Evaluation of a Novel Finite Element Model of Active Contraction in the Heart.

Evaluation of a Novel Finite Element Model of Active Contraction in the Heart.
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DOI:
10.3389/fphys.2018.00425
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发表时间:
2018
影响因子:
4
通讯作者:
Wenk JF
Wenk JF
中科院分区:
医学2区
文献类型:
--
作者:
Zhang X;Liu ZQ;Campbell KS;Wenk JF

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有限元(FE)建模正在成为一种广泛使用的方法,为全球心脏功能的调查。在本研究中,一种新的模型,细胞水平的收缩,其中包括长度和速度依赖性,被实施到一个三维非线性有限元代码。为了验证这种新的FE实现,使用优化程序来确定收缩参数,与肌节功能,通过比较FE预测的压力和应变的实验测量收集的磁共振成像和导管插入术在五个健康大鼠的心室。由有限元模型生成的压力-体积关系与实验数据吻合良好。此外,收缩末期应变和周向-纵向剪切角的区域分布总体上与实验结果具有良好的一致性,主要偏差发生在间隔区域。此外,FE模型预测心室射血后肌节再延长的不均匀分布,这与先前的体内研究一致。总之,新的FE主动收缩模型能够预测整个心动周期内LV的整体性能和局部力学行为。通过包括更准确的细胞水平的机制,该模型可以提供更好的代表性的LV和增强心脏收缩和舒张功能障碍相关的研究。
Finite element (FE) modeling is becoming a widely used approach for the investigation of global heart function. In the present study, a novel model of cellular-level systolic contraction, which includes both length- and velocity-dependence, was implemented into a 3D non-linear FE code. To validate this new FE implementation, an optimization procedure was used to determine the contractile parameters, associated with sarcomeric function, by comparing FE-predicted pressure and strain to experimental measures collected with magnetic resonance imaging and catheterization in the ventricles of five healthy rats. The pressure-volume relationship generated by the FE models matched well with the experimental data. Additionally, the regional distribution of end-systolic strains and circumferential-longitudinal shear angle exhibited good agreement with experimental results overall, with the main deviation occurring in the septal region. Moreover, the FE model predicted a heterogeneous distribution of sarcomere re-lengthening after ventricular ejection, which is consistent with previous in vivo studies. In conclusion, the new FE active contraction model was able to predict the global performance and regional mechanical behaviors of the LV during the entire cardiac cycle. By including more accurate cellular-level mechanisms, this model could provide a better representation of the LV and enhance cardiac research related to both systolic and diastolic dysfunction.
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