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Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis

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 patie...

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Autores principales: Miyahara, Kazuhiro, Hoshina, Katsuyuki, Nitta, Jun, Kimura, Masaru, Yamamoto, Sota, Ohshima, Marie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Japanese College of Angiology / The Japanese Society for Vascular Surgery / Japanese Society of Phlebology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6600102/
https://www.ncbi.nlm.nih.gov/pubmed/31275470
http://dx.doi.org/10.3400/avd.oa.19-00005
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author Miyahara, Kazuhiro
Hoshina, Katsuyuki
Nitta, Jun
Kimura, Masaru
Yamamoto, Sota
Ohshima, Marie
author_facet Miyahara, Kazuhiro
Hoshina, Katsuyuki
Nitta, Jun
Kimura, Masaru
Yamamoto, Sota
Ohshima, Marie
author_sort Miyahara, Kazuhiro
collection PubMed
description 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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spelling pubmed-66001022019-07-03 Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis Miyahara, Kazuhiro Hoshina, Katsuyuki Nitta, Jun Kimura, Masaru Yamamoto, Sota Ohshima, Marie Ann Vasc Dis Original Article 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. Japanese College of Angiology / The Japanese Society for Vascular Surgery / Japanese Society of Phlebology 2019-06-25 /pmc/articles/PMC6600102/ /pubmed/31275470 http://dx.doi.org/10.3400/avd.oa.19-00005 Text en Copyright © 2019 Annals of Vascular Diseases http://creativecommons.org/licenses/by-nc-sa/4.0/ ©2019 The Editorial Committee of Annals of Vascular Diseases. This article is distributed under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided the credit of the original work, a link to the license, and indication of any change are properly given, and the original work is not used for commercial purposes. Remixed or transformed contributions must be distributed under the same license as the original.
spellingShingle Original Article
Miyahara, Kazuhiro
Hoshina, Katsuyuki
Nitta, Jun
Kimura, Masaru
Yamamoto, Sota
Ohshima, Marie
Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title_full Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title_fullStr Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title_full_unstemmed Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title_short Hemodynamic Simulation of Pancreaticoduodenal Artery Aneurysm Formation Using an Electronic Circuit Model and a Case Series Analysis
title_sort hemodynamic simulation of pancreaticoduodenal artery aneurysm formation using an electronic circuit model and a case series analysis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6600102/
https://www.ncbi.nlm.nih.gov/pubmed/31275470
http://dx.doi.org/10.3400/avd.oa.19-00005
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