Lumped-parameter and finite element modeling of heart failure with preserved ejection fraction
Lumped-parameter and finite element modeling of heart failure with preserved ejection fraction
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 threedimensional (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.
Rosalia, Luca
e3f00c11-aa4f-4454-ba25-cd0fd5cfb20a
Ozturk, Caglar
70bbd3bd-fc56-48e8-8b5e-00d5270c1526
Roche, Ellen T.
63e632c8-d821-4c2f-a728-aaf331a5c2a1
13 February 2021
Rosalia, Luca
e3f00c11-aa4f-4454-ba25-cd0fd5cfb20a
Ozturk, Caglar
70bbd3bd-fc56-48e8-8b5e-00d5270c1526
Roche, Ellen T.
63e632c8-d821-4c2f-a728-aaf331a5c2a1
Rosalia, Luca, Ozturk, Caglar and Roche, Ellen T.
(2021)
Lumped-parameter and finite element modeling of heart failure with preserved ejection fraction.
Journal of Visualized Experiments, 168, [e62167].
(doi:10.3791/62167).
Abstract
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 threedimensional (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.
This record has no associated files available for download.
More information
Published date: 13 February 2021
Identifiers
Local EPrints ID: 490960
URI: http://eprints.soton.ac.uk/id/eprint/490960
ISSN: 1940-087X
PURE UUID: 1593493a-b0cd-4675-890d-5a7dbcef4d6b
Catalogue record
Date deposited: 10 Jun 2024 16:50
Last modified: 11 Jun 2024 02:09
Export record
Altmetrics
Contributors
Author:
Luca Rosalia
Author:
Caglar Ozturk
Author:
Ellen T. Roche
Download statistics
Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.
View more statistics