In 2002, Fillinger and colleagues at Dartmouth Hitchcock Medical Center employed FEA to assess the association between wall stress and AAA behavior. Patients who underwent elective repair of asymptomatic AAAs, urgent repair of symptomatic AAAs, and emergent repair of ruptured AAAs were included in the study. The peak wall stress of the symptomatic and ruptured AAAs undergoing nonelective repair was significantly greater than that of the asymptomatic AAAs undergoing elective repair [9]. Moreover, even when accounting for differences in maximum aneurysm diameter, the symptomatic and ruptured AAAs still had a significantly greater peak wall stress than the asymptomatic AAAs. Indeed, the smallest ruptured AAA at 4.8 cm had a peak wall stress equivalent to that of an asymptomatic 6.3 cm abdominal aortic aneurysm. The authors also reported that the location of peak wall stress was not at the point of maximum diameter, but in the posterolateral aspect of the AAA. This location of peak wall stress coincided with the area of rupture in the six patients for whom the location of rupture was known. This seminal study from Fillinger and colleagues highlighted that a noninvasive computational biomechanical analysis of 3D AAA geometry might be superior to maximum diameter alone in predicting an aneurysm rupture risk.

Expanding on their work, Fillinger and colleagues analyzed the ability of maximum diameter versus peak wall stress to predict rupture risk over time in a cohort of patients with AAAs under prospective longitudinal observation [13]. One hundred and three patients with AAAs were assessed in an elective setting: 42 underwent observation without intervention within 1 year of their assessment, 39 underwent elective repair within 1 year, and 22 underwent emergent repair for rupture (n = 8) or symptoms (n = 14). Both index maximum diameter and peak wall stress differed between the groups; however, the latter appeared to better differentiate the AAAs that required emergent repair by receiver operating characteristic curve analysis. Multivariate analysis confirmed that peak wall stress, and not maximum aneurysm diameter, was an independent predictor of rupture risk over time. In addition to these results, the authors reported that almost one-quarter of the patients with ruptured and symptomatic AAAs who underwent emergent repair had maximum aneurysm diameters of 5 cm or less. Approximately three-quarters of the patients who underwent observation without intervention had peak wall stresses lower than the lowest recorded peak wall stress for AAAs that required emergent repair. The findings of this later study by Fillinger and colleagues confirmed those of the previous investigation, suggesting that differences in wall stress could be identified early in the evaluation and treatment of patients with AAA, and thus that FEA might be useful in clinical decision-making.

Additional evidence in support of the role of wall stress in predicting AAA natural history comes from Li and colleagues [14]. Utilizing the rate of AAA expansion as a metric of the risk of aneurysm rupture, these authors sought to analyze the association between wall stress and aneurysm growth. Patients with AAA were included in a longitudinal study with serial computed tomography imaging. Patients with AAA that expanded rapidly (≥4 mm/year) had higher baseline wall stress than slowly expanding AAA (≤4 mm/year). There was no difference in baseline maximum aortic diameter between the two groups. This investigation suggested that AAA with higher wall stress have a greater rate of expansion and consequently a greater risk of rupture. The authors concluded that while the decision to repair AAA remains multifaceted, wall stress could play a role in the management of AAA with diameters in the range of 4–5.5 cm.

As indicated in the prior section, investigators at the University of Pittsburgh have also examined the computationally predicted aortic wall stress in AAAs. However, they have concentrated their efforts on a locally and regionally resolved RPI, instead of peak wall stress alone. They defined the RPI as the ratio between local wall stress and local wall strength, and found that RPI was higher – though the difference was not statistically different – in ruptured than intact AAA [15]. Interestingly, the wall strength was significantly lower in the ruptured group than the intact group, casting some doubt on the clinical utility of wall stress calculations in isolation. Other groups have implemented analyses bases on the RPI formulation: among these is the Munchën group who did find statistically significant increased RPI in symptomatic and ruptured AAA [16].

Our laboratory at the University of Pennsylvania has recently demonstrated the ability to detect the regional aortic wall thickness of the abdominal aorta, including in areas with mural thrombus present [17]. Furthermore, Shang and colleagues in the same lab have shown that the inclusion of locally resolved aortic wall thickness significantly impacts FEA estimates of peak wall stress and that variable wall thickness computational models are more correlated with expansion of AAAs (a putative marker of rupture risk) than are models assuming a uniform aortic wall thickness [10].