BACKGROUND: Morphologically, the risk of aortic aneurysm rupture is mainly evaluated based on its type (e.g., fusiform or saccular) and diameter. Based on the finite element analysis, peak wall stress has been identified as a more sensitive and specific predictor of rupture in recent years. Moreover, in finite analysis, the neck of aneurysm is the highest peak wall stress and is associated with the rupture point.
METHODS: A saccular aortic aneurysm (84 mm) was incidentally detected during preoperative examination for chronic empyema in a 74-year-old male patient with a history of polycythemia. Aortic arch graft replacement using an open stent was performed.
CONCLUSIONS: Morphologically, this case was associated with a very high risk of rupture; nevertheless, it did not rupture. In this case, a mural thrombus (likely formed due to polycythemia) covered the neck of aneurysm that is experiencing the highest peak wall stress and is associated with the rupture point. The mural thrombus decreased peak wall stress and could reduce the risk of rupture even for huge saccular aneurysms. Furthermore, the mural thrombus was fully occupied in aneurysms, such as during coil embolization. Thus, polycythemia could decrease the risk of rupture of huge saccular aneurysms.

OBJECTIVE: This study was an unplanned exploratory analysis of a subset of participants from the Telmisartan in the Management of Abdominal Aortic Aneurysm (TEDY) trial. It aimed to assess the efficacy of the angiotensin 1 receptor blocker telmisartan in reducing abdominal aortic aneurysm (AAA) peak wall stress (PWS) and peak wall rupture index (PWRI) among individuals with small AAAs.
METHODS: Participants with AAAs measuring 35 - 49 mm in maximum diameter were randomised to receive telmisartan 40 mg or identical placebo in the TEDY trial. Participants who had computed tomography angiography performed at entry and at least one other time point during the trial (12 or 24 months) were included in the current study. Orthogonal AAA diameter, PWS, and PWRI were measured using previously validated methods. The annual change in PWS and PWRI from baseline was compared between participants allocated telmisartan or placebo using linear mixed effects models. These models were either unadjusted or adjusted for risk factors that were different in the groups at entry (p < .100) or systolic blood pressure (SBP) at one year.
RESULTS: Of the 207 participants recruited to TEDY, 124 were eligible for inclusion in this study. This study included 65 and 59 participants from the telmisartan and placebo groups, respectively. The PWS and PWRI were not significantly different in the two groups at baseline. Participants allocated telmisartan had a slower annual increase in PWS (-4.19; 95% CI -8.24, -0.14 kPa/year; p = .043) and PWRI (-0.014; 95% CI -0.026, -0.001; p = .032) compared with those allocated placebo after adjusting for risk factors. After adjustment for SBP at one year, telmisartan did not significantly reduce annual increases in PWS or PWRI.
CONCLUSIONS: The findings of this study suggest that telmisartan limits the rate of increase in PWS and PWRI of small AAAs by reducing blood pressure.

BACKGROUND: A biomechanical approach to the rupture risk of an abdominal aortic aneurysm could be a solution to ensure a personalized estimate of this risk. It is still difficult to know in what conditions, the assumptions made by biomechanics, are valid. The objective of this work was to determine the individual biomechanical rupture threshold and to assess the correlation between their rupture sites and the locations of their maximum stress comparing two computed tomography scan (CT) before and at time of rupture.
METHODS: We included 5 patients who had undergone two CT; one within the last 6 months period before rupture and a second CT scan just before the surgical procedure for the rupture. All DICOM data, both pre- and rupture, were processed following the same following steps: generation of a 3D geometry of the abdominal aortic aneurysm, meshing and computational stress analysis using the finite element method. We used two different modelling scenarios to study the distribution of the stresses, a \"wall\" model without intraluminal thrombus (ILT) and a \"thrombus\" model with ILT.
RESULTS: The average time between the pre-rupture and rupture CT scans was 44 days (22-97). The median of the maximum stresses applied to the wall between the pre-rupture and rupture states were 0.817 MPa (0.555-1.295) and 1.160 MPa (0.633-1.625) for the \"wall\" model; and 0.365 MPa (0.291-0.753) and 0.390 MPa (0.343-0.819) for the \"thrombus\" model. There was an agreement between the site of rupture and the location of maximum stress for only 1 patient, who was the only patient without ILT.
CONCLUSIONS: We observed a large variability of stress values at rupture sites between patients. The rupture threshold strongly varied between individuals depending on the intraluminal thrombus. The site of rupture did not correlate with the maximum stress except for 1 patient.

Abdominal aortic aneurysm (AAA) rupture is an important cause of death in older adults. In clinical practice, the most established predictor of AAA rupture is maximum AAA diameter. Aortic diameter is commonly used to assess AAA severity in mouse models studies. AAA rupture occurs when the stress (force per unit area) on the aneurysm wall exceeds wall strength. Previous research suggests that aortic wall structure and strength, biomechanical forces on the aorta and cellular and proteolytic composition of the AAA wall influence the risk of AAA rupture. Mouse models offer an opportunity to study the association of these factors with AAA rupture in a way not currently possible in patients. Such studies could provide data to support the use of novel surrogate markers of AAA rupture in patients. In this review, the currently available mouse models of AAA and their relevance to the study of AAA rupture are discussed. The review highlights the limitations of mouse models and suggests novel approaches that could be incorporated in future experimental AAA studies to generate clinically relevant results.

It has been reported clinically that rupture or dissections in thoracic aortic aneurysms (TAA) often occur due to hypertension which may be modelled with sudden increase of peripheral resistance, inducing acute changes of blood volumes in the aorta. There is clinical evidence that more compliant aneurysms are less prone to rupture as they can sustain such changes of volume. The aim of the current paper is to verify this paradigm by evaluating computationally the role played by the variation of peripheral resistance and the impact of aortic stiffness onto peak wall stress in ascending TAA.
Fluid-structure interaction (FSI) analyses were performed using patient-specific geometries and boundary conditions derived from 4D MRI datasets acquired on a patient. Blood was assumed incompressible and was treated as a non-Newtonian fluid using the Carreau model while the wall mechanical properties were obtained from the bulge inflation tests carried out in vitro after surgical repair. The Navier-Stokes equations were solved in ANSYS Fluent. The Arbitrary Lagrangian-Eulerian formulation was used to account for the wall deformations. At the interface between the solid domain and the fluid domain, the fluid pressure was transferred to the wall and the displacement of the wall was transferred to the fluid. The two systems were connected by the System Coupling component which controls the solver execution of fluid and solid simulations in ANSYS. Fluid and solid domains were solved sequentially starting from the fluid simulations.
Distributions of blood flow, wall shear stress and wall stress were evaluated in the ascending thoracic aorta using the FSI analyses. We always observed a significant flow eccentricity in the simulations, in very good agreement with velocity profiles measured using 4D MRI. The results also showed significant increase of peak wall stress due to the increase of peripheral resistance and aortic stiffness. In the worst case scenario, the largest peripheral resistance (1010 kg s m-4) and stiffness (10 MPa) resulted in a maximal principal stress equal to 702 kPa, whereas it was only 77 kPa in normal conditions.
This is the first time that the risk of rupture of an aTAA is quantified in case of the combined effects of hypertension and aortic stiffness increase. Our findings suggest that a stiffer TAA may have the most altered distribution of wall stress and an acute change of peripheral vascular resistance could significantly increase the risk of rupture for a stiffer aneurysm.

In the paper impact of different material models on the calculated peak wall stress (PWS) and peak wall rupture risk (PWRR) in abdominal aortic aneurysms (AAAs) is assessed. Computational finite element models of 70 patient-specific AAAs were created using two different material models - a realistic one based on mean population results of uniaxial tests of AAA wall considered as reference, and a 100 times stiffer artificial model. The calculated results of PWS and PWRR were tested to evaluate statistical significance of differences caused by the non-realistic material model. It was shown that for majority of AAAs the differences are insignificant but for some 10% of them their relative differences exceed 20% which may lead to incorrect decisions on their surgical treatment. This percentage of failures favours application of realistic material models in clinical practise although they are much more time-consuming.

There is no standard for measuring maximal diameter (Dmax) of abdominal aortic aneurysm (AAA) from computer tomography (CT) images although differences between Dmax evaluated from transversal (axialDmax) or orthogonal (orthoDmax) planes can be large especially for angulated AAAs. Therefore we investigated their correlations with alternative rupture risk indicators as peak wall stress (PWS) and peak wall rupture risk (PWRR) to decide which Dmax is more relevant in AAA rupture risk assessment.
The Dmax values were measured by a trained radiologist from 70 collected CT scans, and the corresponding PWS and PWRR were evaluated using Finite Element Analysis (FEA). The cohort was ordered according to the difference between axialDmax and orthoDmax (Da-o) quantifying the aneurysm angulation, and Spearman\'s correlation coefficients between PWS/PWRR - orthoDmax/axialDmax were calculated.
The calculated correlations PWS/PWRR vs. orthoDmax were substantially higher for angulated AAAs (with Da-o≥3mm). Under this limit, the correlations were almost the same for both Dmax values. Analysis of AAAs divided into two groups of angulated (n=38) and straight (n=32) cases revealed that both groups are similar in all parameters (orthoDmax, PWS, PWRR) with the exception of axialDmax (p=0.024).
It was confirmed that orthoDmax is better correlated with the alternative rupture risk predictors PWS and PWRR for angulated AAAs (DA-O≥3mm) while there is no difference between orthoDmax and axialDmax for straight AAAs (DA-O<3mm). As angulated AAAs represent a significant portion of cases it can be recommended to use orthoDmax as the only Dmax parameter for AAA rupture risk assessment.

Abdominal aortic aneurysm (AAA) rupture is a local event in the aneurysm wall that naturally demands tools to assess the risk for local wall rupture. Consequently, global parameters like the maximum diameter and its expansion over time can only give very rough risk indications; therefore, they frequently fail to predict individual risk for AAA rupture. In contrast, the Biomechanical Rupture Risk Assessment (BRRA) method investigates the wall\'s risk for local rupture by quantitatively integrating many known AAA rupture risk factors like female sex, large relative expansion, intraluminal thrombus-related wall weakening, and high blood pressure. The BRRA method is almost 20 years old and has progressed considerably in recent years, it can now potentially enrich the diameter indication for AAA repair. The present paper reviews the current state of the BRRA method by summarizing its key underlying concepts (i.e., geometry modeling, biomechanical simulation, and result interpretation). Specifically, the validity of the underlying model assumptions is critically disused in relation to the intended simulation objective (i.e., a clinical AAA rupture risk assessment). Next, reported clinical BRRA validation studies are summarized, and their clinical relevance is reviewed. The BRRA method is a generic, biomechanics-based approach that provides several interfaces to incorporate information from different research disciplines. As an example, the final section of this review suggests integrating growth aspects to (potentially) further improve BRRA sensitivity and specificity. Despite the fact that no prospective validation studies are reported, a significant and still growing body of validation evidence suggests integrating the BRRA method into the clinical decision-making process (i.e., enriching diameter-based decision-making in AAA patient treatment).

OBJECTIVE: Abdominal aortic aneurysm is a common degenerative vascular disorder associated with sudden death due to aortic rupture. This review describes epidemiology, predisposing factors, and biology of ruptured abdominal aortic aneurysms (rAAAs).
METHODS: Based on a selective literature search in Medline (PubMed), original publications, meta-analyses, systematic reviews, and Cochrane reviews were evaluated for rAAA.
RESULTS: The hospital admission rate for rAAA is decreasing and is now in the range of approximately 10 per 100,000 population in men. Smoking contributes to about 50 % of population risk for rupture or surgically treated AAA. AAA rupture is a multifaceted biological process involving biochemical, cellular, and proteolytic influences, in addition to biomechanical factors. AAA rupture occurs when the stress (force per unit area) on the aneurysm wall exceeds wall strength. Proteolytic activities of matrix metalloproteinases have been implicated in aneurysm wall weakening and rupture. Aneurysm diameter is the most prominent predisposing factor for aneurysm growth and rupture. Wall stress, aneurysm shape and geometry, intraluminal thrombus, wall thickness, calcification, and metabolic activity influence the rupture risk.
CONCLUSIONS: The best conservative option to avoid AAA rupture consists in smoking cessation and control of hypertension. Many biological factors influence rupture risk.

Abdominal aortic aneurysms are a common health problem and currently the need for surgical intervention is determined based on maximum diameter and growth rate criteria. Since these universal variables often fail to predict accurately every abdominal aortic aneurysms evolution, there is a considerable effort in the literature for other markers to be identified towards individualized rupture risk estimations and growth rate predictions. To this effort, biomechanical tools have been extensively used since abdominal aortic aneurysm rupture is in fact a material failure of the diseased arterial wall to compensate the stress acting on it. The peak wall stress, the role of the unique geometry of every individual abdominal aortic aneurysm as well as the mechanical properties and the local strength of the degenerated aneurysmal wall, all confer to rupture risk. In this review article, the assessment of these variables through mechanical testing, advanced imaging and computational modeling is reviewed and the clinical perspective is discussed.