Institute for Medical Engineering and Science, Massachusetts Institute of Technology; Health Science and Technology Program, Harvard/Massachusetts Institute of Technology.
Institute for Medical Engineering and Science, Massachusetts Institute of Technology.
J Vis Exp. 2021 Feb 13(168). doi: 10.3791/62167.
Scientific efforts in the field of computational modeling of cardiovascular diseases have largely focused on heart failure with reduced ejection fraction (HFrEF), broadly overlooking heart failure with preserved ejection fraction (HFpEF), which has more recently become a dominant form of heart failure worldwide. Motivated by the paucity of HFpEF in silico representations, two distinct computational models are presented in this paper to simulate the hemodynamics of HFpEF resulting from left ventricular pressure overload. First, an object-oriented lumped-parameter model was developed using a numerical solver. This model is based on a zero-dimensional (0D) Windkessel-like network, which depends on the geometrical and mechanical properties of the constitutive elements and offers the advantage of low computational costs. Second, a finite element analysis (FEA) software package was utilized for the implementation of a multidimensional simulation. The FEA model combines three-dimensional (3D) multiphysics models of the electro-mechanical cardiac response, structural deformations, and fluid cavity-based hemodynamics and utilizes a simplified lumped-parameter model to define the flow exchange profiles among different fluid cavities. Through each approach, both the acute and chronic hemodynamic changes in the left ventricle and proximal vasculature resulting from pressure overload were successfully simulated. Specifically, pressure overload was modeled by reducing the orifice area of the aortic valve, while chronic remodeling was simulated by reducing the compliance of the left ventricular wall. Consistent with the scientific and clinical literature of HFpEF, results from both models show (i) an acute elevation of transaortic pressure gradient between the left ventricle and the aorta and a reduction in the stroke volume and (ii) a chronic decrease in the end-diastolic left ventricular volume, indicative of diastolic dysfunction. Finally, the FEA model demonstrates that stress in the HFpEF myocardium is remarkably higher than in the healthy heart tissue throughout the cardiac cycle.
科学研究人员在心血管疾病计算建模领域投入了大量精力，主要集中在射血分数降低的心力衰竭（HFrEF）方面，而广泛忽略了射血分数保留的心力衰竭（HFpEF），HFpEF 最近已成为全球范围内更为普遍的心力衰竭形式。由于 HFpEF 的计算模型很少，本文提出了两种截然不同的计算模型，用于模拟因左心室压力超负荷而导致的 HFpEF 的血液动力学。首先，使用数值求解器开发了一个面向对象的集总参数模型。该模型基于零维（0D）类血管网络，取决于组成元素的几何和机械特性，具有计算成本低的优点。其次，使用有限元分析（FEA）软件包来实现多维模拟。FEA 模型结合了电机械心脏反应、结构变形和基于流腔的血液动力学的三维（3D）多物理模型，并利用简化的集总参数模型来定义不同流腔之间的流量交换轮廓。通过这两种方法，都成功地模拟了因压力超负荷而导致的左心室和近端脉管系统的急性和慢性血液动力学变化。具体而言，通过减小主动脉瓣口面积来模拟压力超负荷，通过降低左心室壁顺应性来模拟慢性重构。与 HFpEF 的科学和临床文献一致，两种模型的结果均显示：（i）左心室和主动脉之间的跨主动脉压力梯度急性升高，心搏量降低；（ii）舒张末期左心室容积慢性降低，表明舒张功能障碍。最后，FEA 模型表明，HFpEF 心肌中的应力在整个心动周期内明显高于健康心脏组织。
