Pathogenesis of Acute Aortic Dissection: A Finite Element Stress Analysis

Pathogenesis of Acute Aortic Dissection: A Finite Element Stress Analysis
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DOI:
10.1016/j.athoracsur.2010.10.042
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发表时间:
2011-02-01
影响因子:
4.6
通讯作者:
Jackson, Benjamin M.
Jackson, Benjamin M.
中科院分区:
医学2区
文献类型:
--
作者:
Nathan, Derek P.;Xu, Chun;Jackson, Benjamin M.

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背景资料。A型和B型主动脉夹层通常分别由窦管交界处上方和左侧锁骨下动脉(LSA)开口远端的内膜撕裂引起。我们假设这种病理是由压力升高引起的局部室壁应力引起的。我们通过心电门控CT血管造影术确定了47例胸主动脉正常的个体。对胸主动脉进行了分割、重建和三角剖分,以创建几何网格。使用120 mm Hg的收缩压负荷进行有限元分析,以预测局部胸主动脉壁的应力。升主动脉窦管交界处以上和主动脉弓内包括LSA在内的主动脉上血管开口远侧存在局部最大壁应力。降主动脉未见局部最大壁应力。窦管交界处以上(0.001.43±-0.0 7)、LSA远端(0.2 1±-0.0 7)和降主动脉(0.0 6+-0.0 1)的平均壁应力对主动脉区域的壁应力有显著影响(p<0.0 5)。在正常胸主动脉中,管壁应力峰值位于窦小管交界处上方和LSA开口远端。考虑到主动脉夹层的共局性,这种应力分布可能与其发病有关。未来有必要进行研究,以确定基于图像的生物力学计算在预测主动脉夹层中的有效性,并设计减少压力负荷引起的胸主动脉壁应力的治疗方法是合理的。(Ann Thorac Surg2011;91:458-)(C)2011年,胸外科医师学会
Background. Type A and type B aortic dissections typically result from intimal tears above the sinotubular junction and distal to the left subclavian artery (LSA) ostium, respectively. We hypothesized that this pathology results from elevated pressure-induced regional wall stress.Methods. We identified 47 individuals with normal thoracic aortas by electrocardiogram-gated computed tomography angiography. The thoracic aorta was segmented, reconstructed, and triangulated to create a geometric mesh. Finite element analysis using a systolic pressure load of 120 mm Hg was performed to predict regional thoracic aortic wall stress.Results. There were local maxima of wall stress above the sinotubular junction in the ascending aorta and distal to the ostia of the supraaortic vessels, including the LSA, in the aortic arch. No local maximum of wall stress was found in the descending thoracic aorta. Comparison of the mean peak wall stress above the sinotubular junction (0.43 +/- 0.07 MPa), distal to the LSA (0.21 +/- 0.07 MPa), and in the descending thoracic aorta (0.06 +/- 0.01 MPa) showed a significant effect for wall stress by aortic region (p < 0.001).Conclusions. In the normal thoracic aorta, there are peaks in wall stress above the sinotubular junction and distal to the LSA ostium. This stress distribution may contribute to the pathogenesis of aortic dissections, given their colocalization. Future investigations to determine the utility of image-derived biomechanical calculations in predicting aortic dissection are warranted, and therapies designed to reduce the pressure load-induced wall stress in the thoracic aorta are rational. (Ann Thorac Surg 2011;91:458-64) (C) 2011 by The Society of Thoracic Surgeons