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模拟球囊血管成形术干预过程中的斑块破裂和夹层形成。

Modeling plaque fissuring and dissection during balloon angioplasty intervention.

作者信息

Gasser T Christian, Holzapfel Gerhard A

机构信息

Department of Solid Mechanics, School of Engineering Sciences, Royal Institute of Technology (KTH), Osquars Backe 1, SE-100 44, Stockholm, Sweden.

出版信息

Ann Biomed Eng. 2007 May;35(5):711-23. doi: 10.1007/s10439-007-9258-1. Epub 2007 Mar 24.

Abstract

Balloon angioplasty intervention is traumatic to arterial tissue. Fracture mechanisms such as plaque fissuring and/or dissection occur and constitute major contributions to the lumen enlargement. However, these types of mechanically-based traumatization of arterial tissue are also contributing factors to both acute procedural complications and chronic restenosis of the treatment site. We propose physical and finite element models, which are generally useable to trace fissuring and/or dissection in atherosclerotic plaques during balloon angioplasty interventions. The arterial wall is described as an anisotropic, heterogeneous, highly deformable, nearly incompressible body, whereas tissue failure is captured by a strong discontinuity kinematics and a novel cohesive zone model. The numerical implementation is based on the partition of unity finite element method and the interface element method. The later is used to link together meshes of the different tissue components. The balloon angioplasty-based failure mechanisms are numerically studied in 3D by means of an atherosclerotic-prone human external iliac artery, with a type V lesion. Image-based 3D geometry is generated and tissue-specific material properties are considered. Numerical results show that in a primary phase the plaque fissures at both shoulders of the fibrous cap and stops at the lamina elastica interna. In a secondary phase, local dissections between the intima and the media develop at the fibrous cap location with the smallest thickness. The predicted results indicate that plaque fissuring and dissection cause localized mechanical trauma, but prevent the main portion of the stenosis from high stress, and hence from continuous tissue damage.

摘要

球囊血管成形术干预对动脉组织具有创伤性。诸如斑块裂隙形成和/或夹层等破裂机制会发生,并对管腔扩大起主要作用。然而,这些基于机械作用对动脉组织造成的创伤类型也是急性手术并发症和治疗部位慢性再狭窄的促成因素。我们提出了物理和有限元模型,这些模型通常可用于追踪球囊血管成形术干预过程中动脉粥样硬化斑块的裂隙形成和/或夹层情况。动脉壁被描述为各向异性、非均质、高度可变形且近乎不可压缩的物体,而组织破坏则通过强不连续运动学和一种新型内聚区模型来捕捉。数值实现基于单位分解有限元法和界面元法。后者用于将不同组织成分的网格连接在一起。通过一个具有V型病变的易患动脉粥样硬化的人体髂外动脉,对基于球囊血管成形术的失败机制进行了三维数值研究。生成了基于图像的三维几何形状,并考虑了组织特异性材料特性。数值结果表明,在初始阶段,纤维帽的两个肩部出现斑块裂隙,并在内弹性膜处停止。在第二阶段,在内膜和中膜之间的局部夹层在纤维帽最薄处形成。预测结果表明,斑块裂隙形成和夹层会导致局部机械创伤,但可防止狭窄的主要部分承受高应力,从而避免持续的组织损伤。

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