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Published on: December 28, 2014
Carotid rupture and intraplaque hemorrhage: immunophenotype and role of cells involved
J Milei1, J C Parodi, G F Alonso
1CARDIOPSIS, Universidad del Salvador and Instituto Cardiovascular de Buenos Aires, Argentina.
Insights
Carotid plaque rupture involves mononuclear cell infiltration. Intraplaque hemorrhage without rupture is linked to extensive plaque vascularization, offering insights into atherosclerosis progression.
Area of Science:
- Cardiovascular Pathology
- Immunohistochemistry
- Atherosclerosis Research
Background:
- Limited immunohistochemical data exists for complicated carotid plaques.
- Cellular components in carotid endarterectomy specimens require detailed analysis.
- Understanding plaque rupture and intraplaque hemorrhage pathogenesis is crucial.
Purpose of the Study:
- To conduct a comprehensive immunohistochemical characterization of complicated carotid plaques.
- To investigate the role of cellular components in plaque rupture.
- To differentiate the cellular mechanisms of plaque rupture versus intraplaque hemorrhage without rupture.
Main Methods:
- Analysis of 165 carotid endarterectomy specimens.
- Immunohistochemical staining for macrophages (CD68+), T-lymphocytes, B-lymphocytes, CD31, and CD34.
- Classification of lipid cores based on vascularization (avascular, mildly vascularized, highly vascularized).
Main Results:
- Ruptured plaques showed significant mononuclear infiltrates (85%) in caps, shoulders, and bases compared to nonruptured plaques (46%).
- Highly vascularized lipid cores were observed in all cases of intraplaque hemorrhage without rupture.
- Neoformed CD34+ vessels, often with surrounding mononuclear infiltrates, were present in 57.5% of plaques, particularly in cases with hemorrhage.
Conclusions:
- Plaque rupture is characterized by mononuclear cell infiltration within the fibrous cap and plaque shoulders.
- Intraplaque hemorrhage without rupture is strongly associated with extensive neovascularization within the lipid core.
- Distinct cellular and vascular features differentiate plaque rupture from intraplaque hemorrhage.
Background:
A complete immunohistochemical characterization in complicated carotid plaques is still lacking. The cellular components of 165 carotid endarterectomy specimens were analyzed to assess their role in the pathogenesis of plaque rupture and intraplaque hemorrhage without rupture.
Methods And Results:
The fibrous caps at the sites of plaque rupture showed CD68+ macrophages, T-lymphocytes, and scarce B-lymphocytes. Ruptured plaques showed mononuclear infiltrates in the caps, shoulders, and bases of the plaques in 85% of the cases. Only 46% of nonruptured plaques showed such infiltrates (P <.0001). Two types of lipid cores were recognized: avascular or mildly vascularized and highly vascularized. The vessels of the latter type reacted with CD31 and CD34. In 57.5% of the cases, the base and the shoulders of the plaques showed neoformed, CD34+ vessels, often surrounded by mononuclear infiltrates. Intraplaque hemorrhage without rupture had highly vascularized lipid cores in all cases. T-lymphocytes and macrophages were in close contact with neoformed vessels.
Conclusions:
Plaque rupture is characterized by mononuclear cell infiltration of the caps, whereas intraplaque hemorrhage without rupture is characterized by extensive vascularization of the plaque.
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