Endografts placed in the aorta for thoracic endovascular aortic repair (TEVAR) may determine malappositioning to the lesser curvature of the aortic wall, thus resulting in a devastating complication known as endograft collapse. This premature device failure commonly occurs in young individuals after TEVAR for traumatic aortic injuries as a result of applications outside the physical conditions for which the endograft was designed. In this study, an experimentally-calibrated fluid-structure interaction (FSI) model was developed to assess the hemodynamic and stress/strain distributions acting on the excessive protrusion extension (PE) of endografts deployed in four young patients underwent TEVAR. Endograft infolding was experimentally measured for different hemodynamic scenarios by perfusion testing and then used to numerically calibrate the mechanical behavior of endograft PE. Results evinced that the extent of endograft can severely alter the hemodynamic and structural loads exerted on the endograft PE. Specifically, PE determined a physiological aortic coarctation into the aortic arch characterized by a helical flow in the distal descending aorta. High device displacement and transmural pressure across the stent-graft wall were found for a PE longer than 21 mm. Finally, marked intramural stress and principal strain distributions on the protruded segment of the endograft wall may suggest failure due to material fatigue. These critical parameters may contribute to the endograft collapse observed clinically and can be used to design new devices more suitable for young individuals to be treated with an endoprosthesis for TEVAR of blunt traumatic aortic injuries.

Rinaudo A., Raffa G.M., Scardulla F., Pilato M., Scardulla C., Pasta S. (2015). Biomechanical implications of excessive endograft protrusion into the aortic arch after thoracic endovascular repair. COMPUTERS IN BIOLOGY AND MEDICINE, 66, 235-241 [10.1016/j.compbiomed.2015.09.011].

Biomechanical implications of excessive endograft protrusion into the aortic arch after thoracic endovascular repair

Rinaudo A.;Raffa G. M.;Scardulla F.;Scardulla C.;Pasta S.
2015-01-01

Abstract

Endografts placed in the aorta for thoracic endovascular aortic repair (TEVAR) may determine malappositioning to the lesser curvature of the aortic wall, thus resulting in a devastating complication known as endograft collapse. This premature device failure commonly occurs in young individuals after TEVAR for traumatic aortic injuries as a result of applications outside the physical conditions for which the endograft was designed. In this study, an experimentally-calibrated fluid-structure interaction (FSI) model was developed to assess the hemodynamic and stress/strain distributions acting on the excessive protrusion extension (PE) of endografts deployed in four young patients underwent TEVAR. Endograft infolding was experimentally measured for different hemodynamic scenarios by perfusion testing and then used to numerically calibrate the mechanical behavior of endograft PE. Results evinced that the extent of endograft can severely alter the hemodynamic and structural loads exerted on the endograft PE. Specifically, PE determined a physiological aortic coarctation into the aortic arch characterized by a helical flow in the distal descending aorta. High device displacement and transmural pressure across the stent-graft wall were found for a PE longer than 21 mm. Finally, marked intramural stress and principal strain distributions on the protruded segment of the endograft wall may suggest failure due to material fatigue. These critical parameters may contribute to the endograft collapse observed clinically and can be used to design new devices more suitable for young individuals to be treated with an endoprosthesis for TEVAR of blunt traumatic aortic injuries.
Rinaudo A., Raffa G.M., Scardulla F., Pilato M., Scardulla C., Pasta S. (2015). Biomechanical implications of excessive endograft protrusion into the aortic arch after thoracic endovascular repair. COMPUTERS IN BIOLOGY AND MEDICINE, 66, 235-241 [10.1016/j.compbiomed.2015.09.011].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/411611
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