作者: Michinori Imazu , Michio Yamakido , Wataru Yasui , Koichi Ono , Hironori Ueda
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摘要: The overgrowth of cells the vessel wall, especially smooth muscle (SMCs), contributes to pathogenesis coronary atherosclerosis and wound repair after angioplasty. However, association between cellular proliferation in lesions clinical pathophysiology remains be clarified humans. Thus, we investigated proliferative activity tissues obtained from patients with ischemia. by using directional atherectomy (DCA) 87 was assessed immunohistochemical staining for proliferating cell nuclear antigen (PCNA). were divided into 34 primary 53 postangioplasty lesions. tissue samples 9 stable angina pectoris (SAP) 25 acute syndromes (ACS). Collectively, 37 SAP 16 ACS. PCNA labeling index (LI) quantified as mean percentage PCNA-positive 3 most positive high-power fields (x 200). LIs high ACS [8.9 +/- 2.1% (p = 0.01)] [2.3 0.8% 0.08) cases 4.1 2.4% 0.06) cases] compared (0.2 0.2%). Intimal hyperplasia, a random SMCs (alpha-actin positive) marked (76%) well (92%) (81%) samples, (33%) < 0.01). expression mainly evident nucleus CD68-positive macrophages. Many localized plaque areas, follows: intimal neovascularized lesions, macrophage clusters, near areas disrupted internal elastic lamina. levels not associated subsequent development restenosis DCA. Our findings suggest that excessive vascular wall cells, SMCs, is involved process angioplasty