Comparisons of Simulation Results between Passive and Active Fluid Structure Interaction Models for Left Ventricle in Hypertrophic Obstructive Cardiomyopathy

Huang, Xueying; Deng, Liangliang; Zuo, Heng; Yang, Chun; Song, Yunhu; Lesperance, Mary; Tang, Dalin

doi:10.21203/rs.3.rs-52784/v3

Cited by 3 publications

(3 citation statements)

References 18 publications

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“…It’s been verified that the results of wall stress in active models were significant different with those obtained from passive model ( Huang et al, 2021 ). To be realistic, the active model was employed in this study for more accurate simulation of cardiac biomechanics.…”

Section: Methodsmentioning

confidence: 80%

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction

Deng

Zuo

et al. 2021

Front. Physiol.

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Apical aneurysm was observed to be associated with midventricular obstruction (MVO) in hypertrophic cardiomyopathy (HCM). To investigate the genesis of the apical aneurysm, the idealized numerical left ventricular models (finite-element left ventricle models) of the healthy left ventricle, subaortic obstruction, and midventricular obstruction in HCM of left ventricle were created. The mechanical effects in the formation of apical aneurysm were determined by comparing the myofiber stress on the apical wall between these three models (healthy, subaortic obstruction, and midventricular obstruction models). In comparing the subaortic obstruction model and MVO model with HCM, it was found that, at the time of maximum pressure, the maximum value of myofiber stress in MVO model was 75.0% higher than that in the subaortic obstruction model (654.5 kPa vs. 373.9 kPa). The maximum stress on the apex of LV increased 79.9, 69.3, 117.8% than that on the myocardium around the apex in healthy model, subaortic obstruction model, and MVO model, respectively. Our results indicated that high myofiber stress on the apical wall might initiate the formation process of the apical aneurysm.

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Section: Methodsmentioning

confidence: 80%

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction

Deng

Zuo

et al. 2021

Front. Physiol.

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“…Finally, focus will be given to the development of a fluid-structure interaction model, to account for the passage of blood through the valve and its interaction with the leaflet tissue (Gao et al, 2017a, Huang et al, 2021. The development version of the toolbox is freely available on GitHub and its future release will be provided with a more complete GUI and pre-processing features as mentioned above.…”

Section: Future Workmentioning

confidence: 99%

A toolbox for generating scalable mitral valve morphometric models

Oliveira

Espino

Deorsola

et al. 2021

Computers in Biology and Medicine

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“…Other computational studies are focused only on obstructive HCM [35] [36], but they did not consider the effects of myofiber disarray.…”

Section: Introductionmentioning

confidence: 99%

Computational Analysis of Ventricular Mechanics in Hypertrophic Cardiomyopathy Patients

Mojumder

Fan

Nguyen

et al. 2022

Preprint

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Hypertrophic cardiomyopathy (HCM) is a genetic heart disease that is associated with many pathological features, such as a reduction in global longitudinal strain (GLS), myofiber disarray and hypertrophy. The effects of these features on left ventricle (LV) function are, however, not clear in two phenotypes of HCM, namely, obstructive and non-obstructive. To address this issue, we developed patient specific computational models of the LV using clinical measurements of 2 female HCM patients and a control subject. Left ventricular mechanics was described using an active stress formulation and myofiber disarray was described using a structural tensor in the constitutive models. Unloaded LV configuration for each subject was first determined from their respective end-diastole LV geometries segmented from the cardiac magnetic resonance images, and an empirical single-beat estimation of the end-diastolic pressure volume relationship. The LV was then connected to a closed-loop circulatory model and calibrated using the clinically measured LV pressure and volume waveforms, peak GLS and blood pressure. Without consideration of myofiber disarray, peak myofiber tension was found to be lowest in the obstructive HCM subject (60 kPa), followed by the non-obstructive subject (242 kPa) and the control subject (375 kPa). With increasing myofiber disarray, we found that peak tension has to increase in the HCM models to match the clinical measurements. In the obstructive HCM patient, however, peak tension is still depressed (cf. normal subject) at the largest degree of myofiber disarray found in the clinic. The computational modeling workflow proposed here can be used in future studies with more HCM patient data.

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Comparisons of Simulation Results between Passive and Active Fluid Structure Interaction Models for Left Ventricle in Hypertrophic Obstructive Cardiomyopathy

Cited by 3 publications

References 18 publications

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction

A toolbox for generating scalable mitral valve morphometric models

Computational Analysis of Ventricular Mechanics in Hypertrophic Cardiomyopathy Patients

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