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Published on: July 1, 2011
Adventitial lymphocytic inflammation in human coronary arteries with intimal atherosclerosis
Fabio Tavora1, Robert Kutys, Ling Li
1Armed Forces Institute of Pathology, Washington, DC, USA.
Insights
Adventitial inflammation, characterized by lymphocyte aggregates and macrophages, is significantly linked to unstable plaque features like rupture and thin caps in coronary arteries. This inflammation increases with arterial stenosis but not calcification.
Area of Science:
- Cardiovascular Pathology
- Immunology
- Atherosclerosis Research
Background:
- The interplay between adventitial inflammation, coronary plaque characteristics, and culprit lesion morphology remains underexplored.
- Understanding these relationships is crucial for diagnosing and managing coronary artery disease.
Purpose of the Study:
- To investigate the association between adventitial inflammation and coronary plaque morphology.
- To determine if adventitial inflammation correlates with plaque instability features.
Main Methods:
- Autopsy analysis of coronary artery segments from patients with severe coronary disease.
- Classification of lesions using modified AHA criteria.
- Assessment of adventitial lymphocyte aggregates and macrophage density (CD68 staining) in relation to plaque characteristics.
Main Results:
- Adventitial lymphocytic inflammation correlated positively with percent stenosis but not calcification.
- Plaque rupture, erosion, and thin caps were associated with increased adventitial lymphocytic inflammation, independent of stenosis.
- Peri-adventitial adipose macrophage density was higher in atherosclerotic plaques and correlated with adventitial lymphocytes and intimal macrophages.
Conclusions:
- Plaque instability features are significantly associated with increased adventitial lymphocytic inflammation, including lymphocyte aggregates and adipocyte-derived macrophages.
- Further research is needed to elucidate the connection between intimal and adventitial inflammation in coronary arteries.
Background:
The relationship between adventitial inflammation, plaque type, and culprit plaque morphology in the epicardial arterial circulation has not been studied in detail.
Methods:
We studied semiserial sections of coronary arteries at autopsy from patients dying with severe coronary disease, 81 men (age 50 + or - 12 years) and 13 women (age 52 + or - 13 years). Lesions were classified at 3- to 5-mm segments according to modified AHA criteria. Adventitial lymphocyte aggregates were assessed at every 5-mm interval and graded semiquantitatively. Macrophage density in the adventitial fat and intima was assessed with anti-CD68 staining.
Results:
Adventitial lymphocytic inflammation increased with percent stenosis (P<.0001) and not calcification (P>.2). Hemorrhage into late core, rupture, erosion, and thin caps all had greater adventitial lymphocytic inflammation independent of percent stenosis (P<.0001). Peri-adventitial adipose macrophage density was increased in plaques with atheromas (206 + or - 22 mm(2) vs. 121 + or - 15 mm(2) in fibrous plaques; P=.02) and correlated positively with adventitial lymphocytes (P<.0001) and intimal macrophage content (P<.0001).
Conclusions:
Features associated with plaque instability are associated with significantly greater degrees of adventitial lymphocytic inflammation, both as lymphocyte aggregates and as adipocyte-derived macrophages. Further study is required to determine the nature of the association between intimal and adventitial lymphocytic inflammation.
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