Computational modeling of mass transfer and links to atherosclerosis.
In the context of atherogenesis, mass transport refers to the movement of atherogenic molecules from flowing blood into the artery wall, or vice versa. Although LDL transport clearly plays a role in atherosclerotic plaque development, it is much less clear whether abnormalities in mass transfer patterns are in themselves atherogenic. A powerful way of addressing this question is through computational modeling, which provides detailed descriptions of local mass transport features. Here we briefly review the strategy and some of the pros and cons of such a modeling approach, and then focus on results gained from studies in a variety of arterial geometries. The general picture is that zones of hypoxia (low oxygen transport from blood to wall) and elevated LDL tend to colocalize with each other, and with areas of atherosclerotic lesion development and/or intimal thickening. The picture is complicated by the fact that such zones also tend to have "abnormal" wall shear stress patterns, which are also believed to be atherogenic. Taken together, these results suggest, but do not prove, a role for mass transport in atherogenesis.
Ethier
C Ross
CR
Department of Mechanical and Industrial Engineering, University of Toronto, Ontario, Canada. ethier@mie.utoronto.ca
D001158:Arteries / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000503:physiopathology*; D001692:Biological Transport; D001783:Blood Flow Velocity; D003198:Computer Simulation; D023921:Coronary Stenosis / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006439:Hemodynamics; D018056:Hemorheology; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008955:Models, Cardiovascular; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D010100:Oxygen / Q000378:metabolism; D013314:Stress, Mechanical; D017539:Tunica Intima / Q000503:physiopathology*
D008077:Lipoproteins, LDL; D010100:Oxygen