title: In-stent restenosis and remote coronary lesion progression are coupled in cardiac transplant vasculopathy but not in native coronary artery disease.
abstract: OBJECTIVE
  The purpose of this study was to describe the clinical, angiographic, and histological features of concomitant in-stent restenosis (ISR) and cardiac allograft vasculopathy (CAV) progression.
  
  
  BACKGROUND
  Cardiac allograft vasculopathy is a major challenge to long-term success of heart transplantation. Coronary stenting for CAV is hampered by ISR.
  
  
  METHODS
  Quantitative coronary angiography compared late lumen loss (LL) at stented and reference, non-stented segments during 1-year follow-up in post-heart transplant and control atherosclerosis patients. Stented and non-stented arteries with CAV were also obtained post-mortem for immunohistochemical analysis.
  
  
  RESULTS
  In 37 stented lesions (25 patients), 1-year binary restenosis occurred in 37.8%. Patients with ISR had higher long-term cardiac death/myocardial infarction rates than patients without ISR (53.8% vs. 9.1%, p = 0.03). In the same 25 patients, 34 CAV lesions with non-significant obstructions were identified as reference controls. After 1 year, patients who developed ISR also had more control lesion LL (0.78 +/- 0.38 mm vs. 0.39 +/- 0.27 mm, p < 0.006) compared to patients without ISR. In the post-transplant patients, in-stent LL was closely coupled to control segment LL (R(2) = 0.63, p < 0.05). Conversely, in native atherosclerosis patients, ISR and remote disease progression were not correlated. Histological staining of stented and control arteries from CAV patients revealed similar pathologies common to ISR and non-intervened CAV segments.
  
  
  CONCLUSIONS
  Progression of CAV at non-intervened segments and ISR correlate strongly and share common histopathology. Optimized treatment for patients with aggressive CAV needs to address the widespread nature of this disease, even when it presents as an initially focal lesion.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. tmjonas@yahoo.com
authors.forename: Michael
authors.initials: M
authors.lastname: Jonas
authors.forename: James C
authors.initials: JC
authors.lastname: Fang
authors.forename: John C
authors.initials: JC
authors.lastname: Wang
authors.forename: Satyendra
authors.initials: S
authors.lastname: Giri
authors.forename: Dan
authors.initials: D
authors.lastname: Elian
authors.forename: Yedael
authors.initials: Y
authors.lastname: Har-Zahav
authors.forename: Hung
authors.initials: H
authors.lastname: Ly
authors.forename: Philip A
authors.initials: PA
authors.lastname: Seifert
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Popma
authors.forename: Campbell
authors.initials: C
authors.lastname: Rogers
mesh_terms: D000368:Aged; D002318:Cardiovascular Diseases / Q000401:mortality; D016022:Case-Control Studies; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000628:therapy; D003327:Coronary Disease / Q000175:diagnosis* / Q000209:etiology / Q000401:mortality / Q000628:therapy*; D023903:Coronary Restenosis / Q000175:diagnosis*; D003331:Coronary Vessels / Q000473:pathology; D018450:Disease Progression; D005260:Female; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology; D015607:Stents; D014184:Transplantation, Homologous