title: Excessive carotid in-stent neointimal formation predicts late cardiovascular events.
abstract: OBJECTIVE
  To examine if excessive in-stent neointimal formation causing a subcritical stenosis may indicate enhanced vascular reactivity in response to injury, thus predicting late cardiovascular events.
  
  
  METHODS
  One hundred consecutive patients (64 men; median age 71 years) with high-grade internal carotid artery stenoses (68 asymptomatic, 32 symptomatic) underwent carotid artery stenting (CAS). High-sensitivity C-reactive protein (hs-CRP) was measured before CAS. Patients were monitored with duplex ultrasound for excessive in-stent neointimal formation (flow-compromising lumen diameter reduction >/=50%), critical restenosis (>/=70%), or the occurrence of late major adverse cardiovascular events (MACE) defined as myocardial infarction (MI), stroke, and death occurring later than 30 days poststenting.
  
  
  RESULTS
  Over a median 23-month follow-up, excessive neointimal formation was observed in 14 (14%) patients, restenosis in 2 (2%), and 30 late MACE in 25 [25%: 4 MIs, 2 ipsilateral strokes (in the patients with restenosis), 8 contralateral strokes, and 16 cardiovascular deaths]. Cumulative MACE-free survival rates at 6, 12, and 24 months were 92%, 84%, and 77%, respectively. Baseline hs-CRP levels were associated both with neointimal hyperplasia (p=0.024) and MACE (p=0.021). Patients with excessive neointimal formation exhibited a significantly increased adjusted risk for MACE (hazard ratio 3.56, p=0.010).
  
  
  CONCLUSIONS
  Excessive in-stent neointimal formation after CAS indicates an increased risk for late MACE, potentially reflecting a state of exaggerated vascular reactivity in response to injury. Inflammation, which is associated both with neointimal hyperplasia and MACE, seems a common characteristic of different vascular pathologies.
authors.affiliation: Department of Angiology, Vienna General Hospital, Medical School, Austria. martin.schillinger@akh-wien.ac.at
authors.forename: Martin
authors.initials: M
authors.lastname: Schillinger
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Schila
authors.initials: S
authors.lastname: Sabeti
authors.forename: Jasmin
authors.initials: J
authors.lastname: Amighi
authors.forename: Oswald
authors.initials: O
authors.lastname: Wagner
authors.forename: Ramazanali
authors.initials: R
authors.lastname: Ahmadi
authors.forename: Erich
authors.initials: E
authors.lastname: Minar
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D016893:Carotid Stenosis / Q000000981:diagnostic imaging / Q000401:mortality / Q000628:therapy*; D002423:Cause of Death; D002544:Cerebral Infarction / Q000401:mortality*; D005260:Female; D005352:Fibromuscular Dysplasia / Q000000981:diagnostic imaging* / Q000401:mortality / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality*; D011475:Prosthesis Failure; D012008:Recurrence; D012306:Risk; D015607:Stents; D016019:Survival Analysis; D017539:Tunica Intima / Q000000981:diagnostic imaging* / Q000473:pathology; D018616:Ultrasonography, Doppler, Duplex
chemical_list: D002097:C-Reactive Protein