The histologic characteristics of primary and restenotic carotid plaque

John M. Marek, Cynthia Koehler, Marie L. Aguirre, Alex Westerband, Andrew T. Gentile, Joseph L Mills, Glenn C. Hunter

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Background. Although smooth muscle cell proliferation is a prominent feature of restenosis in experimental models, the role of cellular proliferation in the initiation and progression of carotid restenosis is not well documented. Methods. Between 1985 and 1995, 35 carotid endarterectomies (CEA) in 34 patients were performed for restenosis. Patient risk factors, cerebrovascular symptoms, and operative findings were recorded. Tissue specimens from 29 of these cases and 14 original specimens from the same patient were examined by light microscopy (H and E, trichrome, elastochrome, and Alcian blue) and immunohistochemistry (α actin, CD 68, vWF, and proliferating nuclear cell antigen (PCNA)) in order to determine the morphologic characteristics and cellular proliferative activity of the plaque. Results. Hemodynamically significant recurrent stenosis occurred in the 29 patients (69% symptomatic) between 2 months and 30 years after their initial CEAs. Eleven of 29 (38%) lesions were removed early (<3 years). Recurrent lesions were characterized based on their components as neointimal thickening, 24% (7/29), neointimal thickening and atherosclerosis, 55% (16/29), or atherosclerotic, 21% (6/29). Nineteen of 29 (66%) plaques were complicated by mural thrombus or intraplaque hemorrhage. An inflammatory cell infiltrate consisting of macrophages and T lymphocytes was observed adjacent to areas of recurrent atherosclerosis and macrophages in regions of intimal thickening. Although infrequently present (generally 1-3% of cells) PCNA- positive cells were detected in 41% (12 of 29) of recurrent and 14% (2 of 14) of primary plaques. No PCNA-positive cells were detected in the remaining 67% (29 of 43) of specimens. There was no statistical difference in the number of PCNA-positive cells in early recurrent lesions compared to those recurring after 3 years (36% vs 44%). PCNA immunoreactivity when present was most commonly noted in macrophages associated with thrombus or atheroma rather than smooth muscle cells. Conclusions. Although evidence of cellular proliferation was observed in 40% of recurrent carotid endarterectomy lesions, the proliferation rate was low (1-3%) and unrelated to the time interval of recurrence. Proliferative activity was most pronounced in macrophages associated with intraplaque hemorrhage or atheroma. The contribution of inflammatory cells to the biologic behavior of restenotic lesions requires further investigation.

Original languageEnglish (US)
Pages (from-to)27-33
Number of pages7
JournalJournal of Surgical Research
Volume74
Issue number1
DOIs
StatePublished - Jan 1998

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Proliferating Cell Nuclear Antigen
Macrophages
Carotid Endarterectomy
Cell Proliferation
Atherosclerotic Plaques
Smooth Muscle Myocytes
Atherosclerosis
Thrombosis
Tunica Intima
Hemorrhage
Alcian Blue
Actins
Microscopy
Pathologic Constriction
Theoretical Models
Immunohistochemistry
T-Lymphocytes
Light
Recurrence

Keywords

  • Carotid plaque
  • Cellular proliferation
  • Restenosis

ASJC Scopus subject areas

  • Surgery

Cite this

Marek, J. M., Koehler, C., Aguirre, M. L., Westerband, A., Gentile, A. T., Mills, J. L., & Hunter, G. C. (1998). The histologic characteristics of primary and restenotic carotid plaque. Journal of Surgical Research, 74(1), 27-33. https://doi.org/10.1006/jsre.1997.5222

The histologic characteristics of primary and restenotic carotid plaque. / Marek, John M.; Koehler, Cynthia; Aguirre, Marie L.; Westerband, Alex; Gentile, Andrew T.; Mills, Joseph L; Hunter, Glenn C.

In: Journal of Surgical Research, Vol. 74, No. 1, 01.1998, p. 27-33.

Research output: Contribution to journalArticle

Marek, JM, Koehler, C, Aguirre, ML, Westerband, A, Gentile, AT, Mills, JL & Hunter, GC 1998, 'The histologic characteristics of primary and restenotic carotid plaque', Journal of Surgical Research, vol. 74, no. 1, pp. 27-33. https://doi.org/10.1006/jsre.1997.5222
Marek, John M. ; Koehler, Cynthia ; Aguirre, Marie L. ; Westerband, Alex ; Gentile, Andrew T. ; Mills, Joseph L ; Hunter, Glenn C. / The histologic characteristics of primary and restenotic carotid plaque. In: Journal of Surgical Research. 1998 ; Vol. 74, No. 1. pp. 27-33.
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title = "The histologic characteristics of primary and restenotic carotid plaque",
abstract = "Background. Although smooth muscle cell proliferation is a prominent feature of restenosis in experimental models, the role of cellular proliferation in the initiation and progression of carotid restenosis is not well documented. Methods. Between 1985 and 1995, 35 carotid endarterectomies (CEA) in 34 patients were performed for restenosis. Patient risk factors, cerebrovascular symptoms, and operative findings were recorded. Tissue specimens from 29 of these cases and 14 original specimens from the same patient were examined by light microscopy (H and E, trichrome, elastochrome, and Alcian blue) and immunohistochemistry (α actin, CD 68, vWF, and proliferating nuclear cell antigen (PCNA)) in order to determine the morphologic characteristics and cellular proliferative activity of the plaque. Results. Hemodynamically significant recurrent stenosis occurred in the 29 patients (69{\%} symptomatic) between 2 months and 30 years after their initial CEAs. Eleven of 29 (38{\%}) lesions were removed early (<3 years). Recurrent lesions were characterized based on their components as neointimal thickening, 24{\%} (7/29), neointimal thickening and atherosclerosis, 55{\%} (16/29), or atherosclerotic, 21{\%} (6/29). Nineteen of 29 (66{\%}) plaques were complicated by mural thrombus or intraplaque hemorrhage. An inflammatory cell infiltrate consisting of macrophages and T lymphocytes was observed adjacent to areas of recurrent atherosclerosis and macrophages in regions of intimal thickening. Although infrequently present (generally 1-3{\%} of cells) PCNA- positive cells were detected in 41{\%} (12 of 29) of recurrent and 14{\%} (2 of 14) of primary plaques. No PCNA-positive cells were detected in the remaining 67{\%} (29 of 43) of specimens. There was no statistical difference in the number of PCNA-positive cells in early recurrent lesions compared to those recurring after 3 years (36{\%} vs 44{\%}). PCNA immunoreactivity when present was most commonly noted in macrophages associated with thrombus or atheroma rather than smooth muscle cells. Conclusions. Although evidence of cellular proliferation was observed in 40{\%} of recurrent carotid endarterectomy lesions, the proliferation rate was low (1-3{\%}) and unrelated to the time interval of recurrence. Proliferative activity was most pronounced in macrophages associated with intraplaque hemorrhage or atheroma. The contribution of inflammatory cells to the biologic behavior of restenotic lesions requires further investigation.",
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AU - Mills, Joseph L

AU - Hunter, Glenn C.

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N2 - Background. Although smooth muscle cell proliferation is a prominent feature of restenosis in experimental models, the role of cellular proliferation in the initiation and progression of carotid restenosis is not well documented. Methods. Between 1985 and 1995, 35 carotid endarterectomies (CEA) in 34 patients were performed for restenosis. Patient risk factors, cerebrovascular symptoms, and operative findings were recorded. Tissue specimens from 29 of these cases and 14 original specimens from the same patient were examined by light microscopy (H and E, trichrome, elastochrome, and Alcian blue) and immunohistochemistry (α actin, CD 68, vWF, and proliferating nuclear cell antigen (PCNA)) in order to determine the morphologic characteristics and cellular proliferative activity of the plaque. Results. Hemodynamically significant recurrent stenosis occurred in the 29 patients (69% symptomatic) between 2 months and 30 years after their initial CEAs. Eleven of 29 (38%) lesions were removed early (<3 years). Recurrent lesions were characterized based on their components as neointimal thickening, 24% (7/29), neointimal thickening and atherosclerosis, 55% (16/29), or atherosclerotic, 21% (6/29). Nineteen of 29 (66%) plaques were complicated by mural thrombus or intraplaque hemorrhage. An inflammatory cell infiltrate consisting of macrophages and T lymphocytes was observed adjacent to areas of recurrent atherosclerosis and macrophages in regions of intimal thickening. Although infrequently present (generally 1-3% of cells) PCNA- positive cells were detected in 41% (12 of 29) of recurrent and 14% (2 of 14) of primary plaques. No PCNA-positive cells were detected in the remaining 67% (29 of 43) of specimens. There was no statistical difference in the number of PCNA-positive cells in early recurrent lesions compared to those recurring after 3 years (36% vs 44%). PCNA immunoreactivity when present was most commonly noted in macrophages associated with thrombus or atheroma rather than smooth muscle cells. Conclusions. Although evidence of cellular proliferation was observed in 40% of recurrent carotid endarterectomy lesions, the proliferation rate was low (1-3%) and unrelated to the time interval of recurrence. Proliferative activity was most pronounced in macrophages associated with intraplaque hemorrhage or atheroma. The contribution of inflammatory cells to the biologic behavior of restenotic lesions requires further investigation.

AB - Background. Although smooth muscle cell proliferation is a prominent feature of restenosis in experimental models, the role of cellular proliferation in the initiation and progression of carotid restenosis is not well documented. Methods. Between 1985 and 1995, 35 carotid endarterectomies (CEA) in 34 patients were performed for restenosis. Patient risk factors, cerebrovascular symptoms, and operative findings were recorded. Tissue specimens from 29 of these cases and 14 original specimens from the same patient were examined by light microscopy (H and E, trichrome, elastochrome, and Alcian blue) and immunohistochemistry (α actin, CD 68, vWF, and proliferating nuclear cell antigen (PCNA)) in order to determine the morphologic characteristics and cellular proliferative activity of the plaque. Results. Hemodynamically significant recurrent stenosis occurred in the 29 patients (69% symptomatic) between 2 months and 30 years after their initial CEAs. Eleven of 29 (38%) lesions were removed early (<3 years). Recurrent lesions were characterized based on their components as neointimal thickening, 24% (7/29), neointimal thickening and atherosclerosis, 55% (16/29), or atherosclerotic, 21% (6/29). Nineteen of 29 (66%) plaques were complicated by mural thrombus or intraplaque hemorrhage. An inflammatory cell infiltrate consisting of macrophages and T lymphocytes was observed adjacent to areas of recurrent atherosclerosis and macrophages in regions of intimal thickening. Although infrequently present (generally 1-3% of cells) PCNA- positive cells were detected in 41% (12 of 29) of recurrent and 14% (2 of 14) of primary plaques. No PCNA-positive cells were detected in the remaining 67% (29 of 43) of specimens. There was no statistical difference in the number of PCNA-positive cells in early recurrent lesions compared to those recurring after 3 years (36% vs 44%). PCNA immunoreactivity when present was most commonly noted in macrophages associated with thrombus or atheroma rather than smooth muscle cells. Conclusions. Although evidence of cellular proliferation was observed in 40% of recurrent carotid endarterectomy lesions, the proliferation rate was low (1-3%) and unrelated to the time interval of recurrence. Proliferative activity was most pronounced in macrophages associated with intraplaque hemorrhage or atheroma. The contribution of inflammatory cells to the biologic behavior of restenotic lesions requires further investigation.

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