title: Extended follow-up by serial angioscopic observation for bare-metal stents in native coronary arteries: from healing response to atherosclerotic transformation of neointima.
abstract: BACKGROUND
  Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated.
  
  
  RESULTS
  Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and >or=4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4+/-17.3% versus 3.6+/-4.2%, respectively; P=0.011).
  
  
  CONCLUSIONS
  This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.
authors.affiliation: Intensive Care Unit, Chiba-Hokusoh Hospital, Nippon Medical School, Chiba, Japan.
authors.forename: Shinya
authors.initials: S
authors.lastname: Yokoyama
authors.forename: Masamichi
authors.initials: M
authors.lastname: Takano
authors.forename: Masanori
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Shigenobu
authors.initials: S
authors.lastname: Inami
authors.forename: Shunta
authors.initials: S
authors.lastname: Sakai
authors.forename: Kentaro
authors.initials: K
authors.lastname: Okamatsu
authors.forename: Shinichi
authors.initials: S
authors.lastname: Okuni
authors.forename: Koji
authors.initials: K
authors.lastname: Seimiya
authors.forename: Daisuke
authors.initials: D
authors.lastname: Murakami
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Ohba
authors.forename: Ryota
authors.initials: R
authors.lastname: Uemura
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Seino
authors.forename: Noritake
authors.initials: N
authors.lastname: Hata
authors.forename: Kyoichi
authors.initials: K
authors.lastname: Mizuno
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000295:instrumentation*; D017546:Angioscopy; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D023903:Coronary Restenosis / Q000209:etiology / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008670:Metals; D008875:Middle Aged; D011474:Prosthesis Design; D012307:Risk Factors; D015607:Stents; D013927:Thrombosis / Q000209:etiology / Q000473:pathology; D013997:Time Factors; D016896:Treatment Outcome; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology*; D014945:Wound Healing
chemical_list: D008670:Metals