Thrombosis Journal
|
Viewing options:Associated material:Related literature:- Articles citing this article
- Other articles by authors
- Related articles/pages
Tools:Post to:
|
Original basic researchHistological composition and progression of carotid plaqueLiz Andréa Villela Baroncini1 , Antonio Pazin Filho1 , Simone Gusmão Ramos2 , Antonio Roberto Martins3 and Luiz Otavio Murta Jr4  1
Department of Internal Medicine, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, São Paulo, Brazil 2
Department of Pathology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, São Paulo, Brazil 3
Department of Pharmacology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, São Paulo, Brazil 4
Department of Physics and Math, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, University of São Paulo, São Paulo, Brazil author email corresponding author email
Thrombosis Journal 2007,
5:4doi:10.1186/1477-9560-5-4
|
| Published: |
26 February 2007 |
Abstract
Background
To analyse histological composition and progression of carotid plaque.
Methods
Thirty-one patients (22 males, mean age 68.03 ± 7.3 years) admitted for carotid endarterectomy for extracranial high-grade internal carotid artery stenosis (≥ 70% luminal narrowing) were enrolled. The patients were divided into 2 groups according to symptomatology (group I, 17 symptomatic patients; and group II, 14 asymptomatic patients). A histological analysis and inflammatory cell quantification of each excised carotid plaque was made. Nine carotid arteries were removed from human cadavers that were not preselected for carotid artery disease. These specimens were used as a control tissue without any macroscopic signs of atherosclerotic plaques.
Results
Fifty eight percent of all carotid plaques were classified as complex plaque with possible surface defect, hemorrhage or thrombus. The inflammatory cells concentration did not differ between the two groups. All specimens from human cadavers were classified as preatheroma with extracellular lipid pools.
Conclusion
Asymptomatic and symptomatic patients could have the same histological components on their carotid plaques. Fibrotic and calcific plaques could become vulnerable as complex plaques with surface defect, hemorrhage and thrombus could remain silent. Asymptomatic carotid stenosis should be followed close with no invasive diagnostic methods and clinical evaluation. |