Publications by authors named "Wilco Kroon"

19 Publications

  • Page 1 of 1

Determinants of biventricular cardiac function: a mathematical model study on geometry and myofiber orientation.

Biomech Model Mechanobiol 2017 04 31;16(2):721-729. Epub 2016 Aug 31.

Department of Biomedical Engineering, Eindhoven University of Technology, P.O. Box 513, 5600 MB, Eindhoven, The Netherlands.

In patient-specific mathematical models of cardiac electromechanics, usually a patient-specific geometry and a generic myofiber orientation field are used as input, upon which myocardial tissue properties are tuned to clinical data. It remains unclear to what extent deviations in myofiber orientation and geometry between model and patient influence model predictions on cardiac function. Therefore, we evaluated the sensitivity of cardiac function for geometry and myofiber orientation in a biventricular (BiV) finite element model of cardiac mechanics. Starting out from a reference geometry in which myofiber orientation had no transmural component, two new geometries were defined with either a 27 % decrease in LV short- to long-axis ratio, or a 16 % decrease of RV length, but identical LV and RV cavity and wall volumes. These variations in geometry caused differences in both local myofiber and global pump work below 6 %. Variation of fiber orientation was induced through adaptive myofiber reorientation that caused an average change in fiber orientation of [Formula: see text] predominantly through the formation of a component in transmural direction. Reorientation caused a considerable increase in local myofiber work [Formula: see text] and in global pump work [Formula: see text] in all three geometries, while differences between geometries were below 5 %. The findings suggest that implementing a realistic myofiber orientation is at least as important as defining a patient-specific geometry. The model for remodeling of myofiber orientation seems a useful approach to estimate myofiber orientation in the absence of accurate patient-specific information.
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http://dx.doi.org/10.1007/s10237-016-0825-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350259PMC
April 2017

In vivo electromechanical assessment of heart failure patients with prolonged QRS duration.

Heart Rhythm 2015 Jun 5;12(6):1259-67. Epub 2015 Mar 5.

Center for Computational Medicine in Cardiology, Institute of Computational Science, University of Lugano, Lugano, Switzerland; Division of Cardiology, Fondazione Cardiocentro Ticino, Lugano, Switzerland. Electronic address:

Background: Combined measurement of electrical activation and mechanical dyssynchrony in heart failure (HF) patients is scarce but may contain important mechanistic and diagnostic clues.

Objective: The purpose of this study was to characterize the electromechanical (EM) coupling in HF patients with prolonged QRS duration.

Methods: Ten patients with QRS width >120 ms underwent left ventricular (LV) electroanatomic contact mapping using the Noga® XP system (Biosense Webster). Recorded voltages during the cardiac cycle were converted to maps of depolarization time (TD). Electrode positions were tracked and converted into maps of time-to-peak shortening (TPS) using custom-made deformation analysis software. Correlation analysis was performed between the 2 maps to quantify EM coupling. Simulations with the CircAdapt cardiovascular system model were performed to mechanistically unravel the observed relation between TD and TPS.

Results: The delay between earliest LV electrical activation and peak shortening differed considerably between patients (TPSmin-TDmin = 360 ± 73 ms). On average, total mechanical dyssynchrony exceeded total electrical activation (ΔTPS = 177 ± 47 ms vs ΔTD = 93 ± 24 ms, P <.001), but a large interpatient variability was observed. The TD and TPS maps correlated strongly in all patients (median R = 0.87, P <.001). These correlations were similar for regions with unipolar voltages above and below 6mV (Mann-Whitney U test, P = .93). Computer simulations revealed that increased passive myocardial stiffness decreases ΔTPS relative to ΔTD and that lower contractility predominantly increases TPSmin-TDmin.

Conclusion: EM coupling in HF patients is maintained, but the relationship between TD and TPS differs strongly between patients. Intra-individual and inter-individual differences may be explained by local and global differences in passive and contractile myocardial properties.
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http://dx.doi.org/10.1016/j.hrthm.2015.03.006DOI Listing
June 2015

Assessment and comparison of left ventricular shear in normal and situs inversus totalis hearts by means of magnetic resonance tagging.

Am J Physiol Heart Circ Physiol 2015 Mar 19;308(5):H416-23. Epub 2014 Dec 19.

Department of Biomedical Engineering, Maastricht University, Maastricht, The Netherlands; and

Situs inversus totalis (SIT) is characterized by complete mirroring of gross cardiac anatomy and position combined with an incompletely mirrored myofiber arrangement, being normal at the apex but inverted at the base of the left ventricle (LV). This study relates myocardial structure to mechanical function by analyzing and comparing myocardial deformation patterns of normal and SIT subjects, focusing especially on circumferential-radial shear. In nine control and nine SIT normotensive human subjects, myocardial deformation was assessed from magnetic resonance tagging (MRT) image sequences of five LV short-axis slices. During ejection, no significant difference in either circumferential shortening (εcc) or its axial gradient (Δεcc) is found between corresponding LV levels in control and SIT hearts. Circumferential-radial shear (εcr) has a clear linear trend from apex-to-base in controls, while in SIT it hovers close to zero at all levels. Torsion as well as axial change in εcr (Δεcr) is as in controls in apical sections of SIT hearts but deviates significantly towards the base, changing sign close to the LV equator. Interindividual variability in torsion and Δεcr values is higher in SIT than in controls. Apex-to-base trends of torsion and Δεcr in SIT, changing sign near the LV equator, further substantiate a structural transition in myofiber arrangement close to the LV equator itself. Invariance of εcc and Δεcc patterns between controls and SIT subjects shows that normal LV pump function is achieved in SIT despite partial mirroring of myocardial structure leading to torsional and shear patterns that are far from normality.
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http://dx.doi.org/10.1152/ajpheart.00502.2014DOI Listing
March 2015

Patient-specific modelling of cardiac electrophysiology in heart-failure patients.

Europace 2014 Nov;16 Suppl 4:iv56-iv61

Center for Computational Medicine in Cardiology, Faculty of Informatics, Università della Svizzera italiana, Via Giuseppe Buffi 13, 6904 Lugano, Switzerland Division of Cardiology, Fondazione Cardiocentro Ticino, 6904 Lugano, Switzerland.

Aims: Left-ventricular (LV) conduction disturbances are common in heart-failure patients and a left bundle-branch block (LBBB) electrocardiogram (ECG) type is often seen. The precise cause of this pattern is uncertain and is probably variable between patients, ranging from proximal interruption of the left bundle branch to diffuse distal conduction disease in the working myocardium. Using realistic numerical simulation methods and patient-tailored model anatomies, we investigated different hypotheses to explain the observed activation order on the LV endocardium, electrogram morphologies, and ECG features in two patients with heart failure and LBBB ECG.

Methods And Results: Ventricular electrical activity was simulated using reaction-diffusion models with patient-specific anatomies. From the simulated action potentials, ECGs and cardiac electrograms were computed by solving the bidomain equation. Model parameters such as earliest activation sites, tissue conductivity, and densities of ionic currents were tuned to reproduce the measured signals. Electrocardiogram morphology and activation order could be matched simultaneously. Local electrograms matched well at some sites, but overall the measured waveforms had deeper S-waves than the simulated waveforms.

Conclusion: Tuning a reaction-diffusion model of the human heart to reproduce measured ECGs and electrograms is feasible and may provide insights in individual disease characteristics that cannot be obtained by other means.
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http://dx.doi.org/10.1093/europace/euu257DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217520PMC
November 2014

Ureter smooth muscle cell orientation in rat is predominantly longitudinal.

PLoS One 2014 21;9(1):e86207. Epub 2014 Jan 21.

Department of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.

In ureter peristalsis, the orientation of the contracting smooth muscle cells is essential, yet current descriptions of orientation and composition of the smooth muscle layer in human as well as in rat ureter are inconsistent. The present study aims to improve quantification of smooth muscle orientation in rat ureters as a basis for mechanistic understanding of peristalsis. A crucial step in our approach is to use two-photon laser scanning microscopy and image analysis providing objective, quantitative data on smooth muscle cell orientation in intact ureters, avoiding the usual sectioning artifacts. In 36 rat ureter segments, originating from a proximal, middle or distal site and from a left or right ureter, we found close to the adventitia a well-defined longitudinal smooth muscle orientation. Towards the lamina propria, the orientation gradually became slightly more disperse, yet the main orientation remained longitudinal. We conclude that smooth muscle cell orientation in rat ureter is predominantly longitudinal, though the orientation gradually becomes more disperse towards the proprial side. These findings do not support identification of separate layers. The observed longitudinal orientation suggests that smooth muscle contraction would rather cause local shortening of the ureter, than cause luminal constriction. However, the net-like connective tissue of the ureter wall may translate local longitudinal shortening into co-local luminal constriction, facilitating peristalsis. Our quantitative, minimally invasive approach is a crucial step towards more mechanistic insight into ureter peristalsis, and may also be used to study smooth muscle cell orientation in other tube-like structures like gut and blood vessels.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0086207PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897663PMC
September 2014

Effects of activation pattern and active stress development on myocardial shear in a model with adaptive myofiber reorientation.

Am J Physiol Heart Circ Physiol 2014 Feb 6;306(4):H538-46. Epub 2013 Dec 6.

Cardiovascular Research Institute Maastricht, Departments of Biomedical Engineering/Physiology, Maastricht University, Maastricht, The Netherlands;

It has been hypothesized that myofiber orientation adapts to achieve a preferred mechanical loading state in the myocardial tissue. Earlier studies tested this hypothesis in a combined model of left ventricular (LV) mechanics and remodeling of myofiber orientation in response to fiber cross-fiber shear, assuming synchronous timing of activation and uniaxial active stress development. Differences between computed and measured patterns of circumferential-radial shear strain E(cr) were assumed to be caused by limitations in either the LV mechanics model or the myofiber reorientation model. Therefore, we extended the LV mechanics model with a physiological transmural and longitudinal gradient in activation pattern and with triaxial active stress development. We investigated the effects on myofiber reorientation, LV function, and deformation. The effect on the developed pattern of the transverse fiber angle α(t,0) and the effect on global pump function were minor. Triaxial active stress development decreased amplitudes of E(cr) towards values within the experimental range and resulted in a similar base-to-apex gradient during ejection in model computed and measured E(cr). The physiological pattern of mechanical activation resulted in better agreement between computed and measured strain in myofiber direction, especially during isovolumic contraction phase and first half of ejection. In addition, remodeling was favorable for LV pump and myofiber function. In conclusion, the outcome of the combined model of LV mechanics and remodeling of myofiber orientation is found to become more physiologic by extending the mechanics model with triaxial active stress development and physiological activation pattern.
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http://dx.doi.org/10.1152/ajpheart.00571.2013DOI Listing
February 2014

U-shaped mechanical activation 4 U?

JACC Cardiovasc Imaging 2013 Aug;6(8):874-6

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http://dx.doi.org/10.1016/j.jcmg.2012.12.014DOI Listing
August 2013

Computational model for estimating the short- and long-term cardiac response to arteriovenous fistula creation for hemodialysis.

Med Biol Eng Comput 2012 Dec 2;50(12):1289-98. Epub 2012 Nov 2.

Department of Biomedical Engineering, Maastricht University, PO Box 616, 6200 MB, Maastricht, The Netherlands.

Creation of an arteriovenous fistula (AVF) for hemodialysis may result in cardiac failure due to dramatic increases in cardiac output. To investigate the quantitative relations between AVF flow, changes in cardiac output, myocardial stress and strain and resulting left ventricular adaptation, a computational model is developed. The model combines a one-dimensional pulse wave propagation model of the arterial network with a zero-dimensional one-fiber model of cardiac mechanics and includes adaptation rules to capture the effect of the baro-reflex and long-term structural remodelling of the left ventricle. Using generic vascular and cardiac parameters based on literature, simulations are done that illustrate the model's ability to quantitatively reproduce the clinically observed increase in brachial flow and cardiac output as well as occurence of eccentric hypertrophy. Patient-specific clinical data is needed to investigate the value of the computational model for personalized predictions.
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http://dx.doi.org/10.1007/s11517-012-0966-9DOI Listing
December 2012

Why SIT works: normal function despite typical myofiber pattern in Situs Inversus Totalis (SIT) hearts derived by shear-induced myofiber reorientation.

PLoS Comput Biol 2012 26;8(7):e1002611. Epub 2012 Jul 26.

Department of Biomedical Engineering/Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

The left ventricle (LV) of mammals with Situs Solitus (SS, normal organ arrangement) displays hardly any interindividual variation in myofiber pattern and experimentally determined torsion. SS LV myofiber pattern has been suggested to result from adaptive myofiber reorientation, in turn leading to efficient pump and myofiber function. Limited data from the Situs Inversus Totalis (SIT, a complete mirror image of organ anatomy and position) LV demonstrated an essential different myofiber pattern, being normal at the apex but mirrored at the base. Considerable differences in torsion patterns in between human SIT LVs even suggest variation in myofiber pattern among SIT LVs themselves. We addressed whether different myofiber patterns in the SIT LV can be predicted by adaptive myofiber reorientation and whether they yield similar pump and myofiber function as in the SS LV. With a mathematical model of LV mechanics including shear induced myofiber reorientation, we predicted myofiber patterns of one SS and three different SIT LVs. Initial conditions for SIT were based on scarce information on the helix angle. The transverse angle was set to zero. During reorientation, a non-zero transverse angle developed, pump function increased, and myofiber function increased and became more homogeneous. Three continuous SIT structures emerged with a different location of transition between normal and mirrored myofiber orientation pattern. Predicted SIT torsion patterns matched experimentally determined ones. Pump and myofiber function in SIT and SS LVs are similar, despite essential differences in myocardial structure. SS and SIT LV structure and function may originate from same processes of adaptive myofiber reorientation.
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http://dx.doi.org/10.1371/journal.pcbi.1002611DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406011PMC
January 2013

A numerical method of reduced complexity for simulating vascular hemodynamics using coupled 0D lumped and 1D wave propagation models.

Comput Math Methods Med 2012 10;2012:156094. Epub 2012 May 10.

Department of Surgery, Maastricht University Medical Center, 6202 AZ Maastricht, The Netherlands.

A computational method of reduced complexity is developed for simulating vascular hemodynamics by combination of one-dimensional (1D) wave propagation models for the blood vessels with zero-dimensional (0D) lumped models for the microcirculation. Despite the reduced dimension, current algorithms used to solve the model equations and simulate pressure and flow are rather complex, thereby limiting acceptance in the medical field. This complexity mainly arises from the methods used to combine the 1D and the 0D model equations. In this paper a numerical method is presented that no longer requires additional coupling methods and enables random combinations of 1D and 0D models using pressure as only state variable. The method is applied to a vascular tree consisting of 60 major arteries in the body and the head. Simulated results are realistic. The numerical method is stable and shows good convergence.
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http://dx.doi.org/10.1155/2012/156094DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361674PMC
September 2012

Patient-specific computational modeling of upper extremity arteriovenous fistula creation: its feasibility to support clinical decision-making.

PLoS One 2012 4;7(4):e34491. Epub 2012 Apr 4.

Department of Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.

Introduction: Inadequate flow enhancement on the one hand, and excessive flow enhancement on the other hand, remain frequent complications of arteriovenous fistula (AVF) creation, and hamper hemodialysis therapy in patients with end-stage renal disease. In an effort to reduce these, a patient-specific computational model, capable of predicting postoperative flow, has been developed. The purpose of this study was to determine the accuracy of the patient-specific model and to investigate its feasibility to support decision-making in AVF surgery.

Methods: Patient-specific pulse wave propagation models were created for 25 patients awaiting AVF creation. Model input parameters were obtained from clinical measurements and literature. For every patient, a radiocephalic AVF, a brachiocephalic AVF, and a brachiobasilic AVF configuration were simulated and analyzed for their postoperative flow. The most distal configuration with a predicted flow between 400 and 1500 ml/min was considered the preferred location for AVF surgery. The suggestion of the model was compared to the choice of an experienced vascular surgeon. Furthermore, predicted flows were compared to measured postoperative flows.

Results: Taken into account the confidence interval (25(th) and 75(th) percentile interval), overlap between predicted and measured postoperative flows was observed in 70% of the patients. Differentiation between upper and lower arm configuration was similar in 76% of the patients, whereas discrimination between two upper arm AVF configurations was more difficult. In 3 patients the surgeon created an upper arm AVF, while model based predictions allowed for lower arm AVF creation, thereby preserving proximal vessels. In one patient early thrombosis in a radiocephalic AVF was observed which might have been indicated by the low predicted postoperative flow.

Conclusions: Postoperative flow can be predicted relatively accurately for multiple AVF configurations by using computational modeling. This model may therefore be considered a valuable additional tool in the preoperative work-up of patients awaiting AVF creation.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0034491PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319586PMC
August 2012

Control of whole heart geometry by intramyocardial mechano-feedback: a model study.

PLoS Comput Biol 2012 Feb 9;8(2):e1002369. Epub 2012 Feb 9.

Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

Geometry of the heart adapts to mechanical load, imposed by pressures and volumes of the cavities. We regarded preservation of cardiac geometry as a homeostatic control system. The control loop was simulated by a chain of models, starting with geometry of the cardiac walls, sequentially simulating circulation hemodynamics, myofiber stress and strain in the walls, transfer of mechano-sensed signals to structural changes of the myocardium, and finalized by calculation of resulting changes in cardiac wall geometry. Instead of modeling detailed mechano-transductive pathways and their interconnections, we used principles of control theory to find optimal transfer functions, representing the overall biological responses to mechanical signals. As biological responses we regarded tissue mass, extent of contractile myocyte structure and extent of the extra-cellular matrix. Mechano-structural stimulus-response characteristics were considered to be the same for atrial and ventricular tissue. Simulation of adaptation to self-generated hemodynamic load rendered physiologic geometry of all cardiac cavities automatically. Adaptation of geometry to chronic hypertension and volume load appeared also physiologic. Different combinations of mechano-sensors satisfied the condition that control of geometry is stable. Thus, we expect that for various species, evolution may have selected different solutions for mechano-adaptation.
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http://dx.doi.org/10.1371/journal.pcbi.1002369DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276542PMC
February 2012

Determination of brachial artery stiffness prior to vascular access creation: reproducibility of pulse wave velocity assessment.

Nephrol Dial Transplant 2012 Jun 20;27(6):2370-6. Epub 2011 Dec 20.

Department of Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.

Background: Despite routine ultrasound mapping of upper extremity arteries and veins, early thrombosis and nonmaturation remain frequent complications following vascular access (VA) surgery. Besides vascular diameters, brachial artery stiffness is assumed to play an important role; however, reproducibility of measurements has never been established. The purpose of this study was to determine within-session and between-session variabilities of pulse wave velocity (PWV) assessment by using ultrasonography and blood pressure registration.

Methods: Beat-to-beat changes in brachial artery diameter and pressure were obtained in 21 subjects in measurement sessions on Day 1 and Day 3. Each session consisted of three acquisitions. For each acquisition, systolic and diastolic diameter and pressure were determined and used for calculation of brachial artery PWV. Within-session variability of diameter and pressure, as well as the estimated PWV, was expressed using the intraclass correlation coefficient with corresponding coefficient of variation (CoV). Between-session variability was reported using Bland-Altman analysis in combination with CoV analysis.

Results: Significant agreement (P < 0.001) was obtained for all diameter and pressure measurements obtained on Day 1 and Day 3. Within-session CoV of pulse pressure, diastolic diameter and distension were 7.0, 1.6 and 18.3%, respectively. Subsequent estimation of local PWV resulted in a CoV of 10.6%. Between-session CoV was 15.1, 3.8 and 18.9% for pulse pressure, diastolic diameter and distension, respectively. For PWV estimation, this resulted in a CoV of 13.5%.

Conclusions: Diameter and pressure can be recorded accurately over the cardiac cycle, and calculations of distensibility, pulse pressure and PWV show a slight to moderate degree of variation. Larger studies elaborating on interindividual differences need to determine the clinical efficacy of PWV measurements prior to VA creation.
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http://dx.doi.org/10.1093/ndt/gfr687DOI Listing
June 2012

Determinants of left ventricular shear strain.

Am J Physiol Heart Circ Physiol 2009 Sep 10;297(3):H1058-68. Epub 2009 Jul 10.

Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven 5600 MB, The Netherlands.

Mathematical models of cardiac mechanics can potentially be used to relate abnormal cardiac deformation, as measured noninvasively by ultrasound strain rate imaging or magnetic resonance tagging (MRT), to the underlying pathology. However, with current models, the correct prediction of wall shear strain has proven to be difficult, even for the normal healthy heart. Discrepancies between simulated and measured strains have been attributed to 1) inadequate modeling of passive tissue behavior, 2) neglecting active stress development perpendicular to the myofiber direction, or 3) neglecting crossover of myofibers in between subendocardial and subepicardial layers. In this study, we used a finite-element model of left ventricular (LV) mechanics to investigate the sensitivity of midwall circumferential-radial shear strain (E(cr)) to settings of parameters determining passive shear stiffness, cross-fiber active stress development, and transmural crossover of myofibers. Simulated time courses of midwall LV E(cr) were compared with time courses obtained in three healthy volunteers using MRT. E(cr) as measured in the volunteers during the cardiac cycle was characterized by an amplitude of approximately 0.1. In the simulations, a realistic amplitude of the E(cr) signal could be obtained by tuning either of the three model components mentioned above. However, a realistic time course of E(cr), with virtually no change of E(cr) during isovolumic contraction and a correct base-to-apex gradient of E(cr) during ejection, could only be obtained by including transmural crossover of myofibers. Thus, accounting for this crossover seems to be essential for a realistic model of LV wall mechanics.
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http://dx.doi.org/10.1152/ajpheart.01334.2008DOI Listing
September 2009

Computational modeling of volumetric soft tissue growth: application to the cardiac left ventricle.

Biomech Model Mechanobiol 2009 Aug 30;8(4):301-9. Epub 2008 Aug 30.

Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

As an initial step to investigate stimulus-response relations in growth and remodeling (G&R) of cardiac tissue, this study aims to develop a method to simulate 3D-inhomogeneous volumetric growth. Growth is regarded as a deformation that is decomposed into a plastic component which describes unconstrained growth and an elastic component to satisfy continuity of the tissue after growth. In current growth models, a single reference configuration is used that remains fixed throughout the entire growth process. However, considering continuous turnover to occur together with growth, such a fixed reference is unlikely to exist in reality. Therefore, we investigated the effect of tissue turnover on growth by incrementally updating the reference configuration. With both a fixed reference and an updated reference, strain-induced cardiac growth in magnitude of 30% could be simulated. However, with an updated reference, the amplitude of the stimulus for growth decreased over time, whereas with a fixed reference this amplitude increased. We conclude that, when modeling volumetric growth, the choice of the reference configuration is of great importance for the computed growth.
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http://dx.doi.org/10.1007/s10237-008-0136-zDOI Listing
August 2009

Computational analysis of the myocardial structure: adaptation of cardiac myofiber orientations through deformation.

Med Image Anal 2009 Apr 8;13(2):346-53. Epub 2008 Jul 8.

Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, NL-6200 MD Maastricht, The Netherlands.

Deformation and structure of the cardiac wall can be assessed non-invasively by imaging techniques such as magnetic resonance imaging. Understanding the (patho-)physiology that underlies the observed deformation and structure is critical for clinical diagnosis. However, much about the genesis of deformation and structure is unknown. In the present computational model study, we hypothesize that myofibers locally adapt their orientation to achieve minimal fiber-cross fiber shear strain during the cardiac cycle. This hypothesis was tested in a 3D finite element model of left ventricular (LV) mechanics by computation of tissue deformations and subsequent adaptation of initial myofiber orientations towards those in the deformed tissue. As a consequence of adaptation, local tissue peak stress, strain during ejection and stroke work density were all found to increase by at least 10%, as well as to become 50% more homogeneous throughout the wall. Global LV work (peak systolic pressure, stroke volume and stroke work) increased significantly as well (>9%). The model-predicted myofiber orientations were found to be similar to those in experiments. To the best of our knowledge the presented model is the first that is able to simultaneously predict a realistic myocardial structure as well as to account for the experimentally observed homogeneity in local mechanics.
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http://dx.doi.org/10.1016/j.media.2008.06.015DOI Listing
April 2009

Structure and torsion of the normal and situs inversus totalis cardiac left ventricle. I. Experimental data in humans.

Am J Physiol Heart Circ Physiol 2008 Jul 25;295(1):H197-201. Epub 2008 Apr 25.

Dept. of Physiology and Pediatrics, Cardiovascular Research Institute Maastricht, Maastricht Univ., Maastricht, The Netherlands.

In 1926, the famous American pediatric cardiologist, Dr. Helen B. Taussig, observed that in situs inversus totalis (SIT) main gross anatomical structures and the deep muscle bundles of the ventricles were a mirror image of the normal structure, while the direction of the superficial muscle bundles remained unchanged (H. B. Taussig, Bull Johns Hopkins Hosp 39: 199-202, 1926). She and we wondered about the implication of this observation for left ventricular (LV) deformation in SIT. We used magnetic resonance tagging to obtain information on LV deformation, rotation, and torsion from a series of tagged images in five evenly distributed, parallel, short-axis sections of the heart of nine controls and eight persons with SIT without other structural (cardiac) defect. In the controls, during ejection, the apex rotated counterclockwise with respect to the base, when looking from the apex. Furthermore, the base-to-apex gradient in rotation (torsion) was negative and similar at all longitudinal levels of the LV. In SIT hearts, torsion was positive near the base, indicating mirrored myofiber orientations compared with the normal LV. Contrary to expectations, torsion in the apical regions of SIT LVs was as in normal ones, reflecting a normal internal myocardial architecture. The transition zone with zero torsion, found between the apex and base, suggests that the heart structure in SIT is essentially different from that in the normal heart. This provides a unique possibility to study regulatory mechanisms for myocardial fiber orientation and mechanical load, which has been dealt with in the companion paper by Kroon et al.
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http://dx.doi.org/10.1152/ajpheart.00876.2007DOI Listing
July 2008

Structure and torsion in the normal and situs inversus totalis cardiac left ventricle. II. Modeling cardiac adaptation to mechanical load.

Am J Physiol Heart Circ Physiol 2008 Jul 18;295(1):H202-10. Epub 2008 Apr 18.

Dept. of Physiology, Cardiovascular Research Institute Maastricht, Maastricht Univ., PO Box 616, Maastricht NL-6200 MD, The Netherlands.

Mathematical models provide a suitable platform to test hypotheses on the relation between local mechanical stimuli and responses to cardiac structure and geometry. In the present model study, we tested hypothesized mechanical stimuli and responses in cardiac adaptation to mechanical load on their ability to estimate a realistic myocardial structure of the normal and situs inversus totalis (SIT) left ventricle (LV). In a cylindrical model of the LV, 1) mass was adapted in response to myofiber strain at the beginning of ejection and to global contractility (average systolic pressure), 2) cavity volume was adapted in response to fiber strain during ejection, and 3) myofiber orientations were adapted in response to myofiber strain during ejection and local misalignment between neighboring tissue parts. The model was able to generate a realistic normal LV geometry and structure. In addition, the model was also able to simulate the instigating situation in the rare SIT LV with opposite torsion and transmural courses in myofiber direction between the apex and base [Delhaas et al. (6)]. These results substantiate the importance of mechanical load in the formation and maintenance of cardiac structure and geometry. Furthermore, in the model, adapted myocardial architecture was found to be insensitive to fiber misalignment in the transmural direction, i.e., myofiber strain during ejection was sufficient to generate a realistic transmural variation in myofiber orientation. In addition, the model estimates that, despite differences in structure, global pump work and the mass of the normal and SIT LV are similar.
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http://dx.doi.org/10.1152/ajpheart.00877.2007DOI Listing
July 2008

Left ventricular apical torsion and architecture are not inverted in situs inversus totalis.

Prog Biophys Mol Biol 2008 Jun-Jul;97(2-3):513-9. Epub 2008 Feb 9.

Department of Pediatrics, Cardiovascular Research Institute Maastricht, University Hospital Maastricht, PO Box 5800, AZ Maastricht, The Netherlands.

Occasionally, individuals have a complete, mirror-image reversal of their internal organ position, called situs inversus totalis (SIT). Whereas gross anatomy is mirror-imaged in SIT, this might not be the case for the internal architecture of organs, e.g. the myofiber pattern in the left cardiac ventricle. We performed a Magnetic Resonance Tagging study in nine controls and in eight subjects with SIT to assess the deformation pattern in the apical half of the LV wall. It appeared that both groups had the same LV apical deformation pattern. This implies that not only the superficial LV apical layers in SIT follow a normal, not inverted pattern, but the deeper layers as well. Apparently, the embryonic L/R controlling genetic pathway does determine situs-specific gross anatomy morphogenesis but it is not the only factor regulating fiber architecture within the apical part of the LV wall. We propose that mechanical forces generated in the not-inverted molecular structure of the basic right-handed helical contractile components of the sarcomere play a role in shaping the LV apex.
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http://dx.doi.org/10.1016/j.pbiomolbio.2008.02.004DOI Listing
September 2008