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Image-based computational models for atherosclerotic plaques have been developed to perform mechanical analysis to quantify critical flow and stress/strain conditions related to plaque rupture which often leads directly to heart attack or stroke. An important modeling issue is how to determine zero stress state from in vivo plaque geometries. This paper presents a method to quantify human carotid artery axial and inner circumferential shrinkages by using patient-specific ex vivo and in vivo MRI images. A shrink-stretch process based on patient-specific in vivo plaque morphology and shrinkage data was introduced to shrink the in vivo geometry first to find the zero-stress state (opening angle was ignored to reduce the complexity), and then stretch and pressurize to recover the in vivo plaque geometry with computed initial stress, strain, flow pressure and velocity conditions. Effects of the shrink-stretch process on plaque stress/strain distributions were demonstrated based on patient-specific data using 3D models with fluid-structure interactions (FSI). The average artery axial and inner circumferential shrinkages were 25

作者:Xueying, Huang;Chun, Yang;Chun, Yuan;Fei, Liu;Gador, Canton;Jie, Zheng;Pamela K, Woodard;Gregorio A, Sicard;Dalin, Tang

来源:Molecular & cellular biomechanics : MCB 2009 年 6卷 2期

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| 浏览:39
作者:
Xueying, Huang;Chun, Yang;Chun, Yuan;Fei, Liu;Gador, Canton;Jie, Zheng;Pamela K, Woodard;Gregorio A, Sicard;Dalin, Tang
来源:
Molecular & cellular biomechanics : MCB 2009 年 6卷 2期
标签:
Atherosclerosis artery shrinkage blood flow carotid artery fluid-structure interactions vulnerable plaques
Image-based computational models for atherosclerotic plaques have been developed to perform mechanical analysis to quantify critical flow and stress/strain conditions related to plaque rupture which often leads directly to heart attack or stroke. An important modeling issue is how to determine zero stress state from in vivo plaque geometries. This paper presents a method to quantify human carotid artery axial and inner circumferential shrinkages by using patient-specific ex vivo and in vivo MRI images. A shrink-stretch process based on patient-specific in vivo plaque morphology and shrinkage data was introduced to shrink the in vivo geometry first to find the zero-stress state (opening angle was ignored to reduce the complexity), and then stretch and pressurize to recover the in vivo plaque geometry with computed initial stress, strain, flow pressure and velocity conditions. Effects of the shrink-stretch process on plaque stress/strain distributions were demonstrated based on patient-specific data using 3D models with fluid-structure interactions (FSI). The average artery axial and inner circumferential shrinkages were 25