BackgroundWe aimed to develop a simple structural model of aortic aneurysms using computer‐assisted drafting (CAD) in order to create a basis of definition for saccular aortic aneurysms.Methods and ResultsWe constructed a simple aortic aneurysm model with 2 components: a tube similar to an aorta and an ellipse analogous to a bulging aneurysm. Three parameters, including the vertical and horizontal diameters of the ellipse and the fillet radius, were altered in the model. Using structural analysis with the finite element method, we visualized the distribution of the maximum principal stress (MPS) in the aortic wall and identified the area(s) of prominent stress. We then selected patients with thoracic aortic aneurysms in whom the aneurysm expansion rates were followed up and applied the theoretical results to the raw imaging data. The maximum MPS drastically increased at areas where the aspect ratio (vertical/horizontal) was <1, indicating that “horizontally long” hypothetical ellipses should be defined as “saccular” aneurysms. The aneurysm expansion rate for the patients with thoracic aneurysms conforming to these parameters was significantly high. Further, “vertically long” ellipses with a small fillet might be candidates for saccular aneurysms; however, the clinical data did not support this.ConclusionsBased on the biomechanical analysis of a simple aneurysm model and the clinical data of the thoracic aortic aneurysms, we defined “horizontally long” aortic aneurysms with an aspect ratio of <1 as “saccular” aneurysms.

Objective : To assess mechanisms underlying aneurysm formation using a simple electronic circuit model. Materials and Methods : We created a simple circuit model connecting the celiac artery (CA) to the superior mesenteric artery via the pancreaticoduodenal arcade. We retrospectively reviewed 12 patients with true pancreaticoduodenal artery aneurysms (PDAAs) who received open or endovascular treatment between 2004 and 2017. We set the resistance of each artery and organ voltage and calculated flow volume and rate in response to degrees of simulated CA stenosis from 0% to 99.9%. Results : Flow volume rates of the anterior pancreaticoduodenal artery and posterior pancreaticoduodenal artery decreased to zero when CA stenosis increased from 0% to 50% and then increased drastically, at which point flow direction reverted and the flow was up to three times the initial rate. The gastroduodenal artery (GDA) also showed reversed flow with severe CA stenosis. In 12 patients with PDAA, eight presented with a CA lesion, and the other patients presented with comorbidities causing the arteries to be pathologically fragile, such as Marfan syndrome, Behçet’s disease, and segmental arterial mediolysis. All four GDA aneurysms were not accompanied by CA lesions. Conclusion : The mechanism underlying CA-lesion-associated PDAA formation may be partially explained using our model.

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The geometric analysis performed in this study revealed that ruptured AAAs had a smaller fillet radius and smaller aspect ratio than nonruptured AAAs did.