# Biomechanical Characterization of Abdominal Aortic Aneurysm: The Rupture Mechanism
## 1 Introduction  
Abdominal aortic aneurysm (AAA) is a progressive, inflammatory disease of the infrarenal aorta leading to irreversible aortic dilation. The consequences of AAA rupture can be severe and life-threatening [1, 2, 3]. AAA diameter has been widely acknowledged as a risk factor of AAA rupture [4]. AAA with a diameter exceeding 5.5 cm is commonly recommended for intervention [5]. This risk factor has raised questions. For example, [PERSON] et al. reported that 60% of AAA cases with a diameter greater than 5 cm did not rupture, while 13% of AAA cases with a diameter less than 5 cm experienced ruptures; more reliable rupture risk markers are needed [6]. In addition, the mechanism of rupture in small AAA, which accounts for 10% of AAA rupture, is still not clear [7]. Various studies have looked into other potential factors, including wall thickness, stiffness, genetic variation, intraluminal thrombus, hemodynamics, and annual growth rate of the AAA [8, 9, 10, 11, 12, 13, 14, 15]. [PERSON] et al. measured the ruptured human aneurysms showing thickened aortic walls in 1.78 \(\pm\) 0.39 mm, while the unruptured ones were in 1.48 \(\pm\) 0.22 mm [16]. [PERSON] et al. also determined the variation in human AAA wall thickness from rupture sites as low as 0.23 mm to the calcified site in 4.26 mm (median = 1.48 mm) [17]. Even though nobetter risk factors have been identified, it is commonly recognized that the progression of AAA is linked to substantial changes in the microarchitecture of the aortic wall and the loss of mechanical integrity, specifically the progression of AAA-induced fragmentation of elastin fibers, elastin degradation, loss of proper functioning of the smooth muscle cells, and the resulting deposition of collagen concentration for repairing/compensating the damaged aortic wall [18; 19]. The newly deposited collagen fibers are typically distributed in a random manner, which might disrupt their intended functionality [20]. An imbalance between collagen degradation and collagen synthesis could lead to catabolic conditions, which might contribute to AAA rupture [18; 21].  
The increased wall stiffness has been quantified in AAA patients utilizing pulse wave velocity measurement [22]. But the way mechanical property changes contribute to AAA rupture is still not clear. One study using uniaxial tensile test has shown that different regions of the AAA have different yield stress, and that lower yield stress may result in the initiation of AAA rupture [23]. Another study has shown that ruptured AAA samples are not weaker than unruptured ones in terms of global failure stress and failure strain [24]. Both studies indicate the necessity of the micromechanical characterization of the AAA. [PERSON] et al. determined the microstructure of AAA through histology and confocal microscopy, and further quantified the mechanical properties of AAA with atomic force microscopy (AFM) [20]. The study has shown that the microstructure of the AAA tissue led to different mechanical properties, and further mechanical failure. The microstructure of AAA and the heterogeneous mechanical behaviors need to be further exploited for better understanding the mechanism of AAA rupture.  
The goal of this work is to identify the AAA rupture prediction using combined histological analysis and micromechanical characterizations. The relationship between aortic wall microstructure and its stiffness in both AAA samples and controlled ones, both of which are obtained from four-week-old male C57 Bl/6 mice, are quantified. The degradation of elastin, density of collagen, and morphology changes in the AAA wall will be inspected with histological analysis. Mechanical characterization will be conducted with AFM indentation.