Kazuhiro Miyahara1, Katsuyuki Hoshina1, Jun Nitta1, Masaru Kimura1, Sota Yamamoto2, Marie Ohshima3. 1. Division of Vascular Surgery, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. 2. Department of Mechanical Engineering, Graduate School, Shibaura Institute of Technology, Tokyo, Japan. 3. Interfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Abstract
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.
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 GDAaneurysms were not accompanied by CA lesions. Conclusion: The mechanism underlying CA-lesion-associated PDAA formation may be partially explained using our model.