Biomechanical weakening of the aorta leads to aneurysm formation and/or dissection and total biomechanical failure results in rupture, which is often fatal. The most common aneurysm is the abdominal aortic aneurysm (AAA) whereas thoracic aortic aneurysms (TAA) involve the ascending or descending segments of the aorta. Biomechanical strength of the aorta is maintained in part via balance between the integrity of the aortic medial and adventitial extracellular matrix and the health of the mural cells. From a biomechanical perspective, aneurysms rupture or dissect when wall stresses locally exceed the wall strength. Pathobiologic mechanisms, pre-disposing disorders and variability of patient demographic characteristics can weaken the aortic wall while increased blood pressure and dilatation increase the stress acting on it, leading to further aneurysm expansion. Thoracic and abdominal aortic aneurysms arise from very different pathophysiologies that ultimately result in a final common outcome of matrix degeneration and biomechanical failure. Therefore, the patient-specific knowledge of both wall stress and wall strength distributions for a given aneurysm will greatly improve the ability to identify those aortic aneurysms that are at highest risk of rupture. Towards this end, the biomechanics of AAA has been studied extensively by many groups whereas TAA biomechanics has not been fully considered. This chapter articulates the state-of-the-art of aortic biomechanics, including the modeling of tensile strength and wall stress distributions and the biological mechanisms which influence them. The potential clinical utility of these biomechanical estimates in predicting AAA rupture is also discussed.

Phillippi J.A., Pasta S., Vorp D.A. (2011). Biomechanics and Pathobiology of Aortic Aneurysms. In Tim McGloughlin (a cura di), Biomechanics and Mechanobiology of Aneurysms (pp. 67-118). Springer [10.1007/8415_2011_84].

Biomechanics and Pathobiology of Aortic Aneurysms

Pasta S.;
2011

Abstract

Biomechanical weakening of the aorta leads to aneurysm formation and/or dissection and total biomechanical failure results in rupture, which is often fatal. The most common aneurysm is the abdominal aortic aneurysm (AAA) whereas thoracic aortic aneurysms (TAA) involve the ascending or descending segments of the aorta. Biomechanical strength of the aorta is maintained in part via balance between the integrity of the aortic medial and adventitial extracellular matrix and the health of the mural cells. From a biomechanical perspective, aneurysms rupture or dissect when wall stresses locally exceed the wall strength. Pathobiologic mechanisms, pre-disposing disorders and variability of patient demographic characteristics can weaken the aortic wall while increased blood pressure and dilatation increase the stress acting on it, leading to further aneurysm expansion. Thoracic and abdominal aortic aneurysms arise from very different pathophysiologies that ultimately result in a final common outcome of matrix degeneration and biomechanical failure. Therefore, the patient-specific knowledge of both wall stress and wall strength distributions for a given aneurysm will greatly improve the ability to identify those aortic aneurysms that are at highest risk of rupture. Towards this end, the biomechanics of AAA has been studied extensively by many groups whereas TAA biomechanics has not been fully considered. This chapter articulates the state-of-the-art of aortic biomechanics, including the modeling of tensile strength and wall stress distributions and the biological mechanisms which influence them. The potential clinical utility of these biomechanical estimates in predicting AAA rupture is also discussed.
Settore ING-IND/34 - Bioingegneria Industriale
Phillippi J.A., Pasta S., Vorp D.A. (2011). Biomechanics and Pathobiology of Aortic Aneurysms. In Tim McGloughlin (a cura di), Biomechanics and Mechanobiology of Aneurysms (pp. 67-118). Springer [10.1007/8415_2011_84].
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10447/432149
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