Passive ventricular mechanics modelling using MRI of structure and function.
Passive ventricular mechanics modelling using MRI of structure and function.
复制标题
使用结构和功能 MRI 进行被动心室力学建模。
DOI：
10.1007/978-3-540-85990-1_98
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Nash,MP
中科院分区：
文献类型：
--
作者：
Wang,VY;Lam,HI;Ennis,DB;Young,AA;Nash,MP
患有扩张型心肌病或心肌梗死的患者可发展为左心室（LV）舒张功能受损。左室重构其结构和功能以适应几何形状和负荷条件的病理生理变化，并且该重构过程可以改变被动心室力学。为了更好地理解被动心室力学，建立了一个左心室有限元模型，该模型包含了来自犬心脏活体磁共振成像（MRI）组织标记、活体左心室腔压力记录和活体扩散张量MRI（DTMRI）的生理和力学信息。MRI组织标记能够以高空间和时间分辨率定量评价心脏机械功能，而DTMRI的每个体素中的最大水扩散方向（主要特征向量）与心肌纤维方向直接相关。通过使用非线性有限元拟合技术拟合来自标记MRI的分段心外膜和心内膜表面数据，该模型被定制为犬LV在扩张期间的几何形状。肌纤维的方向，从DTMRI相同的心脏，被纳入到这个几何模型使用自由形式的变形方法。在时间上与组织标记MRI数据同步的压力记录被用于模拟心室收缩期间的LV变形。舒张期左心室力学的模拟使我们能够根据从标记的MRI获得的运动学数据来估计被动左心室心肌的刚度。这种综合的生理模型将允许更多的洞察局部被动舒张机制的LV在个性化的基础上，从而提高我们的理解的基础结构基础的机械功能障碍的病理条件。
Patients suffering from dilated cardiomyopathy or myocardial infarction can develop left ventricular (LV) diastolic impairment. The LV remodels its structure and function to adapt to pathophysiological changes in geometry and loading conditions and this remodeling process can alter the passive ventricular mechanics. In order to better understand passive ventricular mechanics, a LV finite element model was developed to incorporate physiological and mechanical information derived fromin vivomagnetic resonance imaging (MRI) tissue tagging,in vivoLV cavity pressure recording andex vivodiffusion tensor MRI (DTMRI) of a canine heart. MRI tissue tagging enables quantitative evaluation of cardiac mechanical function with high spatial and temporal resolution, whilst the direction of maximum water diffusion (the primary eigenvector) in each voxel of a DTMRI directly correlates with the myocardial fibre orientation. This model was customized to the geometry of the canine LV during diastasis by fitting the segmented epicardial and endocardial surface data from tagged MRI using nonlinear finite element fitting techniques. Myofibre orientations, extracted from DTMRI of the same heart, were incorporated into this geometric model using a free form deformation methodology. Pressure recordings, temporally synchronized to the tissue tagging MRI data, were used to simulate the LV deformation during diastole. Simulation of the diastolic LV mechanics allowed us to estimate the stiffness of the passive LV myocardium based on kinematic data obtained from tagged MRI. This integrated physiological model will allow more insight into the regional passive diastolic mechanics of the LV on an individualized basis, thereby improving our understanding of the underlying structural basis of mechanical dysfunction in pathological conditions.