title: Hemodynamic simulations and computer-aided designs of graft-artery junctions.
abstract: Severe occlusion of graft-artery junctions due to restenosis, e.g., excessive tissue overgrowth and renewed plaque formation, may occur within a few months or years after bypass surgery. Our hypothesis is that nonuniform hemodynamics, represented by large sustained wall shear stress gradients, trigger abnormal biological processes leading to rapid restenosis and hence early graft failure. In turn, this problem may be significantly mitigated by designing graft-artery bypass configurations for which the wall shear stress gradient (WSSG) is approximately zero and hence nearly uniform hemodynamics are achieved. Focusing on the distal end of several femoral artery bypass junctions, a validated finite volume code has been used to compute the transient three-dimensional velocity vector fields and its first and second surface derivatives in order to test the idea. Specifically, it is shown that the Taylor patch, which generates higher patency rates than standard end-to-side anastomoses, exhibits lower WSSG levels than standard configurations, and that further geometric design improvements reduce the WSSG in magnitude and local extent even more.
authors.affiliation: Department of Mechanical & Aerospace Engineering, North Carolina State University, Raleigh 27695-7910, USA.
authors.forename: M
authors.initials: M
authors.lastname: Lei
authors.forename: C
authors.initials: C
authors.lastname: Kleinstreuer
authors.forename: J P
authors.initials: JP
authors.lastname: Archie
mesh_terms: D000465:Algorithms; D000714:Anastomosis, Surgical / Q000009:adverse effects; D000818:Animals; D001158:Arteries / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001807:Blood Vessel Prosthesis / Q000009:adverse effects; D003198:Computer Simulation; D017076:Computer-Aided Design; D003251:Constriction, Pathologic / Q000209:etiology / Q000503:physiopathology; D005263:Femoral Artery / Q000502:physiology / Q000601:surgery; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular; D012008:Recurrence; D013314:Stress, Mechanical; D014654:Vascular Patency