Plaque inflammation in restenotic coronary lesions of patients with stable or unstable angina
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 atherosc...
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Veröffentlicht in: | Journal of the American College of Cardiology 2000-03, Vol.35 (4), p.963-967 |
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Sprache: | eng |
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Zusammenfassung: | 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-× 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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ISSN: | 0735-1097 1558-3597 |
DOI: | 10.1016/S0735-1097(99)00647-6 |