Cardiac Cine Magnetic Resonance (CMR) Imaging has made a significant paradigm shift in medical imaging technology, thanks to its capability of acquiring high spatial and temporal resolution images of different structures within the heart that can be used for reconstructing patient-specific ventricular computational models. In this work, we describe the development of dynamic patient-specific right ventricle (RV) models associated with normal subjects and abnormal RV patients to be subsequently used to assess RV function based on motion and kinematic analysis. We first constructed static RV models using segmentation masks of cardiac chambers generated from our accurate, memory-efficient deep neural architecture - CondenseUNet - featuring both a learned group structure and a regularized weight-pruner to estimate the motion of the right ventricle. In our study, we use a deep learning-based deformable network that takes 3D input volumes and outputs a motion field which is then used to generate isosurface meshes of the cardiac geometry at all cardiac frames by propagating the end-diastole (ED) isosurface mesh using the reconstructed motion field. The proposed model was trained and tested on the Automated Cardiac Diagnosis Challenge (ACDC) dataset featuring 150 cine cardiac MRI patient datasets. The isosurface meshes generated using the proposed pipeline were compared to those obtained using motion propagation via traditional non-rigid registration based on several performance metrics, including Dice score and mean absolute distance (MAD).
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Robotic right ventricle is a biohybrid platform that simulates right ventricular function in (patho)physiological conditions and intervention
The increasing recognition of the right ventricle (RV) necessitates the development of RV-focused interventions, devices and testbeds. In this study, we developed a soft robotic model of the right heart that accurately mimics RV biomechanics and hemodynamics, including free wall, septal and valve motion. This model uses a biohybrid approach, combining a chemically treated endocardial scaffold with a soft robotic synthetic myocardium. When connected to a circulatory flow loop, the robotic right ventricle (RRV) replicates real-time hemodynamic changes in healthy and pathological conditions, including volume overload, RV systolic failure and pressure overload. The RRV also mimics clinical markers of RV dysfunction and is validated using an in vivo porcine model. Additionally, the RRV recreates chordae tension, simulating papillary muscle motion, and shows the potential for tricuspid valve repair and replacement in vitro. This work aims to provide a platform for developing tools for research and treatment for RV pathophysiology.
more » « less- Award ID(s):
- 1847541
- PAR ID:
- 10478558
- Publisher / Repository:
- Nature Publishing Group
- Date Published:
- Journal Name:
- Nature Cardiovascular Research
- Volume:
- 2
- Issue:
- 12
- ISSN:
- 2731-0590
- Format(s):
- Medium: X Size: p. 1310-1326
- Size(s):
- p. 1310-1326
- Sponsoring Org:
- National Science Foundation
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Abstract Right ventricular (RV) failure remains a significant burden for patients with advanced heart failure, especially after major cardiac surgeries such as implantation of left ventricular assist devices. Device solutions that can assist the complex biological function of heart muscle without the disadvantages of bulky designs and infection‐prone drivelines remain an area of pressing clinical need, especially for the right ventricle. In addition, devices that incur contact between blood and artificial surfaces mandate long‐term use of blood‐thinning medications, carrying increased risks for the patients. This work describes the design of a biomimetic, elastic sleeve to support RV‐specific motion via tuned regional mechanical properties. The RV external device (RVEX) in computational models as well as benchtop models and ex vivo (i.e., explanted heart) setups are evaluated to characterize the device and predict functional benefit. Additionally, long‐term implantation potential is demonstrated in mice. Finally, the ability to sensorize the RVEX device to yield resistive self‐sensing capabilities to continuously monitor ventricular deformation, as demonstrated in benchtop experiments and in live animal surgeries, is proposed.
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Pulmonary arterial hypertension (PAH) presents a significant challenge to right ventricular (RV) function due to progressive pressure overload, necessitating adaptive remodeling in the form of increased wall thickness, enhanced myocardial contractility and stiffness to maintain cardiac performance. However, the impact of these remodeling mechanisms on RV mechanics in not clearly understood. In addition, there is a lack of quantitative understanding of how each mechanism individually influences RV mechanics. Utilizing experimental data from a rat model of PAH at three distinct time points, we developed biventricular finite element models to investigate how RV stress and strain evolved with PAH progression. The finite element models were fitted to hemodynamic and morphological data to represent different disease stages and used to analyze the impact of RV remodeling as well as the altered RV pressure. Furthermore, we performed a number of theoretical simulation studies with different combinations of morphological and physiological remodeling, to assess and quantify their individual impact on overall RV load and function. Our findings revealed a substantial 4-fold increase in RV stiffness and a transient 2-fold rise in contractility, which returned to baseline by week 12. These changes in RV material properties in addition to the 2-fold increase in wall thickness significantly mitigated the increase in wall stress and strain caused by the progressive increase in RV afterload. Despite the PAH-induced cases showing increased wall stress and strain at end-diastole and end-systole compared to the control, our simulations suggest that without the observed remodeling mechanisms, the increase in stress and strain would have been much more pronounced. Our model analysis also indicated that while changes in the RV’s material properties–particularly increased RV stiffness - have a notable effect on its mechanics, the primary compensatory factor limiting the stress and strain increase in the early stages of PAH was the significant increase in wall thickness. These findings underscore the importance of RV remodeling in managing the mechanical burden on the right ventricle due to pressure overload.
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Although pulmonary arterial hypertension (PAH) leads to right ventricle (RV) hypertrophy and structural remodeling, the relative contributions of changes in myocardial geometric and mechanical properties to systolic and diastolic chamber dysfunction and their time courses remain unknown. Using measurements of RV hemodynamic and morphological changes over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we discriminated the contributions of RV geometric remodeling and alterations of myocardial material properties to changes in systolic and diastolic chamber function. Significant and rapid RV hypertrophic wall thickening was sufficient to stabilize ejection fraction in response to increased pulmonary arterial pressure by week 4 without significant changes in systolic myofilament activation. After week 4, RV end-diastolic pressure increased significantly with no corresponding changes in end-diastolic volume. Significant RV diastolic chamber stiffening by week 5 was not explained by RV hypertrophy. Instead, model analysis showed that the increases in RV end-diastolic chamber stiffness were entirely attributable to increased resting myocardial material stiffness that was not associated with significant myocardial fibrosis or changes in myocardial collagen content or type. These findings suggest that whereas systolic volume in this model of RV pressure overload is stabilized by early RV hypertrophy, diastolic dilation is prevented by subsequent resting myocardial stiffening. NEW & NOTEWORTHY Using a novel combination of hemodynamic and morphological measurements over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we found that compensated systolic function was almost entirely explained by RV hypertrophy, but subsequently altered RV end-diastolic mechanics were primarily explained by passive myocardial stiffening that was not associated with significant collagen extracellular matrix accumulation.more » « less
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Introduction: The right ventricle (RV) mechanical property is an important determinant of its function. However, compared to its elasticity, RV viscoelasticity is much less studied, and it remains unclear how pulmonary hypertension (PH) alters RV viscoelasticity. Our goal was to characterize the changes in RV free wall (RVFW) anisotropic viscoelastic properties with PH development and at varied heart rates.Methods: PH was induced in rats by monocrotaline treatment, and the RV function was quantified by echocardiography. After euthanasia, equibiaxial stress relaxation tests were performed on RVFWs from healthy and PH rats at various strain-rates and strain levels, which recapitulate physiological deformations at varied heart rates (at rest and under acute stress) and diastole phases (at early and late filling), respectively.Results and Discussion: We observed that PH increased RVFW viscoelasticity in both longitudinal (outflow tract) and circumferential directions. The tissue anisotropy was pronounced for the diseased RVs, not healthy RVs. We also examined the relative change of viscosity to elasticity by the damping capacity (ratio of dissipated energy to total energy), and we found that PH decreased RVFW damping capacity in both directions. The RV viscoelasticity was also differently altered from resting to acute stress conditions between the groups—the damping capacity was decreased only in the circumferential direction for healthy RVs, but it was reduced in both directions for diseased RVs. Lastly, we found some correlations between the damping capacity and RV function indices and there was no correlation between elasticity or viscosity and RV function. Thus, the RV damping capacity may be a better indicator of RV function than elasticity or viscosity alone. These novel findings on RV dynamic mechanical properties offer deeper insights into the role of RV biomechanics in the adaptation of RV to chronic pressure overload and acute stress.
