Hemodynamics of the Normal Aorta Compared to Fusiform and Saccular Abdominal Aortic Aneurysms with Emphasis on a Potential Thrombus Formation Mechanism |
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Authors: | Jacopo Biasetti T Christian Gasser Martin Auer Ulf Hedin Fausto Labruto |
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Institution: | (1) Department of Solid Mechanics, Royal Institute of Technology (KTH), Stockholm, Sweden;(2) VASCOPS GmbH, Graz, Austria;(3) Department of Molecular Medicine and Surgery, Karolinska University Hospital, Stockholm, Sweden;(4) Department of Radiology, Karolinska University Hospital, Stockholm, Sweden; |
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Abstract: | Abdominal Aortic Aneurysms (AAAs), i.e., focal enlargements of the aorta in the abdomen are frequently observed in the elderly
population and their rupture is highly mortal. An intra-luminal thrombus is found in nearly all aneurysms of clinically relevant
size and multiply affects the underlying wall. However, from a biomechanical perspective thrombus development and its relation
to aneurysm rupture is still not clearly understood. In order to explore the impact of blood flow on thrombus development,
normal aortas (n = 4), fusiform AAAs (n = 3), and saccular AAAs (n = 2) were compared on the basis of unsteady Computational Fluid Dynamics simulations. To this end patient-specific luminal
geometries were segmented from Computerized Tomography Angiography data and five full heart cycles using physiologically realistic
boundary conditions were analyzed. Simulations were carried out with computational grids of about half a million finite volume
elements and the Carreau–Yasuda model captured the non-Newtonian behavior of blood. In contrast to the normal aorta the flow
in aneurysm was highly disturbed and, particularly right after the neck, flow separation involving regions of high streaming
velocities and high shear stresses were observed. Naturally, at the expanded sites of the aneurysm average flow velocity and
wall shear stress were much lower compared to normal aortas. These findings suggest platelets activation right after the neck,
i.e., within zones of pronounced recirculation, and platelet adhesion, i.e., thrombus formation, downstream. This mechanism
is supported by recirculation zones promoting the advection of activated platelets to the wall. |
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