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Published on: January 13, 2012
The carotid bifurcation plaque: pathologic findings associated with cerebral ischemia
Insights
Carotid artery plaques, often fibrous with significant stenosis, develop through pathological changes like intraplaque hemorrhage. Understanding these changes is key for classifying patients and guiding stroke treatment.
Area of Science:
- Neurology
- Vascular Surgery
- Pathology
Background:
- Cervical carotid and vertebral artery embolization or decreased flow cause ischemic stroke.
- Carotid endarterectomy is a surgical procedure to remove plaque from carotid arteries.
Purpose of the Study:
- To analyze pathological findings in carotid plaques from symptomatic patients undergoing endarterectomy.
- To correlate plaque characteristics with preoperative symptoms and long-term outcomes.
Main Methods:
- Detailed analysis of 69 carotid plaques from 50 patients.
- Correlation of gross pathology, microscopy, angiograms, symptoms, and follow-up data.
Main Results:
- Carotid plaques were predominantly fibrous, with 70% showing >70% stenosis.
- Stenoses resulted from intraplaque hemorrhage and atheromatous debris, not just fibrous thickening.
- Ulceration occurred in one-third of plaques; intramural hemorrhage correlated with focal neurologic symptoms.
Conclusions:
- Carotid plaque progression involves fibrointimal thickening and pathological changes, notably intraplaque hemorrhage.
- Non-invasive classification of pathological changes is needed for tailored therapeutic strategies in ischemic stroke.
Abstract:
Embolization from or decreased flow through cervical carotid and vertebral arteries causes ischemic stroke syndromes. Specific pathologic findings were studied in 50 symptomatic patients who underwent 69 carotid endarterectomies. Detailed analyses of their carotid plaques included correlations between photographs of gross specimens, microscopic findings, angiograms, preoperative symptoms and long-term postoperative follow up. Carotid plaques were primarily fibrous with significant (greater than 70%) stenoses encountered in 70% of the arteries. Stenoses were due to simple fibrous thickening in only 20%; the remainder due to intraplaque hemorrhage, atheromatous debris and, least often, luminal thrombus with or without ulceration. Intramural hemorrhage was frequent in plaques associated with focal neurologic symptoms and may have preceded localized collections of atheromatous debris. Ulceration occurred in 1/3 of all plaques, symptomatic or not. It is concluded that the carotid plaques start as fibrointimal thickening evolving to symptomatic stages by the occurrence of one or more of a number of pathologic changes, intraplaque hemorrhage being prominent. A single rational therapeutic regimen seems impossible until patients can be classified according to their pathologic changes diagnosed non-invasively.
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