title: Valsartan prevents neointimal hyperplasia after carotid artery stenting by suppressing endothelial cell injuries.
abstract: OBJECTIVE
  Restenosis or neointimal hyperplasia remains an important complication after carotid artery stenting (CAS) for carotid artery stenosis. The purpose of this study was to examine if an anti-hypertensive drug, angiotensin receptor blocker (ARB), prevents post-CAS neointimal hyperplasia during the first 1-year period after CAS, and to clarify the possible mechanisms.
  
  
  METHODS
  Hypertension had been treated with a calcium channel blocker (CCB) and/or an ARB, valsartan, by the preference of the neurosurgeon in charge in our department. At admission to perform CAS, patients were assigned to normotensive, valsartan (hypertensive patients treated with valsartan with/without any kind of CCBs), and non-valsartan (hypertensive patients treated with any kind of CCBs without ARBs) groups. Post-CAS neointimal hyperplasia was evaluated by carotid duplex ultrasound imaging in terms of intima-media thickening (IMT), which was performed at pre-CAS and at 90, 180, 270, and 360 days post-CAS. Biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine), inflammation (C-reactive protein, tenascin-C) and endothelial cell injury (von Willebrand factor [vWF] antigen) were measured at pre-CAS and at 1, 7, and 180 days post-CAS.
  
  
  RESULTS
  The non-valsartan group (n  =  8) had a higher incidence of maximum in-stent IMT ≧ 1.1 mm compared with the normotensive group (n  =  6). Valsartan (n  =  9) significantly suppressed plasma vWF levels at 7 days post-CAS and decreased the incidence of maximum in-stent IMT ≧ 1.1 mm compared with the non-valsartan group, although clinical parameters were similar between the two groups. Other biomarkers were not significantly different among the three groups.
  
  
  CONCLUSIONS
  These findings suggest that valsartan may prevent post-CAS neointimal hyperplasia possibly by suppressing endothelial cell injury.
authors.forename: Hidenori
authors.initials: H
authors.lastname: Suzuki
authors.forename: Takanori
authors.initials: T
authors.lastname: Sano
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Umeda
authors.forename: Akitaka
authors.initials: A
authors.lastname: Yamamoto
authors.forename: Naoki
authors.initials: N
authors.lastname: Toma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sakaida
authors.forename: Waro
authors.initials: W
authors.lastname: Taki
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology / Q000601:surgery; D016893:Carotid Stenosis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery*; D042783:Endothelial Cells / Q000187:drug effects* / Q000502:physiology; D005260:Female; D006801:Humans; D006965:Hyperplasia / Q000000981:diagnostic imaging / Q000209:etiology / Q000517:prevention & control*; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D008297:Male; D011446:Prospective Studies; D015607:Stents / Q000009:adverse effects*; D013777:Tetrazoles / Q000627:therapeutic use*; D016896:Treatment Outcome; D014463:Ultrasonography; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D015415:Biomarkers; D002121:Calcium Channel Blockers; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine
keywords: Carotid artery stenosis,; Carotid artery stenting,; Endothelial cell injury,; Neointimal hyperplasia,; Restenosis