A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis
A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis
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DOI：
10.1016/j.jtbi.2010.04.023
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发表时间：
2010-08-07
影响因子：
2
通讯作者：
Kuhl, Ellen
中科院分区：
文献类型：
--
作者：
Goktepe, Serdar;Abilez, Oscar John;Kuhl, Ellen
我们提出了一种新的计算模型，在适应不良的心脏生长中，心腔的运动学变化归因于细胞骨架结构和细胞形态的改变。我们采用有限体积增长的概念，其特征在于通过乘法分解成弹性部分和增长部分的变形梯度。其生长张量的功能形式与肌节发生、新肌节单位的产生和沉积相关。在慢性容量超负荷时，舒张期壁应变增加导致肌节串联增加，导致心肌细胞长度相对增加，与离心性肥大和心室扩张相关。在慢性压力超负荷时，收缩期室壁应力增加导致骶骨节平行增加，导致肌细胞横截面积相对增加，与向心性肥大和心室壁增厚相关。两种形式的不适应增长的连续方程离散在空间上使用非线性有限元方法，并离散在时间上使用隐式欧拉向后格式。我们探讨了一个通用的双心室心脏模型，以应对容量和压力超负荷，以证明如何在细胞形态的局部变化转化为全球的心脏形态和功能的改变。(C)2010爱思唯尔有限公司保留所有权利。
We present a novel computational model for maladaptive cardiac growth in which kinematic changes of the cardiac chambers are attributed to alterations in cytoskeletal architecture and in cellular morphology. We adopt the concept of finite volume growth characterized through the multiplicative decomposition of the deformation gradient into an elastic part and a growth part. The functional form of its growth tensor is correlated to sarcomerogenesis, the creation and deposition of new sarcomere units. In response to chronic volume-overload, an increased diastolic wall strain leads to the addition of sarcomeres in series, resulting in a relative increase in cardiomyocyte length, associated with eccentric hypertrophy and ventricular dilation. In response to chronic pressure-overload, an increased systolic wall stress leads to the addition of sacromeres in parallel, resulting in a relative increase in myocyte cross sectional area, associated with concentric hypertrophy and ventricular wall thickening. The continuum equations for both forms of maladaptive growth are discretized in space using a nonlinear finite element approach, and discretized in time using the implicit Euler backward scheme. We explore a generic bi-ventricular heart model in response to volume- and pressure-overload to demonstrate how local changes in cellular morphology translate into global alterations in cardiac form and function. (C) 2010 Elsevier Ltd. All rights reserved.