###### Abstract  
Aortic aneurysms (AA) occur in 4.8% of people causing 150,000 deaths annually. While endovascular aneurysm repairs reduce surgical morbidity, device-related failures (leak/displacement) are frequent highlighting the need for test models that better represent the mural geometry and compliance changes in human AAs. We aimed to develop and characterise an ex vivo porcine aortic model of AA. The optimal duration of tissue elastase exposure to emulate AA changes in elastin microstructure and content was determined using porcine aortic rings. Elastase-induced changes were quantified morphologically, and mechanical properties assessed via ring tensile testing. Subsequent experiments tested the potential for localised elastase treatment in a 1 cm segment of porcine aorta using a specially designed 3D printed rig. The effect on pressure-diameter behaviour was investigated via inflation-extension testing. Elastase treatment produced time dependent decreases in elastin, resulting in an increased tensile modulus and circumferential length in the ring samples in the final phase of the \(J\)-shaped tissue stress-strain curves. In whole aortic segments, localised elastase-induced luminal degradation was successfully limited to a central region. The degree of elastin degradation achieved was sufficient to cause localised dilation with respect to controls under physiological pressures. Localised elastin degradation in porcine aortic segments is feasible and emulates the changes seen clinically in aortic aneurysms. a +
Footnote †: journal: _Sciences_  
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and device kinking and fracture [7; 15].There is a need to optimise endovascular aneurysm repair devices to maintain functionality in the challenging mechanical environment present in aortic aneurysms (AA) [16; 17; 18; 19]. An implanted stent graft must match both the dilation and recoil of the vessel wall during the cardiac cycle and withstand the haemodynamic forces imposed by flowing blood to maintain a proper seal and fixation [7]. Not only are the geometry of the aorta and the pressure-flow characteristics of the blood important, but the compliance of the vessel wall must also be taken into account [20]. The healthy arterial wall exhibits non-linear hyperelastic behaviour characterised by an increasing stiffness with increasing deformation resulting in a J-shaped stress-strain curve [21]. This behaviour is attributed to the initial recruitment of elastin fibres in conjunction with the progressive strain-dependent recruitment of stiff collagen fibres [16; 22]. Destruction and degeneration of mural elastin fibres is widely believed to cause the increases in stiffness seen in AA through the resultant load being taken up by the stiffer collagen fibres [17; 23; 24]. As such, the mechanical environment present in AA differs from that found in healthy aorta because of both the locally dilated vessel geometry and decreased mural compliance. Optimisation of endovascular devices using in vitro benchtop models, which recapitulate these changes in geometry and compliance, offers a means to address, and ultimately reduce, the incidence of endovascular device complications secondary to mechanical failures. In vitro models represent an invaluable tool in facilitating the refinement and optimisation of device designs prior to costly preclinical in vivo trials [25; 26]. The ex vivo porcine aorta is the most utilised model based on its widespread availability and structural similarity to healthy human aorta [27; 28; 29; 30]. However, it does not replicate the dilation nor the stiffening seen in AA [31]. While synthetic models can accurately replicate the geometric features of aneurysms, the materials used poorly replicate the compliance and rupture properties of arterial tissues [20; 32; 33; 34; 35]. Currently available tissue engineered in vitro models are more suited to studies of aneurysm pathophysiology and have not yet been manufactured on a scale suitable for endovascular device testing [36; 37; 38].