title: Vascular injury, repair, and restenosis after percutaneous transluminal angioplasty in the atherosclerotic rabbit.
abstract: BACKGROUND
  Several nonatherosclerotic animal models of restenosis exist and are used for the evaluation of the vascular response to angioplasty-induced injury. However, few studies have evaluated the response of an atherosclerotic vessel to angioplasty. The present study examined the radiographic, histological, immunohistochemical, and morphometric responses over time of atherosclerotic rabbit femoral arteries after percutaneous transluminal angioplasty (PTA).
  
  
  RESULTS
  Rabbits (n = 94) underwent arterial dissection and were fed a hypercholesterolemic diet for 3 weeks, and then PTA was performed. Arteries were obtained before PTA and 1, 3, 5, 7, 14, and 28 days after PTA. PTA caused radial stretching of the artery, medial compression, intramural hemorrhage, injury to normal arterial segments, and dissection within the intima and media. Thrombus filled and cellular accumulation repaired the dissection. Peak smooth muscle cell and macrophage DNA synthesis was noted at 3 to 5 days after angioplasty, generally at the dissection but also in normal sections of the artery. Adventitial injury and subsequent adventitial cellular proliferation and collagen production were observed. A rapid decrease in the radiographic minimal luminal diameter was noted at 3 days, resulting from vascular recoil or thrombus filling the dissection. At 7 to 14 days, only 24% to 33% of the luminal loss was accounted for by an increase in the intimal area, and 22% to 28% of the intima was neointima.
  
  
  CONCLUSIONS
  Restenosis in an atherosclerotic artery results from a variable combination of intimal proliferation, vascular remodeling/wound contraction, and recoil of the normal section of the artery. The variability of an atherosclerotic artery to PTA injury results from variable dissection, thrombus formation, and cellular response to injury as well as variable scar contraction and elastic recoil.
authors.affiliation: Krannert Institute of Cardiology, Department of Medicine, Roudebush VA Medical Center, Indiana University School of Medicine, Indianapolis, 46202-4800, USA.
authors.forename: R L
authors.initials: RL
authors.lastname: Wilensky
authors.forename: K L
authors.initials: KL
authors.lastname: March
authors.forename: I
authors.initials: I
authors.lastname: Gradus-Pizlo
authors.forename: G
authors.initials: G
authors.lastname: Sandusky
authors.forename: N
authors.initials: N
authors.lastname: Fineberg
authors.forename: D R
authors.initials: DR
authors.lastname: Hathaway
mesh_terms: D000800:Angioplasty, Balloon / Q000009:adverse effects*; D000818:Animals; D001161:Arteriosclerosis / Q000473:pathology* / Q000628:therapy; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D003251:Constriction, Pathologic / Q000473:pathology / Q000628:therapy; D005263:Femoral Artery / Q000293:injuries* / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000293:injuries / Q000473:pathology; D011817:Rabbits; D012008:Recurrence; D013927:Thrombosis / Q000209:etiology / Q000473:pathology; D013997:Time Factors; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D014945:Wound Healing
chemical_list: D002791:Cholesterol, Dietary