Computational modeling of cardiac growth and remodeling in pressure overloaded hearts—Linking microstructure to organ phenotype

Niestrawska, Justyna A.; Augustin, Christoph M.; Plank, Gernot

doi:10.1016/j.actbio.2020.02.010

Cited by 23 publications

(20 citation statements)

References 179 publications

(287 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Much work has been done for adult FE modelling for pressure overloaded hearts, 37 including modelling of growth and remodelling. 39 Such work can be very useful if applied to the fetal heart, potentially predicting morphological changes subsequent to disease biomechanics.…”

Section: Discussionmentioning

confidence: 99%

Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis

et al. 2020

View full text Add to dashboard Cite

Critical aortic stenosis (AS) of the fetal heart causes a drastic change in the cardiac biomechanical environment. Consequently, a substantial proportion of such cases will lead to a single-ventricular birth outcome. However, the biomechanics of the disease is not well understood. To address this, we performed Finite Element (FE) modelling of the healthy fetal left ventricle (LV) based on patient-specific 4D ultrasound imaging, and simulated various disease features observed in clinical fetal AS to understand their biomechanical impact. These features included aortic stenosis, mitral regurgitation (MR) and LV hypertrophy, reduced contractility, and increased myocardial stiffness. AS was found to elevate LV pressures and myocardial stresses, and depending on severity, can drastically decrease stroke volume and myocardial strains. These effects are moderated by MR. AS alone did not lead to MR velocities above 3 m/s unless LV hypertrophy was included, suggesting that hypertrophy may be involved in clinical cases with high MR velocities. LV hypertrophy substantially elevated LV pressure, valve flow velocities and stroke volume, while reducing LV contractility resulted in diminished LV pressure, stroke volume and wall strains. Typical extent of hypertrophy during fetal AS in the clinic, however, led to excessive LV pressure and valve velocity in the FE model, suggesting that reduced contractility is typically associated with hypertrophy. Increased LV passive stiffness, which might represent fibroelastosis, was found to have minimal impact on LV pressures, stroke volume, and wall strain. This suggested that fibroelastosis could be a by-product of the disease progression and does not significantly impede cardiac function. Our study demonstrates that FE modelling is a valuable tool for elucidating the biomechanics of congenital heart disease and can calculate parameters which are difficult to measure, such as intraventricular pressure and myocardial stresses.

show abstract

Section: Discussionmentioning

confidence: 99%

Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis

et al. 2020

View full text Add to dashboard Cite

show abstract

“…It some cases, however, it can become non-compensatory and initiate negative feedback mechanisms ( Grossman 1980 ). The underlying structural response to cardiac growth and remodeling manifests itself in two major patterns: eccentric hypertrophy associated with myocyte lengthening caused by a chronic overload in volume and concentric hypertrophy associated with myocyte thickening caused by a chronic overload in pressure ( Niestrawska et al 2020 ). In both cases, these mechanisms lead to pathological structural alterations that compromise the heart’s electrical and mechanical function ( Sahli Costabal et al 2017 ).…”

Section: Cardiac Mechanics—heart Failurementioning

confidence: 99%

Precision medicine in human heart modeling

Peirlinck

Costabal

Jiang

et al. 2021

Biomech Model Mechanobiol

131

View full text Add to dashboard Cite

Precision medicine is a new frontier in healthcare that uses scientific methods to customize medical treatment to the individual genes, anatomy, physiology, and lifestyle of each person. In cardiovascular health, precision medicine has emerged as a promising paradigm to enable cost-effective solutions that improve quality of life and reduce mortality rates. However, the exact role in precision medicine for human heart modeling has not yet been fully explored. Here, we discuss the challenges and opportunities for personalized human heart simulations, from diagnosis to device design, treatment planning, and prognosis. With a view toward personalization, we map out the history of anatomic, physical, and constitutive human heart models throughout the past three decades. We illustrate recent human heart modeling in electrophysiology, cardiac mechanics, and fluid dynamics and highlight clinically relevant applications of these models for drug development, pacing lead failure, heart failure, ventricular assist devices, edge-to-edge repair, and annuloplasty. With a view toward translational medicine, we provide a clinical perspective on virtual imaging trials and a regulatory perspective on medical device innovation. We show that precision medicine in human heart modeling does not necessarily require a fully personalized, high-resolution whole heart model with an entire personalized medical history. Instead, we advocate for creating personalized models out of population-based libraries with geometric, biological, physical, and clinical information by morphing between clinical data and medical histories from cohorts of patients using machine learning. We anticipate that this perspective will shape the path toward introducing human heart simulations into precision medicine with the ultimate goals to facilitate clinical decision making, guide treatment planning, and accelerate device design.

show abstract

“…Longterm disease progression such as the material property adaptation for the LA wall, the MV and the pulmonary vessel, and geometrical changes including LA dilation and wall thickening are not included, since these are chronic effects as the result of the volume and pressure overloading (Cameli et al 2017;Messika-Zeitoun et al 2007). A further extension of the current work is to incorporate tissue growth and remodelling process into our three-dimensional LA-MV model (Niestrawska et al 2020;Gao et al 2017b) following the volumetric growth framework (Rodriguez et al 1994) or the agent-based approach (Zhuan et al 2019).…”

Section: Limitationsmentioning

confidence: 99%

Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model

Feng

Gao

et al. 2021

Biomech Model Mechanobiol

View full text Add to dashboard Cite

This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

show abstract

Computational modeling of cardiac growth and remodeling in pressure overloaded hearts—Linking microstructure to organ phenotype

Cited by 23 publications

References 179 publications

Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis

Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis

Precision medicine in human heart modeling

Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model

Contact Info

Product

Resources

About