Related Experiment Video
Updated: Apr 19, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Evolution of intracranial atherosclerotic disease under modern medical therapy
Thomas W Leung1, Lily Wang, Yannie O Y Soo
1Division of Neurology, Department of Medicine and Therapeutics.
Insights
Intensive medical therapy led to regression or stabilization of most symptomatic intracranial atherosclerotic disease (ICAD) plaques within 12 months. Artery-to-artery embolism was a frequent cause of recurrent strokes in this ICAD cohort.
Area of Science:
- Neurology
- Vascular Neurology
- Cerebrovascular Disease
Background:
- Symptomatic intracranial atherosclerotic disease (ICAD) poses a significant risk for recurrent stroke.
- Understanding the natural evolution of ICAD under contemporary medical management is crucial for optimizing secondary stroke prevention strategies.
Purpose of the Study:
- To investigate the progression and regression of high-grade intracranial atherosclerotic stenosis over 12 months of intensive medical therapy.
- To identify factors influencing plaque evolution and understand mechanisms of recurrent stroke in ICAD patients.
Main Methods:
- A prospective study involving 50 patients with acute stroke due to high-grade (≥70%) ICAD underwent serial 3D rotational angiography over 12 months.
- Intensive medical therapy targeted specific levels for LDL cholesterol, HbA1c, and systolic blood pressure.
- Infarct patterns and microembolic signals were monitored; a historical cohort of 143 ICAD patients served as a reference.
Main Results:
- Intracranial stenosis significantly regressed from a mean of 79% to 63% (p < 0.001) over 12 months.
- Plaque regression (>10% stenosis reduction) occurred in 49% of patients, while 43% remained stable, and 8% progressed.
- Higher baseline HbA1c levels were predictive of plaque regression (OR=4.4; p=0.006).
- Among 6 patients with recurrent strokes related to the stenosis, infarcts often occurred at border zones, with microembolic signals detected in 2.
Conclusions:
- Intensive medical therapy effectively induced regression or quiescence in the majority of symptomatic high-grade ICAD plaques within one year.
- Artery-to-artery thromboembolism leading to border zone infarcts with impaired washout is a key mechanism for stroke recurrence in ICAD.
Objective:
Understanding how symptomatic intracranial atherosclerotic disease (ICAD) evolves with current medical therapy may inform secondary stroke prevention.
Methods:
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.
Results:
Overall, 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.
Interpretation:
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.
Related Concept Videos
01:26Atherosclerosis III: Management
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
01:30Atherosclerosis I: Introduction
01:26Coronary Artery Disease II: Pathophysiology
01:15Ischemic Stroke ll: Pathophysiology
01:30Coronary Artery Disease I: Introduction