title: Mechanism of lumen enlargement with direct stenting versus predilatation stenting: influence of remodelling and plaque characteristics assessed by volumetric intracoronary ultrasound.
abstract: OBJECTIVE
  To compare the effects of arterial remodelling and plaque characteristics on the mechanisms of direct stenting and predilatation stenting. Direct stenting has become routine in some laboratories and differs technically from predilatation stenting.
  
  
  METHODS
  Pre- and post-interventional volumetric intravascular ultrasound (IVUS) was undertaken in 30 patients with direct stenting and in 30 with predilatation stenting of non-calcified native coronary lesions, using the same stent design and stent length. Lumen, vessel (external elastic membrane (EEM)), and plaque (plaque + media) volumes were calculated. Remodelling was determined by comparing the EEM area at the centre of the lesion with the EEM areas at proximal and distal reference sites. Plaque eccentricity was defined as the thinnest plaque diameter to the thickest plaque diameter ratio. Plaque composition was characterised as soft, mixed, or dense.
  
  
  RESULTS
  All volumetric IVUS changes were similar in the two groups. Pre-intervention remodelling remained uninfluenced after direct stenting, but was neutralised after predilatation stenting. Eccentric lesions responded to intervention by a greater luminal gain owing to greater vessel expansion in direct stenting. Plaque composition influenced luminal gain in direct stenting, the gain being greatest in the softest plaques; in predilatation stenting, luminal gain was equivalent but vessel expansion was greater for "dense" plaque and plaque reduction greater for "soft" plaque.
  
  
  CONCLUSIONS
  In non-calcified lesions, the mechanisms of lumen enlargement after direct or predilatation stenting are significantly influenced by atherosclerotic remodelling, plaque eccentricity, and plaque composition.
authors.affiliation: Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Cardiovascular Research Institute, Washington Hospital Center, Washington DC, USA. gerard.finet@creatis.univ-lyon1.fr
authors.forename: G
authors.initials: G
authors.lastname: Finet
authors.forename: N J
authors.initials: NJ
authors.lastname: Weissman
authors.forename: G S
authors.initials: GS
authors.lastname: Mintz
authors.forename: L F
authors.initials: LF
authors.lastname: Satler
authors.forename: K M
authors.initials: KM
authors.lastname: Kent
authors.forename: J R
authors.initials: JR
authors.lastname: Laird
authors.forename: G A
authors.initials: GA
authors.lastname: Adelmann
authors.forename: A E
authors.initials: AE
authors.lastname: Ajani
authors.forename: M T
authors.initials: MT
authors.lastname: Castagna
authors.forename: G
authors.initials: G
authors.lastname: Rioufol
authors.forename: A D
authors.initials: AD
authors.lastname: Pichard
mesh_terms: D002404:Catheterization / Q000379:methods; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000473:pathology* / Q000628:therapy; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology*; D004548:Elasticity; D006801:Humans; D015588:Observer Variation; D019047:Phantoms, Imaging; D011237:Predictive Value of Tests; D011312:Pressure; D012016:Reference Values; D012680:Sensitivity and Specificity; D015607:Stents; D014463:Ultrasonography