北京生物医学工程

基于双心室电力学复合模型的心力衰竭仿真研究

A simulation study of heart failure based on a coupled biventricular electromechanical model

作者：窦建洪贾济徐波夏灵王聪吴凯黄伟毅董训德

单位：1中国人民解放军南部战区总医院麻醉科（广州 510010） 2浙江大学生物医学工程系（杭州 310027） 3华南理工大学自动化科学与工程学院（广州 510641)

关键词：虚拟心脏；建模仿真；心力衰竭；束支阻滞；心肌梗死

分类号：R318.04

出版年·卷·期（页码）：2020·39·5（441-455）

摘要：

目的临床上束支传导阻滞（bundle branch block ,BBB）和心肌梗死（myocardial Infarction, MI）相互影响、同时并存，而国际上相关的心力衰竭（heart failur,HF）宏观数学模型很少见，多集中于电生理方面，且往往采用简单的几何形状和经验的心肌纤维旋向数据，不利于对真实心肌力学特性的研究。本研究旨在建立一个左束支传导阻滞（left bundle branch block ,LBBB）伴急性心肌梗死（acute heart failur ,AMI）的基于真实几何形状和纤维旋向数据的虚拟心脏HF模型，并定量地分析其力学特性。方法首先利用CT数据和激光三维扫描点云相结合的方法，成功构建基于真实人体心脏结构的高精度几何模型；然后基于单域模型的心肌兴奋传播并行算法及八节点等参元法，建立双心室电力学复合模型；最后基于离子通道的心衰细胞模型，建立LBBB伴AMI的心衰数学模型。基于该模型，通过对心室壁运动的仿真来分析心室不同位置和梗塞范围对梗塞区膨展（infarct expansion ,IE）程度的影响；对心室赤道横断面应力的分析，研究心室内的应力分布特征及对力学收缩的影响；对左/右心室中壁最小主应变的仿真，定量研究室内的力学不同步。结果通过对收缩期心壁的运动、主应变和应力分布的定量分析证明，LBBB伴AMI情况下前壁靠心尖部位要比后壁更易产生IE，且透壁性心梗范围越大，IE程度也越大；同时亦证明在LBBB存在时会有更为严重的左心室内的收缩不同步。结论采用沿心肌纤维单元厚度方向分层的方法，我们利用等参元有限元法巧妙地将真实纤维旋向和几何形状融入双心室电力学复合HF模型，仿真结果与临床相符，证明该模型对理解心衰发生的机制具有重大意义。

Objective In clinic, bundle branch block (BBB) and myocardial infarction (MI) often occur simultaneously and interrelate. The macro-level mathematical models of heart failure (HF) are seldom found internationally, and the vast majority are electrophysiological computer models. Furthermore, previous cardiac models were constructed with simple geometry or fictive fiber orientations, which didn’t accord with true characteristics of heart mechanics. The purpose of this paper is to obtain the quantification of characteristics of ventricular mechanics based on the virtual heart model of human of HF caused by left bundle branch block (LBBB) complicated with acute heart failur(AMI）) including real geometry and myofiber orientations. Methods A high accuracy geometric model for a real human heart specimen was built with the combination of CT data and three-dimensional laser scanning point cloud data. After that, the electrical activation conduction sequences of ventricles were simulated based on the implementation of the parallel algorithms for monodomain model equations of myocardial excitation propagation. Then, using the finite element methods (FEM) with an eight-node isoparametric element, a biventricular electromechanical coupled model was built. Finally, the models of HF caused by LBBB complicated with AMI were constructed based on ionic-channel HF models of myocardium. The characteristics of ventricular mechanics based on the HF model were analyzed. First, analyze the influence of location and size of MI to the extent of infarct expansion (IE) through the simulation of ventricular wall motion. Then, the stress around equator site was calculated to study the distribution pattern of ventricular myocardial stress and the effects on the mechanical synchrony of contraction. Finally, the minimum principal strains of left/right ventriclar mid-wall were used to investigate the quantification of mechanical intraventricular asynchrony. Results Successfully simulated a failing heart with LBBB complicated by AMI. Then through the quantitative analyzation of ventricular motion, distributions of principal strain and stress during systole, it showed that IE occurred more in anterior wall near apex than in posterior wall, and larger transmural size may contribute a lot to the development of IE. Furthermore, we proved that more severe intraventricular systolic dyssynchrony of LV happened when LBBB existed. Conclusions By using multilayer division technology in the thickness direction of myofiber unit, a coupled electromechanical biventricular model of HF，including real geometry and fiber orientations， was subtly constructed by means of finite element method with an isoparametric element. The simulation was in agreement with clinical results. Therefore, it has great significance in understanding of the essence of HF diseases.

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