title: Mechanisms of aortic valve incompetence: finite element modeling of aortic root dilatation.
abstract: BACKGROUND
  Idiopathic root dilatation often results in dysfunction of an otherwise normal aortic valve. To examine the effect of root dilatation on leaflet stress, strain, and coaptation, we utilized a finite element model.
  
  
  METHODS
  The normal model incorporated the geometry, tissue thickness, stiffness, and collagen fiber alignment of normal human roots and valves. We evaluated four dilatation models in which diameters of the aortic root were dilated by 5%, 15%, 30%, and 50%. Regional stress and strain were evaluated and leaflet coaptation percent was calculated under diastolic pressure.
  
  
  RESULTS
  Root dilatation significantly increased regional leaflet stress and strain beyond that found in the normal model. Stress increases ranged from 57% to 399% and strain increases ranged from 39% to 189% in the 50% dilatation model. Leaflet stress and strain were disproportionately high at the attachment edge and coaptation area. Leaflet coaptation was decreased by 18% in the 50% root dilatation model.
  
  
  CONCLUSIONS
  Idiopathic root dilatation significantly increases leaflet stress and strain and reduces coaptation in an otherwise normal aortic valve. These alterations may affect valve-sparing aortic root replacement procedures.
authors.affiliation: Department of Bioengineering, University of Washington, Seattle, USA.
authors.forename: K J
authors.initials: KJ
authors.lastname: Grande
authors.forename: R P
authors.initials: RP
authors.lastname: Cochran
authors.forename: P G
authors.initials: PG
authors.lastname: Reinhall
authors.forename: K S
authors.initials: KS
authors.lastname: Kunzelman
mesh_terms: D001021:Aortic Valve / Q000503:physiopathology*; D001022:Aortic Valve Insufficiency / Q000503:physiopathology*; D003187:Compliance; D003198:Computer Simulation; D004108:Dilatation, Pathologic / Q000503:physiopathology; D020342:Finite Element Analysis; D006439:Hemodynamics / Q000502:physiology; D006801:Humans