Investigating the Association Between Carotid Atherosclerotic Plaque Characteristics And Lacunar Infarction Using
Decheng Meng1, Ran Huo1, Huimin Xu1
1Department of Radiology, Peking University Third Hospital, Beijing, China (D.M., R.H., H.X., Y.L.).
Academic Radiology
|July 22, 2026
Summary
Carotid vulnerable plaque calcification is linked to lacunar infarction (LAC). Increased calcification correlates with mild-to-moderate LAC, while severe LAC is associated with intraplaque hemorrhage and lipid-rich necrotic core volumes.
Area of Science:
- Neurology
- Cardiovascular Medicine
- Radiology
Background:
- Large artery atherosclerosis is increasingly linked to cerebral small vessel disease.
- The specific relationship between carotid vulnerable plaque characteristics and lacunar infarction (LAC) requires further investigation, especially in patients with moderate-to-severe carotid stenosis.
Purpose of the Study:
- To investigate the association between carotid vulnerable plaque features and the presence and severity of lacunar infarction (LAC) in patients with moderate-to-severe carotid stenosis.
Main Methods:
- Patients with symptomatic or asymptomatic moderate-to-severe carotid stenosis underwent carotid MRI and brain MRI.
- Carotid plaque burden and composition were assessed, and LAC presence and severity were determined.
- Logistic regression analysis was used to examine the associations between plaque features and LAC.
Main Results:
- Of 194 patients, 110 (56.7%) had LAC. LAC patients exhibited larger calcification volume and calcified area percentage.
- Mild and moderate LAC were associated with larger calcified area percentages.
- Severe LAC was correlated with higher lipid-rich necrotic core (LRNC) and intraplaque hemorrhage (IPH) volumes.
Conclusions:
- Carotid plaque calcification burden is significantly greater in LAC patients, particularly in mild-to-moderate cases.
- Severe LAC shows stronger correlations with IPH and LRNC volumes.
- These findings suggest that vulnerable plaque characteristics may play distinct pathophysiological roles in patients with severe LAC.
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