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

机译:使用电路模型和病例系列分析的胰十二指肠动脉瘤形成的血流动力学模拟

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摘要

>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.
机译:>目的:使用简单的电子电路模型评估动脉瘤形成的机制。>材料和方法:我们创建了将腹腔动脉(CA)与肠系膜上动脉连接的简单电路模型动脉通过胰十二指肠拱门。我们回顾性分析了2004年至2017年间接受开放或血管内治疗的12例真正的胰十二指肠动脉瘤(PDAA)患者。我们设置了每条动脉和器官的阻力,并根据模拟CA狭窄程度从0开始计算流量和速率%至99.9%。>结果:当CA狭窄度从0%增加到50%,然后急剧增加时,胰十二指肠前动脉和胰十二指肠后动脉的流量减少至零,此时流向恢复流量高达初始速率的三倍。胃十二指肠动脉(GDA)也显示血流逆流,伴有严重的CA狭窄。在12例PDAA患者中,有8例出现了CA病变,其他患者出现了合并症,导致动脉在病理上脆弱,例如马凡氏综合症,白塞病和节段性动脉硬化。所有四个GDA动脉瘤均未伴有CA病变。>结论:使用我们的模型可以部分解释CA病变相关的PDAA形成的机制。

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