Carotid rupture and intraplaque hemorrhage: immunophenotype and role of cells involved
- PMID: 9842026
- DOI: 10.1016/s0002-8703(98)70169-3
Carotid rupture and intraplaque hemorrhage: immunophenotype and role of cells involved
Abstract
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.
Comment in
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When neoangiogenesis ricochets.Am Heart J. 1998 Dec;136(6):937-9. doi: 10.1016/s0002-8703(98)70144-9. Am Heart J. 1998. PMID: 9842001 No abstract available.
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