脑心机电建模

N. Filipovic, Christian Helmich, Jasmina Isaković
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引用次数: 0

摘要

大脑通过自主神经系统的交感神经和副交感神经分支控制心脏。它由心肌细胞到周围神经节神经元,再到中枢神经节前神经元和运动前神经元的多突触通路组成。然而,目前还没有可靠的交感神经张力和交感-副交感神经平衡的心血管标志物。为了及早发现和治疗脑心相互作用的病理改变,有必要了解脑心相互作用的相互作用。在这项研究中,我们提出了一个详细的心脏和躯干的电化学力学模型,以模拟药物对心肌病的三种主要作用模式:(i)调节钙瞬态,(ii)改变收缩蛋白的动力学,(iii)改变宏观结构或其边界条件。心脏模型几何包括七个不同的区域。采用改良FitzHugh-Nagumo心肌细胞单域模型。在胸部放置6个电极来模拟心前导联,并将结果与实际临床测量结果进行比较。采用逆心电图法优化心脏电位。整个心脏嵌入整个躯干环境的电活动中,在窦房结自发启动激活,结合整个心脏具有异质动作电位形态的专门传导系统。我们在九个序列中纳入了健康受试者在心室激活过程中的体表电位图。电学模型与Holzapfel实验得到的具有正交各向异性材料特性的力学模型相耦合。在未来的研究中,我们将更多地关注计算机临床试验,目的是将体表的一些临床病理结果与标准的12个ECG电极测量结果进行比较。
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Brain-Heart Electromechanical Modeling
The brain controls the heart through the sympathetic and parasympathetic branches of the autonomic nervous system. It consists of multisynaptic pathways from myocardial cells back to peripheral ganglionic neurons and further to central preganglionic and premotor neurons. Still, there are no reliable cardiovascular markers of the sympathetic tone and of the sympathetic-parasympathetic balance. It is necessary to understand the interaction between the brain and the heart in order to make early detection and treatment of pathological changes in the brain-heart interaction. In this study we present a detailed electro-chemo-mechanical model of heart and torso, so as to simulate the three principal modes of actions of drugs for cardiomyopathy: (i) modulating calcium transients, (ii) changing kinetics of contractile proteins, (iii) changing the macroscopic structure or its boundary conditions. Heart model geometry included seven different regions. Monodomain model of modified FitzHugh-Nagumo model of the cardiac cell was used. Six electrodes were positioned on the chest to model the precordial leads and the results were compared with real clinical measurements. Inverse ECG method was used to optimize potential on the heart. A whole heart was embedded in the electrical activity throughout the torso environment, with spontaneous initiation of activation in the sinoatrial node, incorporating a specialized conduction system with heterogeneous action potential morphologies throughout the heart. We included body surface potential maps in a healthy subject during progression of ventricular activation in nine sequences. The electrical model was coupled with a mechanical model with orthotropic material properties obtained from the experiments of Holzapfel. In future research we will be more focused on in silico clinical trials with the aim to compare some clinical pathology findings on the body surface with standard 12 ECG electrode measurements.
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