{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T02:05:21Z","timestamp":1784081121861,"version":"3.55.0"},"reference-count":54,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T00:00:00Z","timestamp":1422489600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"The Research Grant Council, Hong Kong","award":["470411"],"award-info":[{"award-number":["470411"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Understanding how symptomatic intracranial atherosclerotic disease (ICAD) evolves with current medical therapy may inform secondary stroke prevention.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In a prospective academic\u2010initiated study, we recruited 50 patients (mean age\u2009=\u200963.4\u2009\u00b1\u20099.0 years) with acute strokes attributed to high\u2010grade (\u226570%) intracranial atherosclerotic stenosis for 3\u2010dimensional rotational angiograms before and after intensive medical therapy for 12 months. Treatment targets included low\u2010density lipoprotein\u2009\u2264\u200970mg\/dl, glycosylated hemoglobin (HbA1c)\u2009\u2264\u20096.5%, and systolic blood pressure\u2009\u2264\u2009140 mmHg. We analyzed infarct topography and monitored microembolic signal in recurrent strokes. The reference group was a published cohort of 143 ICAD patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Overall, the stenoses regressed from 79% at baseline (interquartile range [IQR]\u2009=\u200971\u201387%) to 63% (IQR\u2009=\u200954\u201374%) in 1 year (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). Specifically, the qualifying lesions (n\u2009=\u200949) regressed (stenosis reduced &gt;10%) in 24 patients (49%), remained quiescent (stenosis same or \u00b110%) in 21 patients (43%), and progressed (stenosis increased &gt;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\u2009=\u20094.4, 95% confidence interval\u2009=\u20091.4\u201314.5, <jats:italic>p<\/jats:italic>\u2009=\u20090.006). 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>A majority of symptomatic high\u2010grade intracranial plaques had regressed or remained quiescent by 12 months under intensive medical therapy. Artery\u2010to\u2010artery thromboembolism with impaired washout at border zones was a common mechanism in stroke recurrence. 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