Intra- and interventricular asynchrony of electromechanics in the ventricularly paced heart

Intra- and interventricular asynchrony of electromechanics in the ventricularly paced heart
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DOI:
10.1023/b:engi.0000007972.73874.da
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发表时间:
2003-12-01
影响因子:
1.3
通讯作者:
Arts, T
Arts, T
中科院分区:
工程技术4区
文献类型:
--
作者:
Kerckhoffs, RCP;Bovendeerd, PHM;Arts, T

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心室起搏恢复泵功能的程度取决于起搏部位和起搏时机。心脏电动力学的数值模型可以用来研究心室起搏部位和定时之间的关系,在另一方面,泵功能。在患者特定模型中,这些数值模型可用于优化位置和时机,以实现最佳泵功能。本研究的目的是通过扩展现有的右心室LV机电三维有限元模型,证明在心室起搏期间对患者特定机电进行建模的潜力。根据犬(非侵入性获得)电影-MR短轴图像制作LV和RV的参数化几何结构。去极化模型使用eikonal-diffusion方程。力学计算从动量平衡,与非线性各向异性被动和时间,应变和应变率相关的单轴主动行为。在右心室心尖部和左心室游离壁同步激动和心室起搏的情况下,对正常心脏搏动进行完整心动周期的模拟。我们关注LV和RV血流动力学的时间,去极化和肌纤维缩短的时间,局部每搏功和收缩期间隔运动。在模拟窦性心律时,发现右侧心室射血开始早于左侧,这与实验数据一致。在心室起搏的模拟中,除极顺序、肌节长度和每搏作功密度的空间分布主要取决于除极时间、最大压力和最大压力增量均低于窦性心律时的水平、心室肌收缩期的收缩期和舒张期的收缩期,以及心室肌收缩期的收缩期和舒张期的收缩期。(4)最早激活的心室最早开始射血;(5)收缩期开始时室间隔向最后激活的心室移动。作为第一步,通过插入从非侵入性测量的短轴MR图像获得的心室几何形状,已经证明了患者特定建模在模拟传导干扰中的潜力。后续步骤将包括实施适应模型,以估计患者肌纤维方向并评估起搏的长期影响。
The degree of restoration of pump function by ventricular pacing depends on the pacing site and timing of pacing. Numerical models of cardiac electromechanics could be used to investigate the relation between the ventricular pacing site and timing on the one side, and pump function on the other. In patient-specific models, these numerical models could be used to optimize location and timing for best pump function. The aim of this study was to demonstrate the potential for modeling patient-specific electromechanic during ventricular pacing by means of the extension of an existing three-dimensional finite-element model of LV electromechanics with the right ventricle. A parametrized geometry of the LV and RV was made from canine (non-invasively obtained) cine-MR short axis images. Depolarization was modeled using the eikonal-diffusion equation. Mechanics was computed from balance of momentum, with nonlinear anisotropic passive and time-, strain-, and strainrate-dependent uniaxial active behavior. Simulations of complete cardiac cycles were performed for a normal heart beat with synchronous activation and ventricular pacing at the right ventricular apex and left ventricular free wall. We focused on timing of LV and RV hemodynamics, asynchrony in depolarization and myofiber shortening, regional stroke work, and systolic septal motion. In the simulation of sinus rhytm, ventricular ejection was found to start earlier for the right side than for the left side, which is in agreement with experimental data. In simulations with ventricular pacing, results agreed with experimental findings in the following aspects: 1) depolarization sequence; 2) the spatial distributions of sarcomere length and stroke work density depended mainly on timing of depolarization; 3) maximum pressure and maximum increase of pressure were lower than during sinus rhythm; 4) the earliest activated ventricle had the earliest start of ejection, and 5) the septum moved towards the last activated ventricle at the onset of systole. As a first step, the potential of patient-specific modeling in simulating conduction disturbances has been demonstrated by inserting a ventricular geometry, obtained from non-invasively measured short axis MR images. Later steps would include the implementation of adaptation models to estimate patient myofiber orientation and to assess the effects of pacing in the long term.