Longitudinal structural determinants of atherosclerotic plaque vulnerability - A computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging
Longitudinal structural determinants of atherosclerotic plaque vulnerability - A computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging
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DOI：
10.1016/j.jacc.2005.06.069
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发表时间：
2005-10-18
影响因子：
24
通讯作者：
Matsuzaki, M
中科院分区：
文献类型：
--
作者：
Imoto, K;Hiro, T;Matsuzaki, M
目的 本研究利用有限元分析对几种假设血管模型以及三维血管内超声 (IVUS) 图像使用颜色编码应力映射技术，从理论上检验了斑块易损性的纵向结构决定因素。 背景 研究表明，应力过度集中与动脉粥样硬化斑块破裂有关。然而，沿冠状动脉壁斑块内纵向应力分布的局部决定因素仍不清楚。方法使用有限元分析，我们对三维血管模型以及纵向 IVUS 斑块图像 (n = 15) 的斑块内等效应力分布进行了彩色映射。然后，检查了斑块大小、形状、膨胀重塑、钙化和脂质核心对等效应力分布的影响。结果血管模型的颜色图显示等效应力集中在均匀纤维斑块的山顶和肩部。扩张重塑和脂质核心增加了表面等效应力，而管腔狭窄和表面钙化减弱了等效应力。通过脂质核心和钙化的分布来改变过度应力集中的位置。纤维帽的厚度与纤维帽内的等效应力成反比。然而，IVUS斑块图像的彩色图显示，即使纤维帽的厚度保持不变，纤维帽处的等效应力值也会随着斑块形状和浅表钙化的变化而变化。结论纵向应力的分布分析揭示了斑块形状、大小和重塑的特定影响，以及组织成分的内部分布对斑块表面应力集中的影响。此外，相同厚度的纤维帽并不总是表现出相同的破裂脆弱性。
OBJECTIVES This study theoretically examined the longitudinal structural determinants of plaque vulnerability using a color-coded stress mapping technique for several hypothetical vessel models as well as three-dimensional intravascular ultrasound (IVUS) images with use of a finite element analysis.BACKGROUND It has been shown that an excessive concentration of stress is related to atherosclerotic plaque rupture. However, the local determinants of in-plaque longitudinal stress distribution along the coronary arterial wall remain unclear.METHODS Using a finite element analysis, we performed a color mapping of equivalent stress distribution within plaques for three-dimensional vessel models as well as longitudinal IVUS plaque images (n = 15). Then, the effects of plaque size, shape, expansive remodeling, calcification, and lipid core on the equivalent stress distribution were examined.RESULTS The color mapping of vessel models revealed a concentration of equivalent stress at the top of the hills and the shoulders of homogeneous fibrous plaques. Expansive remodeling and the lipid core augmented the surface equivalent stress, whereas luminal stenosis and superficial calcification attenuated the equivalent stress. The location of excessive stress concentration was modified by the distribution of the lipid core and calcification. The thickness of the fibrous cap was inversely related to the equivalent stress within the fibrous cap. However, the color mapping of IVUS plaque images showed that the equivalent stress value at the fibrous cap varied with changes in plaque shape and superficial calcification, even when the thickness of the fibrous cap remained constant.CONCLUSIONS A distribution analysis of longitudinal stress revealed specific effects of plaque shape, size, and remodeling, as well as effects of the interior distribution of tissue components, on the concentration of stress at the plaque surface. Moreover, fibrous caps of the same thickness did not consistently represent the same vulnerability to rupture.