Evolution of intracranial atherosclerotic disease under modern medical therapy.

ObjectiveUnderstanding how symptomatic intracranial atherosclerotic disease (ICAD) evolves with current medical therapy may inform secondary stroke prevention. MethodsIn a prospective academic-initiated study, we recruited 50 patients (mean age=63.49.0 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 lipoprotein70mg/dl, glycosylated hemoglobin (HbA1c)6.5%, and systolic blood pressure140 mmHg. We analyzed infarct topography and monitored microembolic signal in recurrent strokes. The reference group was a published cohort of 143 ICAD patients. ResultsOverall, the stenoses regressed from 79% at baseline (interquartile range [IQR]=71-87%) to 63% (IQR=54-74%) in 1 year (p<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, p=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. InterpretationA 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