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Published on: August 30, 2020
Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke.
Luigi Giusto Spagnoli1, Alessandro Mauriello, Giuseppe Sangiorgi
1Anatomic Pathology, Department of Cardiovascular Diseases, University of Rome Tor Vergata, Rome, Italy. spagnoli@uniroma2.it
JAMA
|October 21, 2004
Summary
Carotid plaque rupture and thrombosis, along with inflammation, are key drivers of ischemic stroke. These findings highlight the importance of plaque characteristics beyond stenosis in stroke pathogenesis.
Area of Science:
- Neurology
- Cardiovascular Science
- Pathology
Background:
- Ischemic stroke pathogenesis involves factors beyond carotid stenosis severity.
- Carotid plaque composition and complications play a significant role.
Purpose of the Study:
- To investigate the role of carotid plaque rupture and thrombosis in ischemic stroke.
- To analyze these factors in patients undergoing carotid endarterectomy, excluding cardiac embolization or severe circle of Willis stenosis.
Main Methods:
- Histological analysis of 269 carotid plaques from an Interinstitutional Carotid Tissue Bank.
- Plaques were obtained from patients with major stroke, transient ischemic attack (TIA), and asymptomatic individuals.
Main Results:
- Thrombotic carotid plaques with high inflammation were found in 74% of stroke patients vs. 35.2% (TIA) and 14.6% (asymptomatic).
- Acute thrombus, often linked to cap rupture, was prevalent in stroke patients.
- Inflammatory infiltrate (monocytes, macrophages, T cells) was more severe in ruptured plaques of stroke patients.
Conclusions:
- Carotid thrombosis and inflammation are major contributors to ischemic stroke in atherosclerotic disease.
- Plaque rupture and associated inflammation are critical in stroke development.
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