Honors & Awards
National Heart Foundation Research Fellowship, New Zealand National Heart Foundation (August 2015)
Best Doctoral Theses Awards, University of Auckland (2013)
Best Poster Prize, Siemens at the “Statistical Atlases and Computational Models of the Heart” workshop (2010)
Best Paper Award, Medical Image Analysis - MICCAI (2009)
Young Investigator Award, Medical Image Computing and Computer Assisted Intervention Society (2008)
Left ventricular geometry during unloading and the end-systolic pressure volume relationship: Measurement with a modified real-time MRI-based method in normal sheep
2020; 15 (6): e0234896
The left ventricular (LV) end-systolic (ES) pressure volume relationship (ESPVR) is the cornerstone of systolic LV function analysis. We describe a 2D real-time (RT) MRI-based method (RTPVR) with separate software tools for 1) semi-automatic level set-based shape prior method (LSSPM) of the LV, 2) generation of synchronized pressure area loops and 3) calculation of the ESPVR. We used the RTPVR method to measure ventricular geometry, ES pressure area relationship (ESPAR) and ESPVR during vena cava occlusion (VCO) in normal sheep. 14 adult sheep were anesthetized and underwent measurement of LV systolic function. Ten of the 14 sheep underwent RTMRI and eight of the 14 underwent measurement with conductance catheter; 4 had both RTMRI and conductance measurements. 2D cross sectional RTMRI were performed at apex, mid-ventricle and base levels during separate VCOs. The Dice similarity coefficient was used to compare LSSPM and manual image segmentation and thus determine LSSPM accuracy. LV cross-sectional area, major and minor axis length, axis ratio, major axis orientation angle and ESPAR were measured at each LV level. ESPVR was calculated with a trapezoidal rule. The Dice similarity coefficient between LSSPM and manual segmentation by two readers was 87.31±2.51% and 88.13±3.43%. All cross sections became more elliptical during VCO. The major axis orientation shifted during VCO but remained in the septo-lateral direction. LV chamber obliteration at the apical level occurred during VCO in 7 of 10 sheep that underwent RTMRI. ESPAR was non-linear at all levels. Finally, ESPVR was non-linear because of apical collapse. ESPVR measured by conductance catheter (EES,Index = 2.23±0.66 mmHg/ml/m2) and RT (EES,Index = 2.31±0.31 mmHg/ml/m2) was not significantly different. LSSPM segmentation of 2D RT MRI images is accurate and allows calculation of LV geometry, ESPAR and ESPVR during VCO. In the future, RTPVR will facilitate determination of regional systolic material parameters underlying ESPVR.
View details for DOI 10.1371/journal.pone.0234896
View details for Web of Science ID 000543547900032
View details for PubMedID 32569290
View details for PubMedCentralID PMC7307770
- Calibration of a fully coupled electromechanical meshless computational model of the heart with experimental data COMPUTER METHODS IN APPLIED MECHANICS AND ENGINEERING 2020; 364
A Novel MRI-Based Finite Element Modeling Method for Calculation of Myocardial Ischemia Effect in Patients With Functional Mitral Regurgitation
FRONTIERS IN PHYSIOLOGY
2020; 11: 158
Functional Mitral Regurgitation (FMR) associated with coronary artery disease affects nearly 3 million patients in the United States. Both myocardial infarction (MI) and ischemia contribute to FMR development but uncertainty as to which patients will respond to revascularization (REVASC) of ischemia alone prevents rational decision making about FMR therapy. The aim of this study was to create patient-specific cardiac MRI (CMR) informed finite element (FE) models of the left ventricle (LV), calculate regional LV systolic contractility and then use optimized systolic material properties to simulate the effect of revascularization (virtual REVASC).We describe a novel FE method able to predict the effect of myocardial ischemia on regional LV function. CMR was obtained in five patients with multi-vessel coronary disease and FMR before and 3 months after percutaneous REVASC and a single healthy volunteer. Patient-specific FE models were created and divided into 17 sectors where the systolic contractility parameter, Tmax of each sector was a function of regional stress perfusion (SP-CMR) and myocardial infarction (LGE-CMR) scores. Sector-specific circumferential and longitudinal end-systolic strain and LV volume from CSPAMM were used in a formal optimization to determine the sector based myocardial contractility, Tmax and ischemia effect, α. Virtual REVASC was simulated by setting α to zero.The FE optimization successfully converged with good agreement between calculated and experimental end-systolic strain and LV volumes. Specifically, the optimized T max for the healthy myocardium for five patients and the volunteer was 495.1, 336.8, 173.5, 227.9, 401.4, and 218.9 kPa. The optimized α was found to be 1.0, 0.44, and 0.08 for Patients 1, 2, and 3, and 0 for Patients 4 and 5. The calculated average of radial strain for Patients 1, 2, and 3 at baseline and after virtual REVASC was 0.23 and 0.25, respectively.We developed a novel computational method able to predict the effect of myocardial ischemia in patients with FMR. This method can be used to predict the effect of ischemia on the regional myocardium and promises to facilitate better understanding of FMR response to REVASC.
View details for DOI 10.3389/fphys.2020.00158
View details for Web of Science ID 000525664500001
View details for PubMedID 32231584
View details for PubMedCentralID PMC7082816
Efficient estimation of load-free left ventricular geometry and passive myocardial properties using principal component analysis.
International journal for numerical methods in biomedical engineering
2020; 36 (3): e3313
Models of cardiac mechanics require a well-defined reference geometry from which deformations and hence myocardial strain and stress can be calculated. In the in vivo beating heart, the load-free (LF) geometry generally cannot be measured directly, since, in many cases, there is no stage at which the lumen pressures and contractile state are all zero. Therefore, there is a need for an efficient method to estimate the LF geometry, which is essential for an accurate mechanical simulation of left ventricular (LV) mechanics, and for estimations of passive and contractile constitutive parameters of the heart muscle. In this paper, we present a novel method for estimating both the LF geometry and the passive stiffness of the myocardium. A linear combination of principal components from a population of diastolic displacements is used to construct the LF geometry. For each estimate of the LF geometry and tissue stiffness, LV inflation is simulated, and the model predictions are compared with surface data at multiple stages during passive diastolic filling. The feasibility of this method was demonstrated using synthetically deformation data that were generated using LV models derived from clinical magnetic resonance image data, and the identifiability of the LF geometry and passive stiffness parameters were analysed using Hessian metrics. Applications of this method to clinical data would improve the accuracy of constitutive parameter estimation and allow a better simulation of LV wall strains and stresses.
View details for DOI 10.1002/cnm.3313
View details for PubMedID 31955509
Myocardial Laminar Organization Is Retained in Angiotensin-Converting Enzyme Inhibitor Treated SHRs
View details for DOI 10.1007/s11340-020-00622-4
Mechanical effects of MitraClip on leaflet stress and myocardial strain in functional mitral regurgitation - A finite element modeling study
2019; 14 (10): e0223472
MitraClip is the sole percutaneous device approved for functional mitral regurgitation (MR; FMR) but MR recurs in over one third of patients. As device-induced mechanical effects are a potential cause for MR recurrence, we tested the hypothesis that MitraClip increases leaflet stress and procedure-related strain in sub-valvular left ventricular (LV) myocardium in FMR associated with coronary disease (FMR-CAD).Simulations were performed using finite element models of the LV + mitral valve based on MRI of 5 sheep with FMR-CAD. Models were modified to have a 20% increase in LV volume (↑LV_VOLUME) and MitraClip was simulated with contracting beam elements (virtual sutures) placed between nodes in the center edge of the anterior (AL) and posterior (PL) mitral leaflets. Effects of MitraClip on leaflet stress in the peri-MitraClip region of AL and PL, septo-lateral annular diameter (SLAD), and procedure-related radial strain (Err) in the sub-valvular myocardium were calculated.MitraClip increased peri-MitraClip leaflet stress at end-diastole (ED) by 22.3±7.1 kPa (p<0.0001) in AL and 14.8±1.2 kPa (p<0.0001) in PL. MitraClip decreased SLAD by 6.1±2.2 mm (p<0.0001) and increased Err in the sub-valvular lateral LV myocardium at ED by 0.09±0.04 (p<0.0001)). Furthermore, MitraClip in ↑LV_VOLUME was associated with persistent effects at ED but also at end-systole where peri-MitraClip leaflet stress was increased in AL by 31.9±14.4 kPa (p = 0.0268) and in PL by 22.5±23.7 kPa (p = 0.0101).MitraClip for FMR-CAD increases mitral leaflet stress and radial strain in LV sub-valvular myocardium. Mechanical effects of MitraClip are augmented by LV enlargement.
View details for DOI 10.1371/journal.pone.0223472
View details for Web of Science ID 000532467000071
View details for PubMedID 31600276
View details for PubMedCentralID PMC6786765
Microstructurally Motivated Constitutive Modeling of Heart Failure Mechanics.
Heart failure (HF) is one of the leading causes of death worldwide. HF is associated with substantial microstructural remodeling, which is linked to changes in left ventricular geometry and impaired cardiac function. The role of myocardial remodeling in altering the mechanics of failing hearts remains unclear. Structurally based constitutive modeling provides an approach to improve understanding of the relationship between biomechanical function and tissue organization in cardiac muscle during HF. In this study, we used cardiac magnetic resonance imaging and extended-volume confocal microscopy to quantify the remodeling of left ventricular geometry and myocardial microstructure of healthy and spontaneously hypertensive rat hearts at the ages of 12 and 24months. Passive cardiac mechanical function was characterized using left ventricular pressure-volume compliance measurements. We have developed a, to our knowledge, new structurally based biomechanical constitutive equation built on parameters quantified directly from collagen distributions observed in confocal images of the myocardium. Three-dimensional left ventricular finite element models were constructed from subject-specific invivo magnetic resonance imaging data. The structurally based constitutive equation was integrated into geometrically subject-specific finite element models of the hearts and used to investigate the underlying mechanisms of ventricular dysfunction during HF. Using a single pair of material parameters for all hearts, we were able to produce compliance curves that reproduced all of the experimental compliance measurements. The value of this study is not limited to reproducing the mechanical behavior of healthy and diseased hearts, but it also provides important insights into the structure-function relationship of diseased myocardium that will help pave the way toward more effective treatments for HF.
View details for DOI 10.1016/j.bpj.2019.09.038
View details for PubMedID 31653449
- A Human iPSC Double-Reporter System Enables Purification of Cardiac Lineage Subpopulations with Distinct Function and Drug Response Profiles CELL STEM CELL 2019; 24 (5): 802-+
A Human iPSC Double-Reporter System Enables Purification of Cardiac Lineage Subpopulations with Distinct Function and Drug Response Profiles.
Cell stem cell
The diversity of cardiac lineages contributes to the heterogeneity of human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs). Here, we report the generation of a hiPSC TBX5Clover2 and NKX2-5TagRFP double reporter to delineate cardiaclineages and isolate lineage-specific subpopulations. Molecular analyses reveal that four different subpopulations can be isolated based on the differential expression of TBX5 and NKX2-5, TBX5+NKX2-5+, TBX5+NKX2-5-, TBX5-NKX2-5+, and TBX5-NKX2-5-, mimicking the first heart field, epicardial, second heart field, and endothelial lineages, respectively. Genetic and functional characterization indicates that each subpopulation differentiates into specific cardiac cells. We further identify CORIN as a cell-surface marker for isolating the TBX5+NKX2-5+ subpopulation and demonstrate the use of lineage-specific CMs for precise drug testing. We anticipate that this tool will facilitate theinvestigation of cardiac lineage specification and isolation of specific cardiac subpopulations for drug screening, tissue engineering, and disease modeling.
View details for PubMedID 30880024
- Quantitative Analysis of Blood Flow in Cerebral Venous Sinus With Stenosis by Patient-Specific CFD Modeling IEEE ACCESS 2019; 7: 3848–54
Left Ventricular Diastolic Myocardial Stiffness and End-Diastolic Myofibre Stress in Human Heart Failure Using Personalised Biomechanical Analysis.
Journal of cardiovascular translational research
2018; 11 (4): 346–56
Understanding the aetiology of heart failure with preserved (HFpEF) and reduced (HFrEF) ejection fraction requires knowledge of biomechanical factors such as diastolic myocardial stiffness and stress. Cine CMR images and intra-ventricular pressure recordings were acquired in 8 HFrEF, 11 HFpEF and 5 control subjects. Diastolic myocardial stiffness was estimated using biomechanical models and found to be greater in HFrEF (6.4 ± 1.2 kPa) than HFpEF (2.7 ± 0.6 kPa, p < 0.05) and also greater than control (1.2 ± 0.4 kPa, p < 0.005). End-diastolic mid-ventricular myofibre stress derived from the personalised biomechanics model was higher in HFrEF (2.9 ± 0.3 kPa) than control (0.9 ± 0.3 kPa, p < 0.01). Chamber stiffness, measured from the slope of the diastolic pressure-volume relationship, is determined by the intrinsic tissue properties as well as the size and shape of the heart, and was unable to distinguish between any of the three groups (p > 0.05). Personalised biomechanical analysis may provide more specific information about myocardial mechanical behaviour than global chamber indices, which are confounded by variations in ventricular geometry.
View details for DOI 10.1007/s12265-018-9816-y
View details for PubMedID 29998358
- Modelling Cardiac Tissue Growth and Remodelling JOURNAL OF ELASTICITY 2017; 129 (1-2): 283–305
Increased cardiac work provides a link between systemic hypertension and heart failure
2017; 5 (1)
The spontaneously hypertensive rat (SHR) is an established model of human hypertensive heart disease transitioning into heart failure. The study of the progression to heart failure in these animals has been limited by the lack of longitudinal data. We used MRI to quantify left ventricular mass, volume, and cardiac work in SHRs at age 3 to 21 month and compared these indices to data from Wistar-Kyoto (WKY) controls. SHR had lower ejection fraction compared with WKY at all ages, but there was no difference in cardiac output at any age. At 21 month the SHR had significantly elevated stroke work (51 ± 3 mL.mmHg SHR vs. 24 ± 2 mL.mmHg WKY; n = 8, 4; P < 0.001) and cardiac minute work (14.2 ± 1.2 L.mmHg/min SHR vs. 6.2 ± 0.8 L.mmHg/min WKY; n = 8, 4; P < 0.001) compared to control, in addition to significantly larger left ventricular mass to body mass ratio (3.61 ± 0.15 mg/g SHR vs. 2.11 ± 0.008 mg/g WKY; n = 8, 6; P < 0.001). SHRs showed impaired systolic function, but developed hypertrophy to compensate and successfully maintained cardiac output. However, this was associated with an increase in cardiac work at age 21 month, which has previously demonstrated fibrosis and cell death. The interplay between these factors may be the mechanism for progression to failure in this animal model.
View details for DOI 10.14814/phy2.13104
View details for Web of Science ID 000392243200001
View details for PubMedID 28082430
View details for PubMedCentralID PMC5256162
- Three-Dimensional Quantification of Myocardial Collagen Morphology from Confocal Images SPRINGER INTERNATIONAL PUBLISHING AG. 2017: 3–12
Image-Based Investigation of Human in Vivo Myofibre Strain
IEEE TRANSACTIONS ON MEDICAL IMAGING
2016; 35 (11): 2486–96
Cardiac myofibre deformation is an important determinant of the mechanical function of the heart. Quantification of myofibre strain relies on 3D measurements of ventricular wall motion interpreted with respect to the tissue microstructure. In this study, we estimated in vivo myofibre strain using 3D structural and functional atlases of the human heart. A finite element modelling framework was developed to incorporate myofibre orientations of the left ventricle (LV) extracted from 7 explanted normal human hearts imaged ex vivo with diffusion tensor magnetic resonance imaging (DTMRI) and kinematic measurements from 7 normal volunteers imaged in vivo with tagged MRI. Myofibre strain was extracted from the DTMRI and 3D strain from the tagged MRI. We investigated: i) the spatio-temporal variation of myofibre strain throughout the cardiac cycle; ii) the sensitivity of myofibre strain estimates to the variation in myofibre angle between individuals; and iii) the sensitivity of myofibre strain estimates to variations in wall motion between individuals. Our analysis results indicate that end systolic (ES) myofibre strain is approximately homogeneous throughout the entire LV, irrespective of the inter-individual variation in myofibre orientation. Additionally, inter-subject variability in myofibre orientations has greater effect on the variabilities in myofibre strain estimates than the ventricular wall motions. This study provided the first quantitative evidence of homogeneity of ES myofibre strain using minimally-invasive medical images of the human heart and demonstrated that image-based modelling framework can provide detailed insight to the mechanical behaviour of the myofibres, which may be used as a biomarker for cardiac diseases that affect cardiac mechanics.
View details for DOI 10.1109/TMI.2016.2580573
View details for Web of Science ID 000388503400011
View details for PubMedID 27323360
Multiphysics and multiscale modelling, data - model fusion and integration of organ physiology in the clinic: ventricular cardiac mechanics
2016; 6 (2): 20150083
With heart and cardiovascular diseases continually challenging healthcare systems worldwide, translating basic research on cardiac (patho)physiology into clinical care is essential. Exacerbating this already extensive challenge is the complexity of the heart, relying on its hierarchical structure and function to maintain cardiovascular flow. Computational modelling has been proposed and actively pursued as a tool for accelerating research and translation. Allowing exploration of the relationships between physics, multiscale mechanisms and function, computational modelling provides a platform for improving our understanding of the heart. Further integration of experimental and clinical data through data assimilation and parameter estimation techniques is bringing computational models closer to use in routine clinical practice. This article reviews developments in computational cardiac modelling and how their integration with medical imaging data is providing new pathways for translational cardiac modelling.
View details for PubMedID 27051509
View details for PubMedCentralID PMC4759748
- Image-driven constitutive modeling of myocardial fibrosis INTERNATIONAL JOURNAL FOR COMPUTATIONAL METHODS IN ENGINEERING SCIENCE & MECHANICS 2016; 17 (3): 211–21
Image-Based Predictive Modeling of Heart Mechanics
ANNUAL REVIEW OF BIOMEDICAL ENGINEERING, VOL 17
2015; 17: 351–83
Personalized biophysical modeling of the heart is a useful approach for noninvasively analyzing and predicting in vivo cardiac mechanics. Three main developments support this style of analysis: state-of-the-art cardiac imaging technologies, modern computational infrastructure, and advanced mathematical modeling techniques. In vivo measurements of cardiac structure and function can be integrated using sophisticated computational methods to investigate mechanisms of myocardial function and dysfunction, and can aid in clinical diagnosis and developing personalized treatment. In this article, we review the state-of-the-art in cardiac imaging modalities, model-based interpretation of 3D images of cardiac structure and function, and recent advances in modeling that allow personalized predictions of heart mechanics. We discuss how using such image-based modeling frameworks can increase the understanding of the fundamental biophysics behind cardiac mechanics, and assist with diagnosis, surgical guidance, and treatment planning. Addressing the challenges in this field will require a coordinated effort from both the clinical-imaging and modeling communities. We also discuss future directions that can be taken to bridge the gap between basic science and clinical translation.
View details for DOI 10.1146/annurev-bioeng-071114-040609
View details for Web of Science ID 000367291800014
View details for PubMedID 26643023
- Identifying Myocardial Mechanical Properties from MRI Using an Orthotropic Constitutive Model SPRINGER-VERLAG BERLIN. 2015: 135–44
- Field-Based Parameterisation of Cardiac Muscle Structure from Diffusion Tensors SPRINGER-VERLAG BERLIN. 2015: 146–54
- Microstructural Remodelling and Mechanics of Hypertensive Heart Disease SPRINGER-VERLAG BERLIN. 2015: 382–89
- Image-based computational cardiology: from data to understanding. Computational and mathematical methods in medicine 2014; 2014: 120960
Estimation of In Vivo Myocardial Fibre Strain Using an Architectural Atlas of the Human Heart
SPRINGER-VERLAG BERLIN. 2013: 208–15
View details for Web of Science ID 000342799600025
Changes in In Vivo Myocardial Tissue Properties Due to Heart Failure
SPRINGER-VERLAG BERLIN. 2013: 216–23
View details for Web of Science ID 000342799600026
UNSUPERVISED SEGMENTATION AND PERSONALISED FE MODELLING OF IN VIVO HUMAN MYOCARDIAL MECHANICS BASED ON AN MRI ATLAS
IEEE. 2012: 1360–63
View details for Web of Science ID 000312384100351
ESTIMATION OF IN VIVO HUMAN MYOCARDIAL FIBRE STRAIN BY INTEGRATING DIFFUSION TENSOR AND TAGGED MRI USING FE MODELLING
IEEE. 2012: 46–49
View details for Web of Science ID 000312384100012
Electromechanical wavebreak in a model of the human left ventricle
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
2010; 299 (1): H134–H143
In the present report, we introduce an integrative three-dimensional electromechanical model of the left ventricle of the human heart. Electrical activity is represented by the ionic TP06 model for human cardiac cells, and mechanical activity is represented by the Niederer-Hunter-Smith active contractile tension model and the exponential Guccione passive elasticity model. These models were embedded into an anatomic model of the left ventricle that contains a detailed description of cardiac geometry and the fiber orientation field. We demonstrated that fiber shortening and wall thickening during normal excitation were qualitatively similar to experimental recordings. We used this model to study the effect of mechanoelectrical feedback via stretch-activated channels on the stability of reentrant wave excitation. We found that mechanoelectrical feedback can induce the deterioration of an otherwise stable spiral wave into turbulent wave patterns similar to that of ventricular fibrillation. We identified the mechanisms of this transition and studied the three-dimensional organization of this mechanically induced ventricular fibrillation.
View details for DOI 10.1152/ajpheart.00862.2009
View details for Web of Science ID 000278888400019
View details for PubMedID 20400690
Investigating Heart Failure Using Ventricular Imaging and Modelling
SPRINGER-VERLAG BERLIN. 2010: 164–73
View details for Web of Science ID 000288721700017
Cardiac Active Contraction Parameters Estimated from Magnetic Resonance Imaging
SPRINGER-VERLAG BERLIN. 2010: 194-+
View details for Web of Science ID 000288721700020
Modelling passive diastolic mechanics with quantitative MRI of cardiac structure and function
ELSEVIER SCIENCE BV. 2009: 773–84
The majority of patients with clinically diagnosed heart failure have normal systolic pump function and are commonly categorized as suffering from diastolic heart failure. The left ventricle (LV) remodels its structure and function to adapt to pathophysiological changes in geometry and loading conditions, which in turn can alter the passive ventricular mechanics. In order to better understand passive ventricular mechanics, a LV finite element (FE) model was customized to geometric data segmented from in vivo tagged magnetic resonance images (MRI) data and myofibre orientation derived from ex vivo diffusion tensor MRI (DTMRI) of a canine heart using nonlinear finite element fitting techniques. MRI tissue tagging enables quantitative evaluation of cardiac mechanical function with high spatial and temporal resolution, whilst the direction of maximum water diffusion in each voxel of a DTMRI directly corresponds to the local myocardial fibre orientation. Due to differences in myocardial geometry between in vivo and ex vivo imaging, myofibre orientations were mapped into the geometric FE model using host mesh fitting (a free form deformation technique). Pressure recordings, temporally synchronized to the tagging data, were used as the loading constraints to simulate the LV deformation during diastole. Simulation of diastolic LV mechanics allowed us to estimate the stiffness of the passive LV myocardium based on kinematic data obtained from tagged MRI. Integrated physiological modelling of this kind will allow more insight into mechanics of the LV on an individualized basis, thereby improving our understanding of the underlying structural basis of mechanical dysfunction under pathological conditions.
View details for DOI 10.1016/j.media.2009.07.006
View details for Web of Science ID 000270264200008
View details for PubMedID 19664952
Passive Ventricular Mechanics Modelling Using MRI of Structure and Function
SPRINGER-VERLAG BERLIN. 2008: 814–21
Patients suffering from dilated cardiomyopathy or myocardial infarction can develop left ventricular (LV) diastolic impairment. The LV remodels its structure and function to adapt to pathophysiological changes in geometry and loading conditions and this remodeling process can alter the passive ventricular mechanics. In order to better understand passive ventricular mechanics, a LV finite element model was developed to incorporate physiological and mechanical information derived from in vivo magnetic resonance imaging (MRI) tissue tagging, in vivo LV cavity pressure recording and ex vivo diffusion tensor MRI (DTMRI) of a canine heart. MRI tissue tagging enables quantitative evaluation of cardiac mechanical function with high spatial and temporal resolution, whilst the direction of maximum water diffusion (the primary eigenvector) in each voxel of a DTMRI directly correlates with the myocardial fibre orientation. This model was customized to the geometry of the canine LV during diastasis by fitting the segmented epicardial and endocardial surface data from tagged MRI using nonlinear finite element fitting techniques. Myofibre orientations, extracted from DTMRI of the same heart, were incorporated into this geometric model using a free form deformation methodology. Pressure recordings, temporally synchronized to the tissue tagging MRI data, were used to simulate the LV deformation during diastole. Simulation of the diastolic LV mechanics allowed us to estimate the stiffness of the passive LV myocardium based on kinematic data obtained from tagged MRI. This integrated physiological model will allow more insight into the regional passive diastolic mechanics of the LV on an individualized basis, thereby improving our understanding of the underlying structural basis of mechanical dysfunction in pathological conditions.
View details for Web of Science ID 000261373800098
View details for PubMedID 18982680
View details for PubMedCentralID PMC2739655