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Association of coronary plaque rupture and atherosclerotic inflammation
1Department of Pathology, Glasgow Royal Infirmary, U.K.
Insights
Inflammation within the fibrous cap of coronary plaques is strongly linked to plaque rupture. This study compared ruptured plaques with intact ones, revealing a significant association between superficial inflammation and rupture events.
Area of Science:
- Cardiovascular Pathology
- Immunohistochemistry
- Atherosclerosis Research
Background:
- Coronary plaque inflammation is a suspected driver of plaque rupture and thrombosis.
- Understanding the specific inflammatory patterns associated with plaque rupture is crucial for cardiovascular disease management.
Purpose of the Study:
- To investigate the association between coronary plaque inflammation and plaque rupture.
- To compare inflammatory cell infiltrates and activation in ruptured plaques versus various control groups.
Main Methods:
- Analysis of 351 coronary plaques from 83 patients across six groups, including ruptured, intact, and control plaques.
- Formalin-fixation, haematoxylin and eosin staining, and serial sectioning for plaque rupture identification.
- Immunohistochemical staining for leukocyte markers (CD68, CD3, CD8) and activation markers (HLA-DR, CD30).
Main Results:
- Significant infiltrates of macrophages (CD68+) and T cells (CD3+, CD8+) were observed adjacent to all plaque ruptures.
- Inflammatory cell activation was indicated by HLA-DR and CD30 labelling.
- Plaque rupture showed a strong statistical association with the severity and frequency of superficial plaque inflammation, but not deep inflammation.
Conclusions:
- Superficial inflammation within the fibrous cap of coronary plaques is particularly associated with plaque rupture.
- These findings support the hypothesis that inflammation plays a key role in the destabilization and rupture of atherosclerotic plaques.
Abstract:
Coronary plaque inflammation may promote plaque rupture and thrombosis. To test this hypothesis, 351 coronary plaques from 83 patients were formalin-fixed and stained with haematoxylin and eosin. There were six groups: (1) ruptured plaques; (2) intact plaques from recently infarcted hearts; (3) plaques from hearts with severe coronary atherosclerosis without identifiable thrombosis; (4) native explanted hearts with severe coronary atherosclerosis; (5) cardiac transplant atherosclerosis; and (6) fatalities unrelated to coronary atherosclerosis. Selected arteries were immunostained for leukocyte markers and serially sectioned to identify plaque rupture. There were infiltrates of CD68-positive macrophages and CD3- and CD8-positive T cells adjacent to all plaque ruptures. Labelling with HLA-DR and CD30 indicated inflammatory cell activation. Plaque rupture was strongly statistically associated with the severity and frequency of superficial plaque inflammation but not that of deep plaque inflammation. Although atherosclerotic inflammation has been identified adjacent to rupture, this is its first comparison with control plaques. These results support the concept that inflammation in the fibrous cap is particularly associated with plaque rupture.