D. Hardman, B. J. Doyle, S. I. K. Semple, J. M. J. Richards, D. E. Newby, W. J. Easson, P. R. Hoskins



Publication year



Proceedings of the Institution of Mechanical Engineers Part H-Journal of Engineering in Medicine

Periodical Number






Author Address

Hoskins, PR Univ Edinburgh, Queens Med Res Inst, Ctr Cardiovasc Sci, 47 Little France Crescent, Edinburgh EH16 4TJ, Midlothian, Scotland Univ Edinburgh, Queens Med Res Inst, Ctr Cardiovasc Sci, Edinburgh EH16 4TJ, Midlothian, Scotland Univ Western Australia, Sch Mech & Chem Engn, Intelligent Syst Med Lab, Crawley, WA, Australia Univ Edinburgh, Clin Res Imaging Ctr, Edinburgh, Midlothian, Scotland Univ Edinburgh, Ctr Clin & Surg Sci Surg, Edinburgh, Midlothian, Scotland Univ Edinburgh, Inst Mat & Proc, Sch Engn & Elect, Edinburgh, Midlothian, Scotland Univ Limerick, Dept Mech Aeronaut & Biomed Engn, Limerick, Ireland

Full version

In abdominal aortic aneurysm disease, the aortic wall is exposed to intense biological activity involving inflammation and matrix metalloproteinase-mediated degradation of the extracellular matrix. These processes are orchestrated by monocytes and rather than affecting the aorta uniformly, damage and weaken focal areas of the wall leaving it vulnerable to rupture. This study attempts to model numerically the deposition of monocytes using large eddy simulation, discrete phase modelling and near-wall particle residence time. The model was first applied to idealised aneurysms and then to three patient-specific lumen geometries using three-component inlet velocities derived from phase-contrast magnetic resonance imaging. The use of a novel, variable wall shear stress-limiter based on previous experimental data significantly improved the results. Simulations identified a critical diameter (1.8 times the inlet diameter) beyond which significant monocyte deposition is expected to occur. Monocyte adhesion occurred proximally in smaller abdominal aortic aneurysms and distally as the sac expands. The near-wall particle residence time observed in each of the patient-specific models was markedly different. Discrete hotspots of monocyte residence time were detected, suggesting that the monocyte infiltration responsible for the breakdown of the abdominal aortic aneurysm wall occurs heterogeneously. Peak monocyte residence time was found to increase with aneurysm sac size. Further work addressing certain limitations is needed in a larger cohort to determine clinical significance.