## 4 Discussion
Lastly, in silico models use solid mechanics and fluid mechanics simulation platforms, in conjunction with material and geometrical data to model the behaviour of the aortic wall, blood, and stent-graft components across preclinical, and clinical settings [15; 19]. However, the accuracy of predictions generated from these models depends on the fidelity of the selected model equations, assumptions, and boundary conditions; alongside the accuracy of the experimentally-derived parameters such as aortic wall geometry and compliance [15; 19]. Ultimately, this methodology is limited by its greater degree of abstraction from the clinical in vivo setting compared to in vitro physical models [15; 19]. Overall, the proposed ex vivo locally elastin-depleted porcine aorta model meets an existing need for a tissue-based non-living physical model which recapitulates the geometric and mechanical properties of the aneurysal aortic wall. The model produced and characterised as part of this work demonstrates several key advantages. First, the proposed model meets an established need for an ex vivo large animal model representative of the geometric and compliance features of aneurysms suitable for endovascular device testing. It represents a comprehensive reproduction of the mechanical features of aneurysm and its use could facilitate better testing and optimisation of endovascular devices prior to in vivo testing. Second, the produced model can be directly assembled from widely available low-cost parts allowing for rapid production and use. Lastly, this approach can produce models of aneurysms demonstrating distinct geometric or anatomical features, e.g., aortic root or arch aneurysms, facilitating the improvement of endovascular treatments in these areas [7]. Overall, our proposed model demonstrates clear advantages: it replicates the mechanical features of AA better than existing in vitro models; requires minimal skill and resource requirements; and has the potential for customisability to specific aneurysm pathologies. However, the produced model requires further optimisation prior to its progression in the testing of endovascular devices. The degree of elastin degradation produced in whole aortae as part of this work resulted in an approximate 5% increase in dilation and no change in compliance under physiological pressures compared to controls. Human aneurysms demonstrate a 50% increased diameter [1] and a 44% and 60% increased circumferential stiffness at thoracic or abdominal locations, respectively, compared to non-aneurysmal aortae [18; 57]. While our findings are consistent with the level of degradation seen, a largerdegree of elastin degradation is needed to produce a more physiologically relevant model. Furthermore, the 1 cm length utilized as part of this study is not representative of the lengths of aneurysmal dilation in human aneurysms [59]. Reproduction of our localised degradation over a longer time period and larger aortic segment, would produce a model more robust for use in endovascular device testing. This work is subject to several methodological limitations. First, the studied group is relatively small comprising samples from 5 animals in the ring analysis and 6 animals in the whole-aorta analysis. However, while the sample number was low, experiments were sufficiently powered to observe statistically meaningful differences. Second, use of an enzyme-soaking method limited direct translation of the 9-h elastase treatment protocol directly from ring-samples to whole aorta in this work most likely due to differences in the exposed surface area to volume ratio. This method was selected for use in this work due to its simplicity and its successful use in relevant background literature to produce the desired changes in arterial geometry and compliance [22; 40; 41; 53]. Future work will explore the importance of controlling diffusion parameters such as the ratio of exposed sample surface area to volume ratio, between experiments when using this technique.