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Background: The natural history of abdominal aortic aneurysm (AAA) can be investigated through longitudinal evaluation of localized aneurysm characteristics exploiting clinical images. The major challenge is to identify corresponding regions between follow-ups. We have recently developed an algorithm (VascForm) based on nonrigid registration that can obtain surface correspondence and quantify surface growth distribution., Methods: A ruptured AAA with an initial computed tomography scan 2 years ago was studied. Following 3-dimensional reconstruction of outer wall and luminal surfaces, the wall/thrombus thickness was obtained. Wall stress distribution was computed with finite element analysis, and computational fluid dynamics simulation was performed. VascForm was applied and allowed for the ruptured wall site to be traced back to the initial wall surface and be correlated with local initial intraluminal thrombus thickness, wall stress, and hemodynamic parameters. It also allowed for the quantification of wall surface growth based on surface element growth., Results: Rupture occurred at the posterolateral side. Initial wall surface growth was in most regions 40%. However, a large section of the posterior wall presented 110% growth. Initial thrombus deposition was more prevalent anteriorly, and a posterior thrombus-free isle was present. Peak wall stress (initial and follow-up) occurred at AAA neck. Nonrigid registration revealed that rupture originated from the vicinity of the initial thrombus-free isle. Furthermore, rupture occurred at the wall region with the largest growth (110%). No clear correlation between hemodynamics and rupture site could be identified., Conclusions: High local surface growth correlates with rupture site and could therefore potentially become a marker of rupture risk. The ongoing application of this methodology to a large cohort of AAA patients will focus on identifying characteristic features of AAA regions that present high surface growth in follow-up evaluations, to assist in improved rupture risk estimation., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Purpose: To investigate the observed inflow stenosis at the O-rings of the Ovation stent-graft and evaluate its hemodynamic and clinical impact., Methods: The study involved 49 consecutive patients (48 men; mean age 71.2 ± 7.7 years) treated successfully with the Ovation abdominal aortic stent-graft between June 2011 and January 2014 at a single center. Cross-sectional area and radius measurements of the infrarenal aorta just proximal to the sealing mechanism, as well at the site of stenosis, were measured from 3D reconstructions of the 1-month postoperative computed tomographic angiograms. Based on Poiseuille's law, the predicted pressure drop was calculated for each patient based on the length of the stenosis. Invasive blood pressure measurements at 3 levels (proximal to the inflatable rings, halfway inside the stenosis, and distal to the stenosis) were obtained in 10 patients intraoperatively. Ankle-brachial index (ABI) values preoperatively were compared to those after the procedure for all patients to assess the clinical impact of this phenomenon., Results: Median internal cross-sectional area at the site of the stenosis was significantly reduced compared to the area just proximal to the O-rings [57% reduction: 123 mm(2) (range 28-254) vs. 283 mm(2) (range 177-531), respectively; p<0.001]. The same was observed for the radius [6.5 mm (range 3-9) vs. 9.5 mm (range 7.5-13), respectively; p<0.001]. Based on the median 15 mm length of the stenosis (range 13-17) observed in the study population, a median pressure drop of 0.13 mmHg (range 0-0.25) along the stenosis was calculated. Invasive blood pressure measurements indicated a non-significant pressure change along the stenosis (e.g., 0.7 mmHg between the proximal level and halfway inside the stenosis). ABI remained practically unchanged postoperatively., Conclusion: The advantages of the Ovation device's unique sealing mechanism come at the expense of a median area inflow stenosis of ∼ 60%. This stenosis does not cause a hemodynamically significant pressure drop. Future modification of the graft ring design may be needed in order to reduce this stenosis.

Object: Hemodynamic insult has been speculated to be a key factor in intracranial aneurysm formation; however, it is unclear whether a sustained insult is necessary. The authors examined whether aneurysmal degradation would continue despite the normalization of wall shear stress (WSS) by adaptive outward vascular remodeling., Methods: Twenty-five rabbits underwent either sham operation (5 animals) or bilateral common carotid artery ligation (20 animals) to augment basilar artery (BA) flow. Basilar termini (BTs) were harvested at 5 days and 3, 12, and 27 weeks postoperation. Histological changes at the BTs were quantified using an aneurysm development score (ADS) wherein the luminal length of the vessel wall exhibiting internal elastic lamina (IEL) loss, media thinning (> 30% media loss), and bulging was multiplied by the percentage of media thinning divided by the BA diameter. This score and its component variables were evaluated over the specified time points and compared with the WSS time course obtained from multiple angiography and BA flow velocity measurements., Results: Serial examination of histological sections from the ligation group (17 rabbits survived the procedure) demonstrated localized, progressive, degenerative, and aneurysmal changes at the BTs. Prominent IEL loss was observed in BT specimens from all ligated animals. Media thinning and luminal bulging significantly progressed over the 27-week follow-up. The composite ADS significantly increased over the study period, indicating progressive aneurysm development, although the WSS returned to preligation baseline values within 5 weeks of ligation., Conclusions: Hemodynamic insult can elicit a pathological vascular response leading to a self-sustaining aneurysmal remodeling that does not require persistence of the original inciting factor to continue its pathological progression.