control between groups of diverging clinical or angiographic outcomes. Higher HbA1c at baseline predicted plaque regression at 1 year (odds ratio = 4.4, 95% confidence interval = 1.4–14.5, <italic>p</italic> = 0.006). Among the 6 patients with recurrent strokes pertaining to the qualifying stenosis, 5 patients had solitary or rosarylike acute infarcts along the internal or anterior border zones, and 2 patients showed microembolic signals in transcranial Doppler ultrasound.</p> </sec> <sec id="ana24340-sec-0004" sec-type="section"> <title>Interpretation</title> <p>A majority of symptomatic high‐grade intracranial plaques had regressed or remained quiescent by 12 months under intensive medical therapy. Artery‐to‐artery thromboembolism with impaired washout at border zones was a common mechanism in stroke recurrence. Ann Neurol 2015;77:478–486</p> </sec> </abstract>