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Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery
Published on: July 31, 2014
Middle cerebral artery atherosclerosis: histological comparison between plaques associated with and not associated
Xiang Yan Chen1, Ka Sing Wong, Wynnie Wai Man Lam
1Department of Medicine and Therapeutics, Chinese University of Hong Kong, Shatin, Hong Kong SAR, China. Fiona.xy2000@gmail.com
Background:
Atherosclerotic stenosis of large intracranial arteries, especially the middle cerebral artery (MCA), is a common cause of stroke in Chinese patients. We aimed to describe the morphological features of atherosclerotic stenosis in the MCA and to investigate their relationship with cerebral infarcts from a postmortem series.
Methods:
We studied the morphological features of the MCAs in consecutive postmortem adults aged 45 years or above. The following parameters were evaluated by a single observer blinded to the clinical history: (1) thickness of fibrous cap; (2) extent of lipid area; (3) degree of luminal stenosis; (4) presence of intraplaque hemorrhage, neovasculature, thrombus and calcification. A semiquantitative assessment of macrophage and T lymphocyte infiltration was made by immunohistochemical staining for CD68 and CD45RO.
Results:
Seventy-six cases were recruited. Atherosclerotic plaques of more than 40% cross-sectional area luminal narrowing stenosis were found in 69 MCAs (45.4%, 69/152). The results demonstrated that the degree of luminal stenosis, the percentage of the plaques containing more than 40% lipid area and the prevalence of intraplaque hemorrhage, neovasculature and thrombus were higher in those plaques associated with infarct, and the mean index of both CD45RO and CD68 was higher among those associated with infarct (p < 0.01). Binary logistic regression showed that stenosis (p = 0.003; odds ratio, OR = 1.050), lipid area (p = 0.048, OR = 1.698) and presence of neovasculature (p = 0.040, OR = 3.471) were independent risk factors of MCA infarcts.
Conclusions:
Luminal stenosis caused by atherosclerotic plaque, percentage of lipid area and presence of intraplaque neovasculature may play a key role in leading to ischemic stroke.
Insights
Atherosclerotic plaques in the middle cerebral artery (MCA) with significant stenosis, large lipid areas, and neovasculature are linked to cerebral infarcts. These features, along with inflammation, are key risk factors for stroke.
Area of Science:
- Neurology
- Pathology
- Vascular Biology
Background:
- Atherosclerotic stenosis of large intracranial arteries, particularly the middle cerebral artery (MCA), is a significant cause of stroke in Chinese populations.
- Understanding the morphological characteristics of MCA atherosclerotic stenosis is crucial for stroke prevention and treatment.
Purpose of the Study:
- To describe the morphological features of atherosclerotic stenosis in the middle cerebral artery (MCA).
- To investigate the relationship between MCA atherosclerotic plaque morphology and cerebral infarcts in a postmortem study.
Main Methods:
- Examined morphological features of MCAs from 76 postmortem adults (≥45 years).
- Evaluated plaque characteristics: fibrous cap thickness, lipid area, luminal stenosis, intraplaque hemorrhage, neovasculature, thrombus, and calcification.
- Assessed macrophage (CD68) and T lymphocyte (CD45RO) infiltration via immunohistochemistry.
Main Results:
- Atherosclerotic plaques causing >40% luminal stenosis were found in 45.4% of MCAs.
- Plaques associated with infarcts showed higher luminal stenosis, larger lipid areas, and more intraplaque hemorrhage, neovasculature, and thrombus.
- Higher CD45RO and CD68 indices were observed in plaques linked to infarcts (p < 0.01).
- Independent risk factors for MCA infarcts included stenosis (OR=1.050), lipid area (OR=1.698), and neovasculature (OR=3.471).
Conclusions:
- Luminal stenosis, lipid area percentage, and intraplaque neovasculature are key contributors to atherosclerotic MCA plaque-related ischemic stroke.
- Inflammatory markers (CD68, CD45RO) correlate with infarct presence, highlighting the role of inflammation in plaque instability and stroke.
