title: Flow reversal promotes intimal thickening in vein grafts.
abstract: OBJECTIVE
  After vascular interventions, unidentified mechanisms disrupt the homeostasis of a focal narrowing to initiate an intimal thickening response. We hypothesize that perturbations in the hemodynamic microenvironment are the initiating event for this disruption of homeostasis and intimal thickening in vein bypass grafts. The objective of this study was to investigate the relation between local flow perturbations and its influence on the vein graft architecture.
  
  
  METHODS
  An external ligature was used to create an 80% focal midgraft stenosis in bilateral rabbit carotid vein grafts. A unilateral distal ligation created a ninefold difference in flow rate between high-flow and low-flow grafts. Ten vein grafts were harvested at 28 days and serially sectioned for morphologic evaluation and vein graft reconstruction. Computational fluid dynamics analyses were performed to examine the hemodynamic environment within these complex flow regions.
  
  
  RESULTS
  The largest intimal thickening occurred exclusively within the region immediately distal to the maximum stenosis in high-flow grafts, which was characterized by persistent flow separation and reversal for the entire cardiac cycle. In regions of low to moderate shear stress (<5 Pa), the typical inverse correlation between intimal thickness and wall shear was observed.
  
  
  CONCLUSIONS
  Regions of vein bypass grafts exposed to persistent flow reversal are most at risk for intimal thickening and loss of lumen.
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, College of Medicine, University of Florida, Gainesville, Fla.
authors.forename: Yong
authors.initials: Y
authors.lastname: He
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Department of Biomedical Engineering, College of Engineering, University of Florida, Gainesville, Fla.
authors.forename: Chessy M
authors.initials: CM
authors.lastname: Fernandez
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, College of Medicine, University of Florida, Gainesville, Fla.
authors.forename: Zhihua
authors.initials: Z
authors.lastname: Jiang
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, College of Medicine, University of Florida, Gainesville, Fla.
authors.forename: Ming
authors.initials: M
authors.lastname: Tao
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, College of Medicine, University of Florida, Gainesville, Fla.
authors.forename: Kerri A
authors.initials: KA
authors.lastname: O'Malley
authors.affiliation: Malcom Randall VAMC, Gainesville, Fla; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, College of Medicine, University of Florida, Gainesville, Fla. Electronic address: bercesa@surgery.ufl.edu.
authors.forename: Scott A
authors.initials: SA
authors.lastname: Berceli
mesh_terms: D000818:Animals; D017536:Carotid Artery, Common / Q000601:surgery; D003198:Computer Simulation; D003251:Constriction, Pathologic; D004195:Disease Models, Animal; D006083:Graft Occlusion, Vascular / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D057446:Hydrodynamics; D007601:Jugular Veins / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D008297:Male; D008955:Models, Cardiovascular; D058426:Neointima; D011817:Rabbits; D012039:Regional Blood Flow; D013997:Time Factors