title: Restenosis after percutaneous transluminal coronary angioplasty--a histopathological study using autopsied hearts.
abstract: Restenosis was studied histopathologically by serial step sectioning of 22 coronary arteries from 21 patients in whom percutaneous transluminal coronary angioplasty (PTCA) had been performed (9 arteries from patients who had died shortly after PTCA and 13 from those who had died considerably later). Nine of the 13 arteries from the patients who had died long after PTCA were immunohistochemically stained using anti-actin antibody for examination of spindle-shaped cells proliferating in the intima. In the patients who had died shortly after PTCA, all 9 arteries showed fresh thrombus formation. In the patients who had died considerably later after PTCA, however, there was fragmentation of the internal elastic lamina (IEL) in 9 arteries. In each of these 9 arteries, a remarkable proliferation of intimal cells was observed on the intimal side, mainly at the site of the IEL fragmentation. These spindle-shaped cells were identified as smooth muscle cells (SMC) because they stained reddish-brown with Masson's trichrome, and because immunohistochemical staining with anti-actin antibody was also positive. In 2 arteries, proliferation of SMC and elastic fibers was observed on the luminal side of the intima, despite absence of fragmentation in the IEL. Proliferation of SMC in false lumens was identified in 2 patients with medial dissection. From the above findings, the following 4 forms of restenosis after PTCA have been identified: 1. thrombus formation; 2. proliferation of SMC on the intimal side, mainly around fragmentation in the IEL; 3. proliferation of SMC on the luminal side of the intima where there was no fragmentation of the IEL; and 4. proliferation of SMC in dissected false lumen. The proliferation of SMC on the intimal side of the disrupted IEL was thought to have been a result of migration of SMC from the media to the intima, because SMC proliferation was seen around the disrupted region.
authors.affiliation: Department of Internal Medicine, Fujita Health University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Morimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Mizuno
authors.forename: S
authors.initials: S
authors.lastname: Hiramitsu
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: N
authors.initials: N
authors.lastname: Kubo
authors.forename: M
authors.initials: M
authors.lastname: Nomura
authors.forename: T
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: H
authors.initials: H
authors.lastname: Kitazume
authors.forename: K
authors.initials: K
authors.lastname: Kodama
authors.forename: H
authors.initials: H
authors.lastname: Kurogane
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D002455:Cell Division; D003251:Constriction, Pathologic / Q000473:pathology / Q000628:therapy; D003327:Coronary Disease / Q000473:pathology* / Q000628:therapy; D003328:Coronary Thrombosis / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D012008:Recurrence