title: [Serial changes of coronary arteries after percutaneous transluminal coronary angioplasty: histopathological and immunohistochemical study].
abstract: Intimal hyperplasia due to fibrocellular proliferation, mainly of smooth muscle cells, leads to restenosis after successful percutaneous transluminal coronary angioplasty (PTCA). The mechanism of intimal proliferation of smooth muscle cells was investigated by histological and immunohistochemical studies of necropsied coronary arteries from 13 patients who died between several hours and 1 year 8 months after PTCA. Immunohistochemical examinations clearly revealed smooth muscle cells already migrating from the media into the injured intima after 10 days. Thereafter, significant proliferation of smooth muscle cells was observed on the intimal side of the affected regions, predominantly around the circumference of the lumen at the PTCA site. Arteries from patients with restenosis who died more than 1 month after PTCA demonstrated proliferating cells with a polygonal shape and large bizarre nuclei. Arteries without restenosis showed smooth muscle cells with a spindle shape and rather elongated or oval nuclei. Although these cells were ordered along the luminal surface, the intercellular space still contained abundant ground substances. A case in which death occurred more than 1 year after PTCA showed these cells were analogous to medial smooth muscle cells. In addition, the extracellular matrix volume was extremely reduced, and composed chiefly of collagen as shown by positive Masson's trichrome stain. These histological findings demonstrated completion of repair and stabilization of the lesion caused by PTCA. Immunohistochemical investigation showed proliferating cells stained positive to vimentin but were negative to desmin, irrespective of the lesion age. This study provides pathological support for clinical reports suggesting that restenosis is predominant between 1 and 6 months and decreases beyond 1 year after PTCA.
authors.affiliation: Department of Cardiology, Matsue Red Cross Hospital.
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: N
authors.initials: N
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Kakio
authors.forename: H
authors.initials: H
authors.lastname: Suyama
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: Y
authors.initials: Y
authors.lastname: Nakazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Nagamatsu
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000032:analysis; D003327:Coronary Disease / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D003893:Desmin / Q000276:immunology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D014746:Vimentin / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D003893:Desmin; D014746:Vimentin