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Published on: May 14, 2013
Plaque inflammation in restenotic coronary lesions of patients with stable or unstable angina
J J Piek1, A C van der Wal, M Meuwissen
1Department of Cardiology, Academic Medical Center, University of Amsterdam, The Netherlands. j.j.piek@amc.uva.nl
Insights
Inflammation in restenotic coronary lesions is linked to unstable angina. Unstable angina patients show higher macrophage and T-lymphocyte levels in plaques compared to stable angina patients.
Area of Science:
- Cardiovascular Pathology
- Immunohistochemistry
- Coronary Artery Disease
Background:
- Limited understanding of plaque inflammation in restenotic coronary lesions.
- Association between inflammation and coronary syndrome severity in restenosis is unknown.
Purpose of the Study:
- To immunohistochemically evaluate inflammation markers in coronary atherectomy specimens.
- To compare inflammation parameters in restenotic lesions of stable angina versus unstable angina patients.
Main Methods:
- 37 patients with stable angina or unstable angina underwent coronary atherectomy for restenotic lesions.
- Immunohistochemistry used for macrophages (CD68), T-lymphocytes (CD3), and smooth muscle cells (alpha-actin).
- Quantification of macrophages, T-lymphocytes, and smooth muscle cells via planimetry and cell counting.
Main Results:
- No significant difference in smooth muscle cell content between stable and unstable angina groups.
- Restenotic lesions in unstable angina patients had significantly higher macrophage and T-lymphocyte infiltration.
- Macrophages: 24.4% vs. 10.5% (p=0.001); T-lymphocytes: 18.8 cells/mm² vs. 8.6 cells/mm² (p=0.034).
Conclusions:
- Inflammation, particularly macrophage and T-lymphocyte presence, is associated with plaque instability.
- Increased inflammation in restenotic lesions may contribute to the development of unstable coronary syndromes.
Objectives:
To evaluate immunohistochemically various parameters of inflammation in coronary atherectomy specimens obtained from restenotic culprit lesions of patients presenting with either stable or unstable angina (UA).
Background:
There is no information regarding the relationship between atherosclerotic plaque inflammation and the severity of the coronary syndromes in patients with restenotic coronary lesions.
Methods:
A total of 37 patients with either stable angina or UA underwent directional coronary atherectomy for restenotic coronary lesions. Cryostat sections of atherectomy specimen were immunohistochemically stained with monoclonal antibodies CD68 (macrophages [MACs]), CD3 (T-lymphocytes) and alpha-actin (smooth muscle cells [SMCs]). Smooth muscle cell contents and MAC contents were planimetrically quantified as the percentage immunopositive tissue area of the total tissue area. T-lymphocytes were counted at 100-X magnification throughout the entire section and expressed as number of cells per mm2.
Results:
Restenotic coronary lesions of patients with UA or stable angina showed no significant difference in SMC areas (31.9%+/-16.3% vs. 38.5%+/-18.8%, respectively; p = NS). However, restenotic coronary lesions of patients presenting with unstable angina contained significantly more MACs (24.4%+/-15.1% vs. 10.5%+/-5.8%, p = 0.001) and T-lymphocytes (18.8 cells/mm2+/-15.1 cells/mm2 vs. 8.6 cells/mm2+/-9.8 cells/mm2; p = 0.034) than patients with stable angina.
Conclusions:
These results suggested that inflammation appears to affect plaque instability in restenotic coronary lesions resulting in unstable coronary syndromes.
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