Computational analysis of coupled blood-wall arterial LDL transport.
The transport of macromolecules, such as low density lipoproteins (LDLs), across the artery wall and their accumulation in the wall is a key step in atherogenesis. Our objective was to model fluid flow within both the lumen and wall of a constricted, axisymmetric tube simulating a stenosed artery, and to then use this flow pattern to study LDL mass transport from the blood to the artery wall. Coupled analysis of lumenal blood flow and transmural fluid flow was achieved through the solution of Brinkman's model, which is an extension of the Navier-Stokes equations for porous media. This coupled approach offers advantages over traditional analyses of this problem, which have used possibly unrealistic boundary conditions at the blood-wall interface; instead, we prescribe a more natural pressure boundary condition at the adventitial vasa vasorum, and allow variations in wall permeability due to the occurrence of plaque. Numerical complications due to the convection dominated mass transport process (low LDL diffusivity) are handled by the streamline upwind/Petrov-Galerkin (SUPG) finite element method. This new fluid-plus-porous-wall method was implemented for conditions typical of LDL transport in a stenosed artery with a 75 percent area reduction (Peclet number=2 x 10(8)). The results show an elevated LDL concentration at the downstream side of the stenosis. For the higher Darcian wall permeability thought to occur in regions containing atheromatous lesions, this leads to an increased transendothelial LDL flux downstream of the stenosis. Increased transmural filtration in such regions, when coupled with a concentration-dependent endothelial permeability to LDL, could be an important contributor to LDL infiltration into the arterial wall. Experimental work is needed to confirm these results.
Stangeby
D Kim
DK
Department of Mechanical Engineering, University of Toronto, Ontario, Canada.
Ethier
C Ross
CR
D001158:Arteries / Q000378:metabolism*; D001161:Arteriosclerosis / Q000503:physiopathology*; D001692:Biological Transport; D002463:Cell Membrane Permeability / Q000502:physiology; D003198:Computer Simulation; D003251:Constriction, Pathologic / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism*; D020342:Finite Element Analysis; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008955:Models, Cardiovascular; D010100:Oxygen / Q000378:metabolism; D016062:Porosity; D011312:Pressure; D012212:Rheology; D012680:Sensitivity and Specificity
D008077:Lipoproteins, LDL; D010100:Oxygen