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Published on: February 20, 2019
Quantification of Various Inflammatory Cells in Advanced Atherosclerotic Plaques
Veronica Soundra Veena Paul1, Christina Mary Priya Paul2, Sarah Kuruvilla3
1Assistant Professor, Department of Pathology, A.C.S Medical College , Chennai, India .
Insights
Advanced atherosclerotic plaques are primarily infiltrated by T-lymphocytes, with CD8+ cells outnumbering CD4+ cells. Understanding these inflammatory cells in atherosclerosis may offer new therapeutic strategies.
Area of Science:
- Cardiovascular Pathology
- Immunohistochemistry
- Histomorphometry
Background:
- Atherosclerosis, the underlying pathology of coronary artery disease, involves complex inflammatory processes crucial for understanding disease progression.
- This autopsy study investigates the types and quantities of inflammatory cells within advanced atherosclerotic plaques.
Purpose of the Study:
- To identify and categorize inflammatory cells in advanced atherosclerotic plaques.
- To determine the distribution and quantify inflammatory cells using histomorphometry.
- To compare inflammatory cell profiles between different American Heart Association (AHA) plaque types (IV and V).
Main Methods:
- Analysis of heart specimens from 3 autopsy cases with coronary artery disease.
- Classification of 50 advanced atherosclerotic plaques (AHA Type IV and V) using H&E staining.
- Immunohistochemical staining for T-lymphocytes (CD4+, CD8+), B-lymphocytes, and neutrophils.
- Histomorphometric quantification of identified inflammatory cells and comparison between plaque types.
Main Results:
- Advanced atherosclerotic plaques were predominantly infiltrated by T-lymphocytes (CD3+).
- T-lymphocytes were mainly located in the plaque's shoulder region and fibrous cap.
- CD8+ T-cells were consistently more abundant than CD4+ T-cells in advanced lesions.
- Neutrophils were not detected, and inflammatory cell differences between AHA Type IV and V plaques were not statistically significant.
Conclusions:
- T-lymphocytes, particularly CD8+ cells, are key inflammatory components in advanced atherosclerotic plaques.
- The distribution and quantification of inflammatory cells offer insights into plaque pathophysiology.
- Further understanding of inflammatory cell roles in atherosclerosis may lead to novel therapeutic interventions.
Introduction:
Atherosclerosis, the pathological basis of coronary artery disease is being extensively studied as understanding of the complex processes involved in the formation and progression that can provide an insight into prevention and treatment of the same. This is an autopsy study to identify and quantify various inflammatory cells in advanced atherosclerotic plaques.
Aim:
This study aims at identifying and categorizing the various inflammatory cells present in advanced atherosclerotic plaques, noting their distribution in the plaque, quantifying them using histomorphometry and comparing them across plaques of different AHA types.
Materials And Methods:
Post-mortem angiogram was performed on 3 heart specimens obtained at autopsy of random Road Traffic Accident (RTA) cases which revealed evidence of coronary artery disease. End-arterectomy was done and the arteries with atherosclerotic plaques were cut into serial sections and made into tissue blocks. Sections from these blocks were stained with H & E stain and the plaques were classified based on AHA classification. 50 advanced atherosclerotic plaques of AHA Type IV and V were chosen for this study and were screened for inflammatory cells, first with H & E stain and then with different immunohistochemical stains for T-lymphocytes, B-lymphocytes and neutrophils. The T-lymphocytes thus identified was further sub-typed into CD4+ and CD8+ cells again using IHC markers and the percentage area of each was measured using histomorphometry. Then, these values were compared between AHA Type IV and AHA Type V lesions.
Results:
It was found that the inflammatory cells found in advanced atherosclerotic plaques were predominantly T-lymphocytes as evidenced by their CD3 positivity and they were found to be distributed mainly around the shoulder region and fibrous cap of the plaque. When categorized further, it was found that CD8+ T-cells were always more than CD4+ T-cells in advanced lesions. Meloperoxidase stain for neutrophils was negative in all the plaques examined. The difference in the amount of inflammatory cells between AHA type IV and Type V was not statistically significant.
Conclusion:
The study of the amount of inflammatory cells in atherosclerotic plaques and understanding their role in the pathophysiology of advanced plaques may have therapeutic implications.
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