Abdominal aortic aneurysm
Analysis of the role of emofluidodynamic forces in AAA expansion
Abdominal aortic aneurysm (AAA) is a degenerative disease of the last segment of the abdominal aorta. It represents the 13th leading cause of death in the western world, with a greater incidence in the male population over age of 65 years.
If not treated an AAA may rupture, a severe clinical event associated with high rate of mortality and morbidity. All the repair techniques are not without risks. Clinicians are therefore faced with a major dilemma: determining and deciding whether the risk of rupture justifies the risks associated with surgery. Since long clinicians have struggle in an attempt to identify the mechanisms that lead to aneurysm wall failure; nevertheless, rupture risk indexes are mostly based on empirical meas- urements, such as maximum AAA diameter, wall stress or peak wall stress, rather than on the physical principles that might trigger rupture.
Anisotropy of AAA wall displacements was observed in ultrasound investigations along the cardiac cycle, a crucial phenomenon that from one side supposedly may affects wall stress and strain
distributions on different areas of the aneurysm shape, and on the other, influences wall remodeling processes and rupture.
A reasonable hypothesis is that anisotropic displacements are partially due to the action of bulk hemodynamics, i.e. to the dynamic pressure of the jet impinging on the wall, which is in turn associated with the altered anatomy of the abdominal aorta and the AAA. This is an important issue to address, since if this hypothesis were verified, hemodynamics would acquire a new role in AAA progression studies and in the design of rupture risk indexes.
Technological advances in both biomedical imaging and CFD fields give us the chance to directly and quantitatively focus on this problem: in fact, the retrieval of in vivo AAA wall displacements non- invasively is made possible by means of time resolved CT scanner, while CFD provides a reliable mean to simulate patient-specific hemodynamics.
For each dataset, the 3D surface model of the lumen boundary of the abdominal aorta was reconstructed using a gradient-driven level set approach for all the available time frames. Once the geometry of the specific patient was reconstructed, the surface model has then been successively turned into volumetric meshes of linear tetrahedra (in the range 1100000-2200000 elements) in view of computational fluid-dynamics simulations. The mesh size was set after a mesh refinement study, with the aim of obtaining a mesh-independent numerical solution.
Unsteady numerical simulations are performed using the finite element code LifeV (LifeV). At the inlet, a physiological flow rate is chosen as representative of the physiological impulse. At the outlets, a zero-stress condition is prescribed, since the region of interest is in the aneurismatic sack.
WSS was here used as a compact measure of fluid dynamic features and to localize the impingement area on the AAA wall. Comparisons between WSS and displacement fields were performed: the presence of the WSS peak can be associated with a distinctive area of enlargement along the AAA wall with respect to the mid-diastolic reference position.
Statistical analysis of the correlation between WSS maps and displacement fields will be per- formed as a quantitative measure of the associations identified so far.
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