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ORIGINAL ARTICLES |
| Acute coronary syndromes |
1 Division of Cardiology, Kitano Hospital, Tadukekofukai Medical Research Institute, Osaka, Japan
2 Department of Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan
3 Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan
4 Department of Cardiology, Osaka City General Hospital, Osaka, Japan
5 Division of Cardiology, Takeda Hospital, Kyoto, Japan
6 Third Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan
7 Heart Bio-Mechanics Centre, Doshisha University, Kyoto, Japan
Correspondence to:
Professor M Fujita, Human Health Sciences, Kyoto University Graduate School of Medicine, 53 Kawaharacho, Shogoin, Sakyo-ku, Kyoto 606–8507, Japan; mfujita{at}kuhp.kyoto-u.ac.jp
ABSTRACT
Background: The S100A8/A9 complex is expressed in a subset of activated neutrophils and macrophages in acute inflammatory lesions associated with various diseases.
Objective: To investigate (a) whether serum S100A8/A9 levels are increased in patients with unstable angina (UA); and (b) whether S100A8/A9 expression is upregulated in coronary atherosclerotic plaques of patients with UA.
Design: Serum S100A8/A9 levels in 39 patients with stable angina (SA) and 53 patients with UA were measured. In addition, the presence of the S100A8/A9 complex in directional coronary atherectomy specimens was studied immunohistochemically. Cell types which stain positive for S100A8/A9 were identified by immunodouble staining with neutrophils and macrophages.
Results: Mean (SD) serum S100A8/A9 levels were significantly higher in patients with UA than in those with SA (3.25 (3.08) µg/ml vs 0.77 (0.31) µg/ml, p<0.05). In patients with UA, immunodouble staining clearly showed that the S100A8/A9 complex was expressed in infiltrated neutrophils and occasional macrophages. The S100A8/A9-positive area was significantly higher in UA than in SA (mean (SD) 18.3 (14.2)% vs 1.3 (2.4)%, respectively, p<0.001).
Conclusions: The S100A8/A9 complex may be involved in the inflammatory process of coronary atherosclerotic plaques in patients with UA.
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