Multiphysics simulation of blood flow and LDL transport in a porohyperelastic arterial wall model.
Atherosclerosis localizes at a bend andor bifurcation of an artery, and low density lipoproteins (LDL) accumulate in the intima. Hemodynamic factors are known to affect this localization and LDL accumulation, but the details of the process remain unknown. It is thought that the LDL concentration will be affected by the filtration flow, and that the velocity of this flow will be affected by deformation of the arterial wall. Thus, a coupled model of a blood flow and a deformable arterial wall with filtration flow would be invaluable for simulation of the flow field and concentration field in sequence. However, this type of highly coupled interaction analysis has not yet been attempted. Therefore, we performed a coupled analysis of an artery with multiple bends in sequence. First, based on the theory of porous media, we modeled a deformable arterial wall using a porohyperelastic model (PHEM) that was able to express both the filtration flow and the viscoelastic behavior of the living tissue, and simulated a blood flow field in the arterial lumen, a filtration flow field and a displacement field in the arterial wall using a fluid-structure interaction (FSI) program code by the finite element method (FEM). Next, based on the obtained results, we further simulated LDL transport using a mass transfer analysis code by the FEM. We analyzed the PHEM in comparison with a rigid model. For the blood flow, stagnation was observed downward of the bends. The direction of the filtration flow was only from the lumen to the wall for the rigid model, while filtration flows from both the wall to the lumen and the lumen to the wall were observed for the PHEM. The LDL concentration was high at the lumenwall interface for both the PHEM and rigid model, and reached its maximum value at the stagnation area. For the PHEM, the maximum LDL concentration in the wall in the radial direction was observed at the position of 3% wall thickness from the lumenwall interface, while for the rigid model, it was observed just at the lumenwall interface. In addition, the peak LDL accumulation area of the PHEM moved about according to the pulsatile flow. These results demonstrate that the blood flow, arterial wall deformation, and filtration flow all affect the LDL concentration, and that LDL accumulation is due to stagnation and the presence of filtration flow. Thus, FSI analysis is indispensable.
Koshiba
Nobuko
N
Graduate School of Frontier Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. koshiba@sml.k.u-tokyo.ac.jp
Ando
Joji
J
Chen
Xian
X
Hisada
Toshiaki
T
D001158:Arteries / Q000378:metabolism* / Q000502:physiology; D001692:Biological Transport; D001783:Blood Flow Velocity; D003331:Coronary Vessels / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D004547:Elastic Tissue / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D020342:Finite Element Analysis; D008077:Lipoproteins, LDL / Q000032:analysis / Q000378:metabolism*; D008955:Models, Cardiovascular; D016062:Porosity; D011673:Pulsatile Flow; D013997:Time Factors; D017539:Tunica Intima / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D017540:Tunica Media / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D014783:Viscosity
D008077:Lipoproteins, LDL