Home LiteratureArticle Details
PMID: 8281670 Published · ppublish English Journal Article

Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology.

Circulation ·Vol. 89 ·No. 1 ·1994-01-00 ·Pages 36-44

van der Wal AC, Becker AE, van der Loos CM, Das PK

Abstract

The study was designed to verify the concept of plaques "at risk" and whether inflammation could play a role in plaque rupture and thrombosis. In 20 patients who had died of acute myocardial infarction, the thrombosed coronary artery was identified and the site of plaque rupture was traced in serial sections. The cellular characteristics of the fibrous cap at the immediate site of rupture were analyzed and compared with the adjacent cap tissue by use of monoclonal antibodies reactive with macrophages, T lymphocytes, and smooth muscle cells. A deep intimal rupture, extending into the lipid core, was encountered in 12 plaques, whereas 8 had superficial erosions only. Ten atherosclerotic plaques had a distinctly attenuated fibrous cap covering a large atheroma, 7 showed a thick fibrocellular cap overlying a lipid pool, and 3 showed a fibrocellular lesion without a clear lipid core. Macrophages, and to a lesser extent T lymphocytes, were the dominant cells at the immediate site of either rupture or superficial erosion in each instance. These sites, moreover, were always characterized by abundant expression of HLA-DR antigens on both inflammatory cells and adjacent smooth muscle cells, suggesting an active inflammatory reaction. In terms of overall cellular composition of the ruptured plaques, the dominant cell types were macrophages and T cells in 11, smooth muscle cells in 3, and mixtures of both in 6. The underlying atherosclerotic plaque morphology in complicated coronary artery lesions causing acute myocardial infarction is heterogeneous with respect to both plaque architecture and cellular composition. However, the immediate site of plaque rupture or erosion is always marked by an inflammatory process. This suggests that inflammation plays a role in destabilizing the fibrous cap tissue and, thus, in enhancing the risk of coronary thrombosis.

MeSH Terms
Coronary Artery Disease/metabolism,pathology Coronary Thrombosis/metabolism,pathology Coronary Vessels/chemistry,pathology HLA-DR Antigens/analysis Humans Immunoenzyme Techniques Inflammation/pathology Macrophages/pathology Middle Aged Muscle, Smooth, Vascular/chemistry,pathology Myocardial Infarction/pathology T-Lymphocytes/pathology Tunica Intima/chemistry,pathology
Chemicals
HLA-DR Antigens
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
van der Wal A C
Department of Cardiovascular Pathology, University of Amsterdam, The Netherlands.
Becker A E
van der Loos C M
Das P K
Article Info
Journal
Circulation
Abbr.
Circulation
ISSN
0009-7322
Published
1994-01-00
Pages
36-44
Language
English
Region
United States
NLM ID
0147763
Subset
IM
Corrections
CommentIn
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]