In the first part of this study we develop a realistic subject-specific aorta finite element model derived from a dual-venc MRI scan. We investigate if spontaneous dissection will occur under extreme hypertensive lumen blood pressure loading, or if significant reduction in interface strength must occur in order for dissection to initiate. Importantly, we also demonstrate that dissection initiation is a pure mode II fracture process, rather than a mixed mode or mode I process. In the second part of this study we construct a parameterised idealised aorta model in order to assess the relative contribution for several anatomical and physiological factors to dissection risk. Such parametric analyses provide fundamental insight into the mechanics of stress localisation and delamination in the aorta. Overall, our detailed series of simulations suggest that variations in anatomical features and hypertensive loading will not result in a sufficient elevation of the stress state in the aorta wall to initiate dissection. Our results suggest that initiation of aortic dissection requires a significant reduction in the mode II fracture strength of the aortic wall, suggesting that dissection is preceded by structural and biomechanical remodelling.
Fatigue Fracture Analysis of Dissimilar Residual Stress in Dissimilar Aluminum Alloy Friction Stir Welded Joints