title: Redilation of endovascular stents in congenital heart disease: factors implicated in the development of restenosis and neointimal proliferation.
abstract: OBJECTIVE
  We sought to determine the incidence of and risk factors for the development of restenosis and neointimal proliferation after endovascular stent implantation for congenital heart disease (CHD).
  
  
  BACKGROUND
  Risk factors for the development of restenosis and neointimal proliferation are poorly understood.
  
  
  METHODS
  This was a retrospective review of patients who underwent endovascular stent redilation between September 1989 and February 2000.
  
  
  RESULTS
  Of 368 patients who had 752 stents implanted, 220 were recatheterized. Of those 220 patients, 103 underwent stent redilation. Patients were classified into three groups: 1) those with pulmonary artery stenosis (n = 94), tetralogy of Fallot/pulmonary atresia (n = 72), congenital branch pulmonary stenosis (n = 9), status post-Fontan operation (n = 6), status post-arterial switch operation (n = 7); 2) those with iliofemoral venous obstruction (n = 6); and 3) those with miscellaneous disorders (n = 3). The patients' median age was 9.9 years (range 0.5 to 39.8); their mean follow-up duration was 3.8 years (range 0.1 to 10). Indications for stent redilation included somatic growth (n = 67), serial dilation (n = 27) and development of neointimal proliferation or restenosis, or both (n = 9). There was a low incidence of neointimal proliferation (1.8%) and restenosis (2%). There were no deaths. Complications included pulmonary edema (n = 1), hemoptysis (n = 1) and contralateral stent compression (n = 2).
  
  
  CONCLUSIONS
  Redilation or further dilation of endovascular stents for CHD is effective as late as 10 years. The risk of neointimal proliferation (1.8%) and restenosis (2%) is low and possibly avoidable. Awareness of specific risk factors and modification of the stent implantation technique, including avoidance of minimal stent overlap and sharp angulation of the stent to the vessel wall and avoidance of overdilation, have helped to reduce the incidence of restenosis.
authors.affiliation: LillieFrank Abercrombie Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston 77030, USA.
authors.forename: C J
authors.initials: CJ
authors.lastname: McMahon
authors.forename: H G
authors.initials: HG
authors.lastname: El-Said
authors.forename: R G
authors.initials: RG
authors.lastname: Grifka
authors.forename: J K
authors.initials: JK
authors.lastname: Fraley
authors.forename: M R
authors.initials: MR
authors.lastname: Nihill
authors.forename: C E
authors.initials: CE
authors.lastname: Mullins
mesh_terms: D000293:Adolescent; D000328:Adult; D000800:Angioplasty, Balloon; D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging / Q000209:etiology* / Q000628:therapy; D002455:Cell Division; D002648:Child; D002675:Child, Preschool; D005260:Female; D005500:Follow-Up Studies; D006083:Graft Occlusion, Vascular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000628:therapy; D006330:Heart Defects, Congenital / Q000150:complications / Q000601:surgery*; D006801:Humans; D007223:Infant; D008297:Male; D011651:Pulmonary Artery / Q000000981:diagnostic imaging / Q000473:pathology; D011859:Radiography; D012189:Retrospective Studies; D012307:Risk Factors; D015607:Stents / Q000009:adverse effects*