Colli Franzone P, Pavarino L F, Scacchi S
Dipartimento di Matematica, Università di Pavia, Via Ferrata 1, Pavia 27100, Italy.
Dipartimento di Matematica, Università di Milano, Via Saldini 50, Milano 20133, Italy.
Math Biosci. 2016 Oct;280:71-86. doi: 10.1016/j.mbs.2016.08.003. Epub 2016 Aug 18.
The aim of this work is to investigate, by means of numerical simulations, the influence of myocardial deformation due to muscle contraction and relaxation on the cardiac repolarization process in presence of transmural intrinsic action potential duration (APD) heterogeneities. The three-dimensional electromechanical model considered consists of the following four coupled components: the quasi-static transversely isotropic finite elasticity equations for the deformation of the cardiac tissue; the active tension model for the intracellular calcium dynamics and cross-bridge binding; the anisotropic Bidomain model for the electrical current flow through the deforming cardiac tissue; the membrane model of ventricular myocytes, including stretch-activated channels. The numerical simulations are based on our finite element parallel solver, which employs Multilevel Additive Schwarz preconditioners for the solution of the discretized Bidomain equations and Newton-Krylov methods for the solution of the discretized non-linear finite elasticity equations. Our findings show that: (i) the presence of intrinsic transmural cellular APD heterogeneities is not fully masked by electrotonic current flow or by the presence of the mechanical deformation; (ii) despite the presence of transmural APD heterogeneities, the recovery process follows the activation sequence and there is no significant transmural repolarization gradient; (iii) with or without transmural APD heterogeneities, epicardial electrograms always display the same wave shape and discordance between the polarity of QRS complex and T-wave; (iv) the main effects of the mechanical deformation are an increase of the dispersion of repolarization time and APD, when computed over the total cardiac domain and over the endo- and epicardial surfaces, while there is a slight decrease along the transmural direction.
本研究旨在通过数值模拟,研究在存在跨壁固有动作电位时程(APD)异质性的情况下,肌肉收缩和舒张引起的心肌变形对心脏复极过程的影响。所考虑的三维机电模型由以下四个耦合部分组成:用于心脏组织变形的准静态横向各向同性有限弹性方程;用于细胞内钙动力学和横桥结合的主动张力模型;用于电流通过变形心脏组织流动的各向异性双域模型;心室肌细胞的膜模型,包括牵张激活通道。数值模拟基于我们的有限元并行求解器,该求解器采用多级加法施瓦茨预条件器来求解离散化的双域方程,并采用牛顿-克里洛夫方法来求解离散化的非线性有限弹性方程。我们的研究结果表明:(i)固有跨壁细胞APD异质性的存在不会被电紧张电流流动或机械变形的存在完全掩盖;(ii)尽管存在跨壁APD异质性,但恢复过程遵循激活顺序,且不存在明显的跨壁复极梯度;(iii)无论有无跨壁APD异质性,心外膜电图始终显示相同的波形以及QRS波群和T波极性之间的不一致;(iv)当在整个心脏区域以及心内膜和心外膜表面计算时,机械变形的主要影响是复极时间和APD离散度的增加,而沿跨壁方向则略有降低。