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A New MRI-Based Model of Heart Function with Coupled Hemodynamics and Application to Normal and Diseased Canine Left Ventricles.

Choi YJ, Constantino J, Vedula V, Trayanova N, Mittal R - Front Bioeng Biotechnol (2015)

Bottom Line: The time-dependent endocardial surfaces are registered using a diffeomorphic mapping algorithm, while the intraventricular blood flow patterns are simulated using a sharp-interface immersed boundary method-based flow solver.The utility of the combined heart-function model is demonstrated by comparing the hemodynamic characteristics of a normal canine heart beating in sinus rhythm against that of the dyssynchronously beating failing heart.We also discuss the potential of coupled CE and hemodynamics models for various clinical applications.

View Article: PubMed Central - PubMed

Affiliation: Department of Mechanical Engineering, Johns Hopkins University , Baltimore, MD , USA ; Institute for Computational Medicine, Johns Hopkins University , Baltimore, MD , USA.

ABSTRACT
A methodology for the simulation of heart function that combines an MRI-based model of cardiac electromechanics (CE) with a Navier-Stokes-based hemodynamics model is presented. The CE model consists of two coupled components that simulate the electrical and the mechanical functions of the heart. Accurate representations of ventricular geometry and fiber orientations are constructed from the structural magnetic resonance and the diffusion tensor MR images, respectively. The deformation of the ventricle obtained from the electromechanical model serves as input to the hemodynamics model in this one-way coupled approach via imposed kinematic wall velocity boundary conditions and at the same time, governs the blood flow into and out of the ventricular volume. The time-dependent endocardial surfaces are registered using a diffeomorphic mapping algorithm, while the intraventricular blood flow patterns are simulated using a sharp-interface immersed boundary method-based flow solver. The utility of the combined heart-function model is demonstrated by comparing the hemodynamic characteristics of a normal canine heart beating in sinus rhythm against that of the dyssynchronously beating failing heart. We also discuss the potential of coupled CE and hemodynamics models for various clinical applications.

No MeSH data available.


Related in: MedlinePlus

Blood transport analyzed using Lagrangian particle tracking. Red and green dots represent the atrial and ventricular blood cells, respectively. (A) Normal heart with SR activation; (B) normal heart with LBBB activation; (C) failing heart with SR activation; (D) failing heart with LBBB activation. SR, sinus rhythm; LBBB, left bundle branch block.
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Figure 9: Blood transport analyzed using Lagrangian particle tracking. Red and green dots represent the atrial and ventricular blood cells, respectively. (A) Normal heart with SR activation; (B) normal heart with LBBB activation; (C) failing heart with SR activation; (D) failing heart with LBBB activation. SR, sinus rhythm; LBBB, left bundle branch block.

Mentions: Figure 9 shows the Lagrangian blood transport in the LV; blood cells that enter the ventricle from the atrium during diastole are represented by red dots and blood cells located within the ventricle at the start of diastole by green dots. The number density (i.e., number of blood cells per unit volume) for both is assumed to be the same. For the normal hearts (Figures 9A,B), the fresh atrial inflow moves toward the apex during diastole and reach the vicinity of the apex by end-diastole. It is interesting to point out that even through the ventricular vortex only convects slightly more than half way into the ventricle (Figures 6 and 8), blood cells from the atrium are induced to penetrate deeper into the ventricle. By end-systole, the atrial and ventricular blood cells are found to be well-mixed and this is in line with the study of Seo and Mittal (2013b) for the normal human ventricles. For the failing hearts (Figures 9C,D), the atrial blood does not penetrate far into the ventricle, and therefore does not significantly displace the ventricular blood. During systole, this atrial bolus of A-wave (or atrial kick) that persists near the mitral annulus, is ejected out of the ventricle. Thus, the atrial and ventricular blood cells remain mostly unmixed throughout the entire cycle and the ventricular blood cells in the LV remain stagnant in the majority of the LV for failing hearts (Figures 9C,D).


A New MRI-Based Model of Heart Function with Coupled Hemodynamics and Application to Normal and Diseased Canine Left Ventricles.

Choi YJ, Constantino J, Vedula V, Trayanova N, Mittal R - Front Bioeng Biotechnol (2015)

Blood transport analyzed using Lagrangian particle tracking. Red and green dots represent the atrial and ventricular blood cells, respectively. (A) Normal heart with SR activation; (B) normal heart with LBBB activation; (C) failing heart with SR activation; (D) failing heart with LBBB activation. SR, sinus rhythm; LBBB, left bundle branch block.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4585083&req=5

Figure 9: Blood transport analyzed using Lagrangian particle tracking. Red and green dots represent the atrial and ventricular blood cells, respectively. (A) Normal heart with SR activation; (B) normal heart with LBBB activation; (C) failing heart with SR activation; (D) failing heart with LBBB activation. SR, sinus rhythm; LBBB, left bundle branch block.
Mentions: Figure 9 shows the Lagrangian blood transport in the LV; blood cells that enter the ventricle from the atrium during diastole are represented by red dots and blood cells located within the ventricle at the start of diastole by green dots. The number density (i.e., number of blood cells per unit volume) for both is assumed to be the same. For the normal hearts (Figures 9A,B), the fresh atrial inflow moves toward the apex during diastole and reach the vicinity of the apex by end-diastole. It is interesting to point out that even through the ventricular vortex only convects slightly more than half way into the ventricle (Figures 6 and 8), blood cells from the atrium are induced to penetrate deeper into the ventricle. By end-systole, the atrial and ventricular blood cells are found to be well-mixed and this is in line with the study of Seo and Mittal (2013b) for the normal human ventricles. For the failing hearts (Figures 9C,D), the atrial blood does not penetrate far into the ventricle, and therefore does not significantly displace the ventricular blood. During systole, this atrial bolus of A-wave (or atrial kick) that persists near the mitral annulus, is ejected out of the ventricle. Thus, the atrial and ventricular blood cells remain mostly unmixed throughout the entire cycle and the ventricular blood cells in the LV remain stagnant in the majority of the LV for failing hearts (Figures 9C,D).

Bottom Line: The time-dependent endocardial surfaces are registered using a diffeomorphic mapping algorithm, while the intraventricular blood flow patterns are simulated using a sharp-interface immersed boundary method-based flow solver.The utility of the combined heart-function model is demonstrated by comparing the hemodynamic characteristics of a normal canine heart beating in sinus rhythm against that of the dyssynchronously beating failing heart.We also discuss the potential of coupled CE and hemodynamics models for various clinical applications.

View Article: PubMed Central - PubMed

Affiliation: Department of Mechanical Engineering, Johns Hopkins University , Baltimore, MD , USA ; Institute for Computational Medicine, Johns Hopkins University , Baltimore, MD , USA.

ABSTRACT
A methodology for the simulation of heart function that combines an MRI-based model of cardiac electromechanics (CE) with a Navier-Stokes-based hemodynamics model is presented. The CE model consists of two coupled components that simulate the electrical and the mechanical functions of the heart. Accurate representations of ventricular geometry and fiber orientations are constructed from the structural magnetic resonance and the diffusion tensor MR images, respectively. The deformation of the ventricle obtained from the electromechanical model serves as input to the hemodynamics model in this one-way coupled approach via imposed kinematic wall velocity boundary conditions and at the same time, governs the blood flow into and out of the ventricular volume. The time-dependent endocardial surfaces are registered using a diffeomorphic mapping algorithm, while the intraventricular blood flow patterns are simulated using a sharp-interface immersed boundary method-based flow solver. The utility of the combined heart-function model is demonstrated by comparing the hemodynamic characteristics of a normal canine heart beating in sinus rhythm against that of the dyssynchronously beating failing heart. We also discuss the potential of coupled CE and hemodynamics models for various clinical applications.

No MeSH data available.


Related in: MedlinePlus