# Biomechanical Characterization of Abdominal Aortic Aneurysm: The Rupture Mechanism
## 4 Discussion  
The mechanical characterization of AAA at the micro-length scale is essential for disease management, especially the prediction of AAA rupture. In this work, the microstructures and mechanical properties of AAA were quantified using AFM, along with histology analysis. The AAA samples were dissected from the elastase-treated mouse AAA model. It is clear from AFM scanning that the control group has aligned texture, while the AAA group has a fragmented texture. The heterogeneity of AAA was investigated with two AFM probe tip sizes of 5 \(\upmu\)m and 20 nm. From tip size of 20 nm, the histogram of the stiffnesses clearly shows two frequency peaks in the AAA group, which was not observed in the control group. The AAA group showed a significant higher stiffness than the control group with a tip size of 5 \(\upmu\)m. The two frequency peaks in the AAA group with the 20 nm  
Figure 6: (**a**) Average Young’s modulus of AAA and healthy control artery conducted with a 5 \(\upmu\)m probe. Asterisks (**) represent a significant difference between the groups’ \(p\)-value \(<\) 0.01 significance level T test. (**b**) Average Young’s modulus of AAA and healthy control artery conducted with a 20 nm probe. Asterisk (*) represents a significant difference between groups’ \(p\)-value \(<\) 0.05 significance level T test. probe indicate that the weak region may contribute to the initiation and propagation of AAA rupture. Our mouse AAA model was successfully developed using elastase treatment, as shown in our histological analysis. The enlargement of the lumen, degradation of the elastin, increased density of collagen, and formation of microvessels were clearly observed in AAA samples. [PERSON] et al. have shown a detailed surgical procedure to maintain a stable AAA growth rate by directly applying the porcine pancreatic elastase to the adventitia layer of the artery [28]. Another study has shown that a chronic AAA model could be induced with the combination of \(\beta\)-aminopropionitrile (BAPN) administration and periaortic elastase, which demonstrated persistent long-term aneurysm growth, thrombus formation, and spontaneous rupture [29]. In our AAA model, a complete degradation of elastin lamellae was observed in the artery, with minimal local residual elastin observed. Additionally, the thickening of the artery wall and microvessels' formation were observed in this work, which is consistent with the documented studies [30; 31]. Although quite a few studies have shown the decline of the wall thickness during AAA progression [32], wall thickening and microvessel formation at the initial stage of AAA have not been sufficiently studied. The thickening process might be result from the endocytic regulation of growth factors against AAA [31], which has been described as \"good intentions to try and make more smooth muscle, but actually it makes the problem worse\" [33]. This wall thickening and microvessel formation at the initial stage of AAA may provide a window into understanding the initiation of AAA for the development of an early method of detection and treatment. Rupture prediction is essential for AAA management, including the decision to undertake elective repair of AAA [34]. Current surgery decisions are based on an AAA maximum diameter of 5.5 mm [5]. A retrospective study on massive untreated large AAA in patients has shown that the risk of death from causes other than AAA was higher than the risk of death from rupture [35]. On the other hand, the rupture rate of the small AAA (size \(<\) 5.5 mm) appears to be between less than 1.61 per 100 person years [36], and accounts for 10% of AAA rupture [7]. These observations indicate a dire need to improve rupture prediction for small AAA, and to rethink the mechanism of rupture in large AAA. It is well acknowledged, based on the Laplace formula \(\sigma_{h}=PD/2t\), that a larger AAA size (D) correlates with high hoop stress (\(\sigma_{h}\)) in the vessel wall for a certain blood pressure \(P\) and wall thickness \(t\).