Left Ventricle Biomechanics of Low-Flow, Low-Gradient Aortic Stenosis: A Patient-Specific Computational Model

Wisneski, Andrew D.; Cutugno, Salvatore; Pasta, Salvatore; Stroh, Ashley; Jiang, Yao; Nguyen, Tom C.; Mahadevan, Vaikom S.; Guccione, Julius M.

doi:10.3389/fphys.2022.848011

Cited by 6 publications

(4 citation statements)

References 32 publications

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“…We utilized the Living Left Heart Human Model by Dassault Systèmes Simulia Corporation (LLHH), capable of simulating LV performance, pressure–volume loops and stress and strain analyses, all correlating with clinical observations [ 18 , 19 ]. The finite element model included the AA, LV, left atrium, mitral valve, aortic root and pericardium.…”

Section: Methodsmentioning

confidence: 99%

The Stiffness of the Ascending Aorta Has a Direct Impact on Left Ventricular Function: An In Silico Model

Goetz,

Yao,

Brener

et al. 2024

Bioengineering

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During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta (AA). An in silico study (Living Left Heart Human Model, Dassault Systèmes Simulia Corporation) demonstrated that stiffening of the AA affects myocardial stress and LV strain patterns. With AA stiffening, myofiber stress increased overall in the LV, with particularly high-stress areas at the septum. The most pronounced reduction in strain was noted along the septal longitudinal region. The pressure–volume loops showed that AA stiffening caused a deterioration in LV function, with increased end-systolic volume, reduced systolic LV pressure, decreased stroke volume and effective stroke work, but elevated end-diastolic pressure. An increase in myofiber contractility indicated that stroke volume and effective stroke work could be recovered, with an increase in LV end-systolic pressure and a decrease in end-diastolic pressure. Longitudinal and radial strains remained reduced, but circumferential strains increased over baseline, compensating for lost longitudinal LV function. Myofiber stress increased overall, with the most dramatic increase in the septal region and the LV apex. We demonstrate a direct mechanical pathophysiologic link between stiff AA and reduced longitudinal left ventricular strain which are common in patients with HFpEF.

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Section: Methodsmentioning

confidence: 99%

The Stiffness of the Ascending Aorta Has a Direct Impact on Left Ventricular Function: An In Silico Model

Goetz,

Yao,

Brener

et al. 2024

Bioengineering

Self Cite

View full text Add to dashboard Cite

show abstract

“…We utilized the Living Left Heart Human Model by Dassault Systémes Simulia Corporation (LLHH) which is capable of simulating LV performance, pressure-volume loops, and stress and strain analyses all of which correlate with clinical observations [9,10]. Our finite element model includes the AA, LV, left atrium, mitral valve, aortic root and the pericardium.…”

Section: Computational Modelmentioning

confidence: 99%

Inversion of Left Ventricular Axial Shortening: In Silico Proof of Concept for Treatment of HFpEF

Goetz,

Yao,

Brener

et al. 2024

Preprint

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Left ventricular (LV) longitudinal function is mechanically coupled to the elasticity of the ascending aorta (AA). The pathophysiologic link between stiff AA and reduced longitudinal strain and subsequent deterioration in longitudinal LV systolic function is likely relevant in heart failure with preserved ejection fraction (HFpEF). A proposed therapeutic effect of freeing the LV apex and allowing for LV inverse longitudinal shortening was studied in-silico utilizing Living Left Heart Human Model (Dassault Systémes Simulia Corporation). LV function was evaluated in a model with A) Elastic AA; B) Stiff AA; and C) Stiff AA with free LV apex. The cardiac model simulation demonstrated that freeing the apex caused inverse LV longitudinal shortening that can abolish the deleterious mechanical effect of a stiff AA on LV function. A stiff AA and impairment of LV longitudinal strain are common in patients HFpEF. The hypothesis-generating model strongly suggests that freeing the apex and inverse longitudinal shortening may improve LV function in HFpEF patients with a stiff AA.

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“…We utilized the Living Left Heart Human Model by Dassault Systemes Simulia Corporation (LLHH), capable of simulating LV performance, pressure-volume loops, and stress and strain analyses all correlateing with clinical observations. [14] [15] The nite element model included the AA, LV, left atrium, mitral valve, aortic root, and pericardium. The dynamic response is governed by realistic structural and blood ow physics, and the heart contraction is driven by electrical excitation.…”

Section: Computational Modelmentioning

confidence: 99%

Stiffness of ascending aorta has a direct impact on left ventricular function: In silico model

Goetz,

Brener,

Puri

et al. 2023

Preprint

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During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta. Effects of stiffening the ascending aorta (AA) on cardiac function was evaluated with potential implications for heart failure with reduced ejection fraction (HFpEF). Living left heart human model (Dassault Systemes Simulia Corporation) was utilized to simulate LV function in normal and stiff AA model. In a model simulating a normal elastic AA, the ascending aorta was stretched by 11.0mm, baseline computed stroke volume was 92.2ml, and effective stroke work was 8747.5 Joules. Simulations show a typical pressure-volume loop, normal myofiber stress and strain patterns. In a model with a stiffened AA, end-diastolic pressure increased by 8.5%, while end-systolic LV pressure was reduced by 9.1%, stroke volume by 10.8% and effective stroke work by 19.0%. LV shape tended to be more ovalized at end-systole. Average tensile radial strain was reduced by 20.2 ± 2.4% compressive circumferential strain by 6.8 ± 10.9%, and average compressive longitudinal stain by 48.4 ± 36.9%, while septal longitudinal strain was reduced by 94.1%, anterior, lateral and posterior strain by 41.2%, 13.3% and 40.0% respectively. Average myofiber stress increased by 37.0 ± 42.9%, with high-stress areas noted at the LV septum. To restore baseline stroke volume, contractility was doubled, resulting in nearly identical pressure-volume loop, end-diastolic and end-systolic pressures, stroke volume, and effective stroke work as at baseline. Average tensile radial and compressive longitudinal strain remained reduced by 3.7 ± 8.8% and 37.5%±35.0%, respectively, while compressive circumferential strain increased by 13.6 ± 29.1% over baseline. Septal, anterior, lateral, and posterior longitudinal strain remained reduced by 82.3%, 23.5%, 6.7%, and 33.3% respectively. The calculated average myofiber stress was 61.8 ± 88.3% higher compared to baseline, with remarkably increased stress along the LV septum, papillary muscles, and apex. Hypothesis-generating computational study demonstrated deleterious effects of AA stiffening upon longitudinal LV function, indicating that the LV is directly linked to the AA through mechanical coupling. Since a stiff AA and impairment of left ventricular longitudinal strain is common in patients with HFpEF, we hypothesize a direct mechanical pathophysiologic link between reduced aortic stretching and reduced longitudinal left ventricular strain.

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Left Ventricle Biomechanics of Low-Flow, Low-Gradient Aortic Stenosis: A Patient-Specific Computational Model

Cited by 6 publications

References 32 publications

The Stiffness of the Ascending Aorta Has a Direct Impact on Left Ventricular Function: An In Silico Model

The Stiffness of the Ascending Aorta Has a Direct Impact on Left Ventricular Function: An In Silico Model

Inversion of Left Ventricular Axial Shortening: In Silico Proof of Concept for Treatment of HFpEF

Stiffness of ascending aorta has a direct impact on left ventricular function: In silico model

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