Ascending thoracic aortic aneurysm (ATAA) is among the most devastating forms of cardiovascular disease, causing a significant mortality despite current medical and surgical treatments [1]. Moreover these therapies themselves are associated with great risk of mortality or morbidity, complicated by the advanced age of the typical patient, and high surgical costs. The mechanics of spontaneous aortic dissection is not fully understood. It is generally believed that aortic dissection initiates as an intimal tear in which a separation of wall layers produces the formation of a 'false' lumen. The dissection may propagate axially and/or circumferentially due to blood flow and pressure. Dissection may lead to several possible complications. For example, the septum between the false lumen and true lumen may fracture, resulting in embolism and ischemic damage. Another possibility is that the thinned and weakened residual outer aortic wall may fail, resulting in rapid blood loss and tamponade. From a mechanical point of view, aortic dissection is due to the combination of hemodynamic loads acting on the intimal layer and the laminar structure of the aortic wall with different elastic properties. Since the aorta is an anisotropic and inhomogeneous body, it is possible that the hemodynamic loads (including mural shear) produce stresses of the appropriate types and magnitudes that result in delamination of the aortic layers [2]. That is, dissection initiates when the hemodynamic loads overcome the adhesive forces holding the layers together. The effects of the loads are of course accentuated in the case of a disorganized microstructure and degenerated tissue that is typical in aneurysmal disease.
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