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1

Paun, Bruno. "Image based analysis and modeling of the detailed cardiac ventricular anatomy." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/456042.

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The role of trabeculations and their normal morphological expression in the human heart is still unclear. Clinical studies have shown that excessive trabeculation can cause heart failure due to diastolic and systolic dysfunction, thromboembolism and arrhythmias. Quantifying and modeling those structures could provide us insights into their function, their influence on cardiac performance and also their connection with cardiomyopathies. The contributions of this thesis can be summarized as follows: 1) a simplified model of the trabeculated left ventricle (LV) to study the impact of trabeculations on stroke volume, strain and pump capacity of the LVs of different geometries, 2) a simple as well as a more elaborate method for geometry independent parametrization of the detailed cardiac left and right ventricular anatomy, 3) a framework for visualization and statistical analysis of the trabeculations, and 4) a longitudinal analysis of the cardiac trabeculations in a mouse embryo at different gestational stages.
El papel de las trabéculas cardíacas y su morfología normal en el corazón humano todavía es desconocido. Estudios clínicos han demostrado que la trabeculacíon excesiva puede causar insuficiencia cardíaca debido a disfunción diastólica y sistólica, tromboembolismo y arritmias. El modelado y cuantificación de estas nos puede dar una idea de su función, su influencia en el rendimiento cardíaco y también su conexión con cardiomiopatías. Las contribuciones de la presente tesis son los siguientes: 1) un modelo simplificado del ventrículo izquierdo trabeculado para estudiar el impacto de las trabéculas sobre el volumen, la deformación y el gasto cardíaco de los ventrículos con diferentes geometrías, 2) un método simplificado, así como un método más complejo para la parametrización independiente de la geometría cardíaca detallada de los ventrículos izquierdo y derecho, 3) un framework para la visualización y el análisis estadístico de las trabeculaciones, y 4) un análisis longitudinal de las trabéculas cardíacas en un embrión de ratón en diferentes etapas gestacionales.
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2

Frandon, Julien. "IRM cardiaque : mise au point d'un logiciel semi-automatique pour l'étude de la trabéculation du ventricule gauche Semiautomatic detection of myocardial contours in order to investigate normal values of the left ventricular trabeculated mass using MRI Semi-automatic detection of myocardial trabeculation using cardiovascular magnetic resonance: correlation with histology and reproducibility in a mouse model of non-compaction." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAS045.

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La non compaction du ventricule gauche est une pathologie rare, avec une incidence chez l’adulte estimée à 0,014 %. Son pronostic est mal connu, avec une symptomatologie variable (insuffisance cardiaque, trouble du rythme cardiaque, épisodes emboliques) pouvant aller jusqu’à la transplantation cardiaque et au décès.Il n’existe pas de gold standard diagnostique. Une non compaction est suspectée devant un aspect hypertrabéculé du myocarde avec un épaississement de la couche non compactée et de profonds récessus. Certains auteurs ont proposé des critères 2D basés sur des rapports de longueurs entre couche compactée et non compactée comme Jenni et al en échographie cardiaque ou Petersen et al en IRM. Jacquier et al ont proposé une mesure de la masse non compactée totale en utilisant le volume complet de l’acquisition IRM mais avec une segmentation manuelle incluant le sang entre les trabéculations.L’objectif de ce travail est la mise au point d’un logiciel de segmentation semi automatique de la trabéculation en IRM cardiaque pour avoir des mesures plus précises et reproductibles des trabécules en supprimant le sang. Le logiciel a été validé techniquement sur des IRM 1,5 et 3 Tesla de pratique clinique courante. Il permet une segmentation précise et reproductible en 15 minutes de la masse compactée et non compactée du myocarde. Les mesures de masse ont été comparées à des mesures histologiques réelles sur modèle murin, avec une corrélation excellente. Le logiciel a été testé sur une large cohorte de patients sains, permettant de définir les valeurs normales de trabéculation par tranche d’âge et par sexe. Il est en cours de validation sur les patients atteints de non compaction
Left ventricular non-compaction is a rare cardiomyopathy with an incidence of 0,014 % in adult patients. Its prognosis remains little known. Untreated, it can lead to heart failure, cardioembolic events, tachyarythmia, heart transplant and death.Non compaction is suspected on echocardiography or CMR when a characteristic double-layered aspect of the myocardium with a thick, non-compacted endocardial layer, prominent trabeculations and deep recesses are observed, but there is no gold standard for the diagnosis. Some have proposed 2D criteria based on ratios of lengths between compacted and non compacted layers evaluated by sonography or MRI. Jacquier and al have proposed a quantification of the total amount of LV trabeculation on CMR but with a manual contouring including blood inside the trabeculae.Our purpose was the development of a semi-automatic software package to calculate the non-compacted mass that suppresses blood from the trabeculae and evaluates the total amount of compacted and non compacted mass. The feasibility of this trabeculation quantification algorithm was illustrated in multicenter, multivendor 1,5 and 3 T MRI. The software allows a precise and reproductible segmentation in about 15 mins. The quantification software was compared with histology, and tested for accuracy and reproducibility in a mouse model of non-compaction. The software was tested in a large cohort of healthy subjects to provide the range of normal values of trabeculae across age and gender. Clinical validation on patients with non compaction is in progress
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3

Remme, Espen W. "A Model-based Approach for Clinical Evaluation of Left Ventricular Deformation." Doctoral thesis, Norwegian University of Science and Technology, Faculty of Information Technology, Mathematics and Electrical Engineering, 2004. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-249.

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Assessment of left ventricular (LV) deformation is essential for clinical evaluation of LV function and cardiac images are frequently used to evaluate the LV motion and function. By combining the images with mathematical models more information may be extracted from the images. The work presented in this thesis has focused on using the finite element (FE) method to describe the LV and its deformation and combining this method with images of the heart to extract more information about the deformation.

We developed a method that estimated the LV deformation by manually tracking distinct anatomical landmarks (fiducial markers) through the cardiac cycle in 3 dimensional (3D) images of the heart. The motion of the nodal parameters of an FE mesh shaped to the geometry of the LV was fitted to the motion of the fiducial markers and thus provided a means to describe the motion. The sparsity of the fiducial markers made the fitting problem under-constrained so a parameter distribution model (PDM) of likely motions were constructed from a historical database of cases where FE meshes had been fitted to the motion of magnetic resonance (MR) tagged data. The estimated deformation from the fiducial marker fitting was filtered through the PDM and the resulting deformation corresponded well when compared to the deformation obtained from MR tagging in 13 normal subjects.

A method that decomposed the LV deformation into different deformation modes such as longitudinal shortening, wall thickening, and twisting was developed. The nodes of a subject’s LV FE mesh were displaced according to each deformation mode and the relative contribution of each mode to the total deformation measured by MR tagging was quantified by calculating a coefficient for each mode. A study that compared 13 young normal subjects with 13 older diabetes patients showed that the patients had a significantly lower degree of longitudinal shortening and wall thickening but a higher degree of longitudinal twist.

The LV deformation is influenced by cardiac disease via the material properties of the myocardium. We investigated the effects of the material parameter values on the LV deformation in a simulation study using an FE model of the LV. A description of the myocardial microstructure and a passive and active constitutive law was included in the model. The cardiac cycle was simulated from the beginning of diastasis through to the end of ejection by applying appropriate boundary conditions. The different deformation modes between end diastole and end systole were extracted and quantified for different sets of material parameters. We found that stiffer material properties particularly in the myocardial sheet direction impaired longitudinal shortening and wall thickening.

A sensitivity analysis was carried out to look at the various material parameters’ influence on LV wall strains during passive inflation. The analysis showed a high degree of coupling of the parameters in the constitutive law, which indicated an overparameterization of the law. A parameter estimation study revealed the same problem. Most of the parameters were set to constant values and only one parameter in each of the three microstructural directions were estimated during the passive inflation phase using synthetic strain data as measurements. This still gave good estimates of the stress-strain relationships in the fiber and sheet directions.


Papers I and II reprinted with kind permission of Elsevier, ScienceDirect
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4

Au, Colin L. "Left ventricular volume estimation from radionuclide images using an ellipsoidal model." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34160.pdf.

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5

Gonzalez, Erick. "Development of a three-dimensional model of left ventricular flow dynamics." FIU Digital Commons, 1994. https://digitalcommons.fiu.edu/etd/3980.

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The most common cause of death in the USA is coronary artery disease, which manifests itself by abnormal left ventricular (LV) wall motion. Diagnostic and prognostic parameters in use do not take into account regional and temporal changes in the heart wall. A three-dimensional numerical model was developed to simulate the flow patterns in a spherical left ventricle using the finite analytical method. Velocity boundary conditions were computed from LV wall motion for normal and simulated abnormal cases. A central ejection region (CER) was defined as the region in which velocity vectors were aligned +/- °5 from the long axis. The CER was extended to a quantitative CER coefficient. The Ejection Pressure Gradients were defined as the pressures along line segments from the center of the outlet to points on the LV wall.
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6

A'roch, Roman. "Left ventricular function's relation to load, experimental studies in a porcine model." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-43605.

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Background: Loading conditions are recognized to influence ventricular function according to the Starling relationship for length/stretch and force.  Many modern echocardiographic parameters which have been announced as describing ventricular function and contractile status, may be confounded by uncontrolled and unmeasured load.  These studies aimed to measure the relation between four differ­ent types of assessments of ventricular dysfunction and degrees of load.  Study examined the ‘myo­cardial performance index’ (MPI).  Study II examined long axis segmental mechanical dyssynchrony.  Study III examined tissue velocities, and Study IV examined ventricular twist.  All studies aimed to describe the relation of these parameters both to load and to inotropic changes. Methods:  In anesthetized juvenile pigs, left ventricular (LV) pressure and volume were measured continuously and their relationship (LVPVR) was analysed.  Preload alterations were brought about by inflation of a balloon tipped catheter in the inferior vena cava (IVCBO).  Inotropic interventions were brought about by either an overdose of anesthetic (combine intravenous pentobarbital and inhaled isoflurane, Study I), or beta blocker and calcium channel blocker given in combination (Stud­ies III and IV).  In one study (II), global myocardial injury and dysfunction was induced by endotoxin infusion.  MPI measurements were derived from LVPVR heart cycle intervals for isovolumic contrac­tion and relaxation as well as ejection time.  Long axis segmental dyssynchrony was derived by ana­lyzing for internal flow and time with segmental dyssynchronous segment volume change during systole, hourly before and during 3 hours of endotoxin infusion.  Myocardial tissue velocities were measured during IVCBO at control, during positive and then later negative inotropic interventions.  The same for apical and base circumferential rotational velocities by speckle tracking.  Load markers (including end-diastolic volume) were identified for each beat, and the test parameters were analysed together with load for a relation.  The test parameters were also tested during single apneic beats for a relation to inotropic interventions. Results: MPI demonstrated a strong and linear relationship to both preload and after-load, and this was due to changes in ejection time, and not the isovolumic intervals.  Long axis segmental dyssyn­chrony increased during each hour of endotoxin infusion and global myocardial injury.  This dysyn­chrony parameter was independent of load when tested by IVCBO. Peak systolic velocities were strongly load-independent, though not in all the inotropic situations and by all measurement axes.  Peak systolic strain was load-dependent, and not strongly related to inotropic conditions.  Peak sys­tolic LV twist and untwist were strongly load-dependent. Conclusions: MPI is strongly load-dependent, and can vary widely in value for the same contractile status if the load is varied.  Mechanical dyssynchrony measures are load-independen in health and also in early global endotoxin myocardial injury and dysfunction.  Peak sytole velocities are a clinically robust parameter of LV regional and global performance under changing load, though peak systolic strain seems to be load-dependent.  Left ventricular twist and untwist are load-dependent in this pig model.
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7

Nagasawa, Atsushi. "Basic fibroblast growth factor attenuates left-ventricular remodeling following surgical ventricular restoration in a rat ischemic cardiomyopathy model." Kyoto University, 2020. http://hdl.handle.net/2433/259712.

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8

Spotswood, Timothy C. "Echocardiographic changes of left ventricular size and function in a canine normovolaemic anaemia model." Diss., University of Pretoria, 2006. http://hdl.handle.net/2263/23732.

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The objective of this study was to non-invasively document the changes in echocardiographic variables of left ventricular size and function during acute normovolaemic anaemia. This model was developed as a pilot study with the purpose of providing baseline information to investigate the pathophysiology, and more specifically the effect on the heart, of canine babesiosis-induced anaemia. The study group comprised of 11 mature healthy Beagle dogs that weighed between 9 and 15 kg. Severe normovolaemic anaemia was induced over a 3-4 day period by serial bleeding while maintaining normovolaemia by autotransfusing plasma and infusing crystalloids. The dogs were then allowed to recover. Pre-anaemic [mean haematocrit (Hct) 46.7%, standard deviation (SD) 2.4%)] echocardiographic variables of left ventricular size and performance were statistically compared to those in the severely [mean Hct 15.3 %, SD 1.1%], moderately [mean Hct 24.7%, SD 1.5%] and mildly [mean Hct 33.5%, SD 2.5%] anaemic states, and between the anaemic states. The following variables were measured: left atrial size; left ventricular fractional shortening, ejection fraction, end-systolic and end-diastolic ventricular volumes and their derivatives [stroke volume, stroke index, cardiac output, cardiac index]; systolic time intervals [left ventricular ejection time (LVET), pre-ejection period (PEP), velocity of circumferential shortening, LVET/PEP and LVET index (LVETI)]; and heart rate. With the exception of end diastolic volume, left atrial size, LVET/PEP and LVETI, there was a statistically significant (p < 0.05) change in all variables in the severely anaemic state versus the pre-anaemic and the mild and moderate anaemic states. In accordance with previous invasive models, this study demonstrates the hyperdynamic state of the left ventricle that develops in response to experimentally induced acute canine normovolaemic anaemia in the conscious dog, and shows promise as a non-invasive technique of evaluating the cardiac changes in dogs suffering from canine babesiosis.
Dissertation (MMedVet(Diagnostic Imaging))--University of Pretoria, 2005.
Companion Animal Clinical Studies
unrestricted
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9

Ding, Tong. "Development and experimental verification of a three-dimensional model of left ventricular flow dynamics." FIU Digital Commons, 1997. http://digitalcommons.fiu.edu/etd/2822.

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Ischemic heart disease, which results from the insufficient coronary artery blood flow is a leading cause of mortality in developed countries. It manifests itself by abnormal left ventricular wall motion during systole. A three dimensional numerical model was developed to simulate the flow patterns in the left ventricle. Numerical solutions were obtained by discretizing the Navier-Stokes equations for viscous, incompressible, steady flow using finite element method. A diagnostic index Central Ejection Region (CER) as well as its quantitative version CER coefficient which are based on the flow patterns were defined as the region in which velocity vectors were aligned 5 degrees from the long axis. They seem to be very sensitive to the degrees and size of ischemia. To validate the numerical method, experimental measurements as well as the numerical computation were performed on sphere-shape normal and the ischemic left ventricle model A good agreement has been achieved.
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10

Wilson, Gayle. "Alterations in myofilament properties in a rabbit coronary artery ligation model of left ventricular dysfunction." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265534.

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11

Nishina, Takeshi. "Initial effects of the left ventricular volume reduction surgery in a rat ischemic cardiomyopathy model." Kyoto University, 2005. http://hdl.handle.net/2433/144475.

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12

Elliott, Elspeth B. A. "Investigation of factors affecting the sodium/calcium exchanger in a rabbit model of left ventricular dysfunction." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433518.

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13

Yousef, Zaheer Raza. "Post-infarction left ventricular remodelling and the open artery hypothesis : an experimental model and a clinical trial." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405634.

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14

Ben-Amotz, Ron. "Effects Of Intraperitoneal Bilirubin Administration On Infarct Area And Left Ventricular Function In A Rat Model Of Acute Coronary Occlusion." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306520603.

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15

Horii, Taiko. "Residual fibrosis affects a long-term result of left ventricular volume reduction surgery for dilated cardiomyopathy in a rat model." Kyoto University, 2005. http://hdl.handle.net/2433/144700.

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16

Towner, Kali Jean, and Kali Jean Towner. "Hemodynamic Changes Associated with Sub-Optimal Inflow Cannula Angle in the Heartware HVAD - A Hemostatic Model." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624116.

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Pump thrombosis is the epitome of left ventricular assist device dysfunction for end-stage heart failure patients. With the increased utilization of implantable, long-term, left ventricular assist devices (LVADs), understanding the implications associated with device orientation and interaction with the body is exceedingly important. Components associated with pump thrombosis in the Thoratec© HeartMate II™ (HMII) and the HeartWare© HVAD® devices include the inflow cannula, the outflow graft, and the pump elements as well as pump pocket depth for the HMII specifically. Several studies have been conducted to analyze these interactions with the HMII, however there is minimal to no data available analyzing how the device orientation of the HeartWare HVAD affects hemodynamics and a patient’s risk for developing pump thrombosis. Therefore, the purpose of this pilot study is the simulate the hemodynamic implications associated with Sub-optimal cannula angulation of the HVAD. Using Solidworks 2016 Ed., a simplified, hemo-static model of the left side of the heart was created. Dimensions for the atria, ventricle, and mitral valve were determined through the combination of Trans-Esophageal Echo cardiogram data as well as literature references. Three different inflow cannula angle scenarios were developed including a Control, a Clinically Optimal, and a Sub-optimal. Assumptions included body temperature, no accumulation within the ventricle, and no ejection or contraction. The model consists of static continuous flow set to 5 liters per minute with the assumption that the HeartWare HVAD is completely supporting the left ventricle. The results include both qualitative and quantitative data. Flow trajectory plots for each cannula scenario depict the hemodynamic flow patterns for different time points. Results show visible changes in the Sub-optimal orientation when compared to both the Control and the Clinically Optimal scenario. Additionally, it was determined that there were no statistically significant differences in the velocity vectors for any of the scenarios however, the shear stress values were determined to be significantly different for all time points, p < 0.001 for all scenarios when compared to Control. Though there are several limitations of this study, with sub-optimal inflow cannula angulation, there is a potential increased risk of hemolysis due to increased shear stress.
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17

Veerassamy, Shalini. "Revisiting hemodynamic analysis of pulmonary edema after the onset of left ventricular dysfunction using a mathematical model of the cardiovascular system." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31075.

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The aim of this project was to extend a mathematical model of the cardiovascular circulation, originally built by Burkhoff and Tyberg [6]. The model was implemented in Simulink and consists of 6 lumped vascular compartments interconnected by segments allowing unidirectional blood flow. A set of 6 differential equations describe changes in blood volume in the four systemic and two ventricular compartments as functions of time in terms of the pressure across each compartment and the resistances between them. The model was used to investigate why pulmonary venous pressure rises after the onset of left ventricular dysfunction. Special attention was given to the pericardial and peripheral resistance effects. Sensitivity analysis showed that our parameter values and ratios were more appropriate than those of Burkhoff and Tyberg [6]. We conclude that, although stressed volume has a fundamental role in raising the pulmonary venous pressure, contractile strength and systemic arterial resistance also contribute considerably.
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18

Balan, Bharat. "Novel Orally Active Hydrogen Sulfide-Releasing Compound, SG1002, Improves Left Ventricular Function and Survival in a Murine Model of Ischemic Cardiomyopathy." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4937.

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Hydrogen sulfide (H2S) is a gasotransmitter that has shown cardioprotective effects in the setting of myocardial injury such as acute myocardial infarction (MI) and pressure overload-induced heart failure. However, there are shortcomings in precision and control release from the use of traditional formulations of H2S in the form of inorganic salts. In this thesis, we sought to determine if the novel, orally active, slow-releasing H2S-compound SG1002 plays a role in attenuating MI-induced left ventricular (LV) dysfunction and adverse remodeling. We also evaluated the effect of SG1002 on changes in ECG parameters such as QT interval, in addition to 28-day survival post MI. SG1002 protects against ischemic cardiomyopathy in mice by mitigating LV dysfunction as measured by echocardiography and decreasing LV scar size as measured by histopathological methods. The improvement in survival might be due to the reduction in QT interval prolongation hence lessening the likelihood of forming lethal arrhythmias post MI. Western blot analyses of SG1002 treated mice showed restoration of VEGF levels indicating a pivotal role played by pro-angiogenic signaling in the improvement of cardiac function and attenuation of adverse remodeling. We propose that SG1002 can be a promising pharmacotherapeutic means for the treatment of ischemic heart failure.
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19

Pierrakos, Olga. "Hemodynamic Flow Characterization of St. Jude Medical Bileaflet Mechanical and Bioprosthetic Heart Valve Prostheses in a Left Ventricular Model via Digital Particle Image Velocimetry." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31262.

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The performance of the heart after a valve replacement operation will greatly depend on the flow character downstream the mitral valve thus a better understanding of the flow character is essential. Most in vitro studies of the flow downstream of a MHV have been conducted with the valve in the aortic position. Researchers reported detailed measurements most of which were obtained by Laser Doppler Velocimetry (LDV) in rigid models of the aorta. Digital Particle Image Velocimetry (DPIV) has also been utilized to reveal intricate patterns of interacting shed vortices downstream of the aortic valve. The orientation of the valves may considerably affect the flow development and slight difference may produce significant differences in the ventricular flow fields. Two orientations, respectively anatomical and anti-anatomical, of the St. Jude Medical (SJM) bileaflet valve are presented and compared with the SJM Biocor porcine valve, which served to more closely represent the natural valve. In this effort, we employ a powerful tool to monitor the velocity field in a flexible, transparent LV and study the evolution of large eddies and turbulence through a complete cardiovascular cycle. Both time average and instantaneous results of velocity, vorticity, and turbulent kinetic energy distributions are presented. The presence and location of vortical structures were deduced as well as the level of coherence of these structures. The presence of three distinct flow patterns were identified, by the location of vortical structures and level of coherence, for the three configurations corresponding to significant differences in the turbulence level distribution inside the LV.
Master of Science
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20

Rose, David D. "The use of transesophageal echocardiography for the assessment of left ventricular volume and function in patients undergoing acute normovolemic hemodilution as a human hemorrhagic model." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3261239.

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21

Evani, Om A. "A Novel, Orally Active Hydrogen Sulfide-Releasing Compound, SG1002, Improves Left Ventricular Function with an Associated Induction of Angiogenesis in a Murine Model of Ischemia/Reperfusion." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5389.

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Hydrogen sulfide (H2S) is the newest member of the gasotransmitter family and is becoming well known for its cardioprotective effects in preclinical trials. Many recent studies have shown the benefits of exogenous H2S in the setting of acute myocardial infarction (AMI) and pressure overload-induced heart failure, but current formulations are derived from inorganic salts which have shortcomings in the precision and control of release of H2S. The main objective of this thesis was to determine if the novel, orally active, slow-releasing compound, SG1002, can attenuate the severity of damage and adverse remodeling caused by ischemia/reperfusion injury through an induction of angiogenesis. A traditional sodium salt, Na2S, which has been previously shown to be cardioprotective, was used as a positive control. SG1002 improved overall left ventricular function as measured by increased ejection fraction from echocardiography and decreased QRS interval from electrocardiography compared to untreated animals following MI. SG1002 therapy was also associated with an induction of angiogenesis, which was determined through qRT-PCR, western blot, and histological methods. SG1002 increased VEGF protein levels, which was paralleled with an increase in capillary density in the infarct region. SG1002 also upregulated microRNA-126, which is thought to repress the inhibitor of VEGF, Spred-1. It is possible that this “angiomiR” plays a key role in the angiogenesis-related cardioprotection of H2S. The combination of increased pro-angiogenic factors along with greater vascular density resulting from SG1002 therapy indicates the therapeutic potential for this drug in the prevention and/or treatment of ischemic heart failure.
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22

Li, Zipeng. "Sustained-release of basic fibroblast growth factor using gelatin hydrogel improved left ventricular function through the alteration of collagen subtype in a rat chronic myocardial infarction model." Kyoto University, 2018. http://hdl.handle.net/2433/235987.

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23

Kassem, Sara. "Simpsons biplan metod jämfört med Philips Heart Model vid bestämning av vänsterkammares ejektionsfraktion." Thesis, Örebro universitet, Institutionen för hälsovetenskaper, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-92907.

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Introduktion: Vänsterkammarens ejektionsfraktion (VKEF) är ett central mått på systolisk funktion i vänster kammare och är en av de mest betydelsefulla parametrar vid ekokardiografiska undersökningar. Idag är Simpson biplan metoden den mest använda metoden för bestämning av ejektionsfraktionen. Vid ekokardiografiska undersökningar sänder givaren med piezoelektriska kristaller ut ultraljudsvågor med en frekvens över 20 000 Hz. Ljudvågorna som skickas ut i kroppen reflekteras och sedan återvänder de till givaren för att skapa en bild. Denna studie jämför den tvådimensionella (2D) ultraljudsmetoden Simpsons biplan med Philips Heart Model som är en automatiserad tredimensionella (3D) funktion för bedömning av VKEF.  Material och metod: I studien inkluderades 31 hjärtfriska försökspersoner mellan åldrarna 21-64. Det samlades in bilder på apikala 4- och 2 kammarbilder från alla försökspersoner där Simpsons biplan metoden användes för att beräkna ejektionsfraktion. Apikala 4-kammarbilder samlades in för att beräkna ejektionsfraktionen med Philips Heart Model 3D funktion.  Resultat: Resultatet från denna studie visade att det inte föreligger någon signifikant skillnad mellan Simpsons biplan metoden och Philips Heart Model metoden för bestämning av ejektionsfraktion. Båda metoderna visade likvärdiga mätresultat.  Diskussion: Philips Heart Model metoden är en relativ ny funktion som använder sig av artificiell intelligens för att analysera 3D bilder. Philips Heart Model metoden är en säker funktion att använda då de flesta studier bevisar likvärdiga och säkra mätresultat i jämförelse med andra metoder.  Konklusion: Enligt denna studie ger Philips Heart Model funktionen likvärdiga mätresultat av vänsterkammarens ejektionsfraktion i jämförelse med Simpsons biplan.
Introduction: Simpson’s biplane method is the most used method for determining the left ventricular ejection fraction (LVEF) in echocardiographic examinations. Ejection fraction is a central measurement of the heart's global systolic function. The probe with piezoelectric crystals emits ultrasound waves with a frequency above 20,000 Hz. The sound waves that are sent out into the body are reflected and then return to the probe to create an image. This study compares the two-dimensional (2D) ultrasound Simpson's biplane method with the Philips Heart Model method, which is an automated three-dimensional (3D) function for assessment of LVEF.                                                                                                                          Material and method: 31 subjects with no recorded heart pathologies between the ages of 21-64 were included in the study. Apical 4- and 2-chamber images were collected from the test subjects, where the Simpson's biplane method was applied to calculate the ejection fraction. 2D apical 4-chamber images were collected to convert to 3D and used to calculate the ejection fraction with the Philips Heart Model.    Results: The results of this study showed that there is no significant difference between the Simpson’s biplane method and the Philips Heart Model method for determining ejection fraction.    Discussion: The Philips Heart Model method is a relatively new feature that uses artificial intelligence to analyze 3D images. The Philips Heart Model method is a reliable feature to use as most studies have proven similar and reliable measurements when comparing it with other methods for determining LVEF.    Conclusion: According to this study, the Philips Heart Model feature provides equivalent measurements in comparison with the manual method Simpson's biplane.
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24

Mäkelä, J. (Jussi). "Bone marrow-derived stem cell therapy in acute myocardial infarction:an experimental porcine model." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514296697.

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Abstract Stem cell therapy has several mechanisms for repairing damaged myocardium and improving functional capacity of the left ventricle reduced by myocardial infarction. Despite the increase in scientific data, details of these mechanisms are still partly unexplained. The optimal number and type of stem cells as well as timing and route of transplantation are unclear. The purpose of this study was to clarify therapeutic potential of bone marrow-derived stem cells (BM-MNCs) using experimental porcine acute myocardial infarction model. Myocardial infarction was caused by occluding the circumflex coronary artery for 90 minutes. Immediately after reperfusion BM-MNCs were injected directly into the damaged myocardium or by angioplastic catheter into the infarct-related coronary artery. Left ventricular ejection fraction (LVEF) improved 3 weeks after infarction in animals that received BM-MNCs intramyocardially whereas in animals that received intracoronary transplantation or saline LVEF failed to recover. Radionuclide imaging and histological analysis showed intramyocardially transplanted cells remaining in the infarcted myocardium, whereas after intracoronary transplantation a major fraction of cells flushed into the lungs. In histological analysis minor fraction of BM-MNCs showed differentiation towards myocyte form and proliferation. Significantly lower collagen density and higher levels of smooth muscle actin and skeletal muscle actin were detected in the infarcted myocardium after intramyocardial or intracoronary BM-MNC transplantation compared with animals that received saline. Proteomic screening indicated that mitochondrial energy metabolism recovered after BM-MNC transplantation. Additionally, two proteins showed elevated levels after BM-MNC transplantation, which indicates that they are actively involved in the pathological mechanisms. BM-MNCs appear to enhance recovery of the infarcted myocardium by restoring the reduced LVEF after infarction. Intramyocardial stem cell therapy showed best results in recovery. Stem cell therapy moulds the infarct scar by reducing collagen density and by increasing components typical for muscle cells. The effects of stem cell therapy are mainly paracrine
Tiivistelmä Kantasoluterapian on havaittu korjaavan infarktissa vaurioitunutta sydänlihasta toimintakykyisemmäksi usealla mekanismilla sekä parantavan sydänlihaksen pumppaustoimintaa. Huolimatta lisääntyneestä tutkimustiedosta näiden monimutkaisten mekanismien yksityiskohdat ovat edelleen paljolti selvittämättä. Samoin käytettävien kantasolujen tyypin, määrän, siirtotekniikan ja siirron ajoituksen optimointi on vielä epäselvää. Tämän tutkimuksen tavoitteena oli selvittää kokeellista sian infarktimallia käyttäen luuytimen kantasolujen kykyä tehostaa vaurioituneen sydänlihaksen toipumista akuutin infarktin jälkeen. Mallissa aiheutettiin sydäninfarkti sulkemalla vasemman sepelvaltimon kiertävähaara 90 minuutiksi. Välittömästi verenkierron uudelleen avaamisen jälkeen luuytimen soluja ruiskutettiin infarktialueelle joko suoraan sydänlihakseen tai sepelvaltimoon. Kolmen viikon kuluttua infarktista kantasoluja suoraan sydänlihakseen saaneiden eläinten vasemman kammion ejektiofraktio (LVEF) parani tilastollisesti merkitsevästi verrattuna kantasoluja sepelvaltimoon saaneisiin eläimiin ja keittosuolaa saaneisiin eläimiin, joiden LVEF pysyi infarktin jälkeisellä alentuneella tasolla. Isotooppitutkimus ja histologinen analyysi osoittivat, että suoraan sydänlihakseen ruiskutetuista kantasoluista valtaosa säilyy infarktialueella kun taas sepelvaltimoon siirretyt solut pääasiassa ajautuvat keuhkoihin. Histologisessa analyysissa sydänlihakseen ruiskutettujen solujen todettiin vähäisessä määrin erilaistuvan lihassolujen suuntaan ja jakautuvan. Kantasoluja saaneiden eläinten ryhmissä todettiin infarktialueella merkitsevästi alhaisempi kollageenipitoisuus sekä enemmän sileälihassolujen aktiinia ja poikkijuovaisten lihassolujen aktiinia kuin keittosuolaa saaneilla eläimillä. Proteomiikka-analyysin tulokset viittaavat kantasoluterapian saaneilla eläimillä mitokondrioiden energiatalouden tehostumiseen. Lisäksi esille tuli kaksi kantasoluterapian jälkeen aktiivista proteiinia, joilla todennäköisesti on keskeinen tehtävä infarktin patogeneesissä. Tutkimuksen perusteella luuytimen kantasolut tehostavat sydänlihaksen toipumista infarktista palauttamalla sydämen alentunutta pumppaustehoa. Suoraan sydänlihakseen annettu kantasoluterapia vaikuttaa tehokkaimmalta menetelmältä. Kantasoluterapia muovaa infarktiarpea vähentämällä kollageenin ja lisäämällä lihassoluille tyypillisten komponenttien määrää. Kantasoluterapian vaikutukset ovat pääasiassa parakriinisiä
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25

Sharp, III Thomas E. "DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/445275.

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Physiology
Ph.D.
Remarkable advances have been made in the treatment of cardiovascular diseases (CVD), however, CVD still accounts for the most deaths in industrialized nations. Ischemic heart disease (IHD) can lead to acute coronary syndrome (ACS) (myocardial infarction [MI]). The standard of care is reperfusion therapy followed by pharmacological intervention to attenuate clinical symptoms related to the MI. While survival from MI has dramatically increased with the implementation of reperfusion therapy, these individuals will inevitably suffer progressive pathological remodeling leaving them predispose to develop heart failure (HF). HF is a clinical syndrome defined as the impairment of the heart to maintain organ perfusion at rest and/or during times of exertion (i.e. exercise intolerance). Clinically, this is accompanied by dyspnea, pulmonary or splanchnic congestion and peripheral edema. Physiologically, there is neurohormal activation through the classical β–adrenergic and PKA–dependent signalin
Temple University--Theses
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26

Chen, Shi-Kai, and 簡士凱. "Four-dimensional Wall Motion Model for Application of Left Ventricular Myocardial Function." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/44362626436246045430.

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碩士
中原大學
生物醫學工程研究所
105
The synergy of myocardial contraction creates an effective cardiovascular pumping system. Regional dysfunction of myocardium will be leading to functional abnormality of cardiac wall motion that is one of the risk factors for ventricular remodeling and heart failure. Early detecting abnormality of wall motion and treated could prevent further deterioration. This study sought to characterize global and regional systolic function abnormalities. The self-developed 4D image processing software will be extracting the wall motion of left ventricle from a 4D cardiac images. A seeded region growing incorporated active contour method was designed to locate the edge of endocardial and epicardium. A 3D harmonic phase method using 3D triangle mesh was utilized to construct a 3D grid model of heart. Myocardial wall motion value in different extent will be marked with colors in 3D model. With 10 frames of 3D heart model and the shortening of ventricular long axis, the left ventricular wall motion could be predicted. The region of wall motion with less than 2mm that was lower than average will be marked with dark blue color for illustration. The coordinates of lower motion areas and related LV parameters were characterized and recorded. Four data set of fibrotic scar delay enhanced cardiac images and 4D cardiac wall motion images was used to test this non-invasive method of early detection cardiac abnormality. The patient after surgery with fibrotic scar tissue necessarily has lower myocardial motion value. However, fibrotic scar tissue will not show up in 40% of patients after surgery but the operated area may still have lower myocardial motion. The detection wall motion could effectively reflect the dysfunction of myocardium. Thus, this study provides a new approach to assess the degree and site dysfunction area of myocardium.
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27

Ketout, Hussin Shaban. "Fusion of Deformable and Biomechanical Models for Tracking Left Ventricular Endocardium by Echocardiography." 2013. http://hdl.handle.net/10222/38669.

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Biomedical image processing is a very important research area. Image analysis is one of the most important techniques in studies related to heart functions. The clinical assessment of LV function is very important to evaluate the heart function for patients or suspected heart disease sufferers. 2D echocardiography allows us to study the dynamic analysis of the heart which results in obtaining the quantitative and qualitative analysis of the LV. Cardiac function quantitative analysis depends on the heart’s shape characteristics like the enclosed area and heart wall thickness. The segmentation of medical images and obtaining the traces of the LV boundaries is an essential procedure to get the quantitative and qualitative analysis. Yet, in clinical procedure, this task depends on manual tracing which is slow, tedious and time consuming job. Hence, automating this clinical procedure during the cardiac cycle is of great importance. The aim of this thesis is to automate the manual process of detecting and tracking the LV boundaries of 2D echocardiographic image sequence. Instead of depending only on the imaging based techniques, the designed and implemented framework utilizes the LV mechanics beside the imaging based techniques. When it comes to information extraction from patterns which have been classified, it has been proved that the different contour detection methods complement each other. As a result, efficient combination of different contour detectors is expected to achieve better contour detection than if only one detector is used. This combination of contour detectors produces incremental gains in overall performance. In the first framework, the detection and tracking are accomplished by employing the extended Kalman filter framework to combine the contours estimated by the biomechanical model and the contours extracted using the deformable models. An alternative framework is used by employing averaging fusion followed by level set method. A gold standard is created from three manual outlines and utilized in the experimental results to evaluate the automated results. The tracking and segmentation of LV during the cardiac cycle was accomplished successfully in all cases. The results showed limits of agreement for an average perpendicular distance of 1.277 ±0.252 mm versus the created gold standard. This proved that this framework achieved better performance in tracking and segmenting the LV through the cardiac cycle.
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28

Xiao, Sheng-Han, and 蕭聖翰. "Based on Deep Neural Network to Analyze Electrocardiogram and Construct Left Ventricular Hypertrophy Prediction Model." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/f3x493.

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碩士
國立中興大學
資訊管理學系所
106
Heart disease ranks second in Taiwan’s top ten cause of death in 2016 and the number of deaths in heart disease increases by about 700 people each year. Therefore, how to improve the accuracy of heart disease diagnosis is urgent. This study combined the deep neural network and ECG data to develop an ECG left ventricular hypertrophy classifier. The classification system uses data preprocessing technology to impute missing values of ECG data and transform ECG data for the requirement of the deep neural network. Then, input the data into the six-layers deep neural network designed in this study was used to predict left ventricular hypertrophy. L2-Regularization and Dropout are used to avoid overfitting in each model iteration. The system has been named the Electrocardiographic left ventricular hypertrophy classifier (ELVHC). The experimental results show that the accuracy of the prediction model is 73%, the sensitivity is 66%, and the specificity is 78%. The deep neural network model that the study proposed is significantly higher than two clinical methods in the sensitivity and the accuracy.
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29

Stram, Amanda R. "Mitochondrial protein acetylation and left ventricular function in a model of hypertrophic cardiomyopathy and heart failure." Diss., 2017. http://hdl.handle.net/1805/14329.

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Indiana University-Purdue University Indianapolis (IUPUI)
Rationale: The childhood heart disease of Friedreich’s Ataxia (FRDA) is characterized by hypertrophy and failure. It is caused by loss of frataxin (FXN), a mitochondrial protein involved in energy homeostasis. FRDA model hearts have increased mitochondrial protein acetylation and impaired sirtuin 3 (SIRT3) deacetylase activity. Protein acetylation is an important regulator of cardiac metabolism and SIRT3 is protective in heart disease. The underlying pathophysiology of heart failure in FRDA is unclear. I suspect that increased acetylation in FRDA heart mitochondria damages cardiac energy homeostasis by inhibiting activity of key enzymes involved in heart metabolism. Objective: My project tested the hypothesis that altered acetylation of mitochondrial proteins contributes to the cardiomyopathy of FRDA. Methods: Conditional mouse models of FRDA cardiomyopathy with ablation of FXN (FXN KO) or FXN and SIRT3 (FXN/SIRT3 DKO) in the heart were compared to healthy controls. Hearts were evaluated using echocardiography, cardiac catheterization, histology, protein acetylation and expression. FXN KO mice were treated with NAD+ replacement therapy with nicotinamide riboside (NR), and FXN/SIRT3 DKO mice were treated with FXN protein replacement therapy. Results: Acetylation was temporally progressive and paralleled evolution of heart failure in the FXN KO model. High levels of acetylation were associated with cardiac fibrosis, mitochondrial damage, impaired fat metabolism, and diastolic and systolic dysfunction. Acetylation correlated strongly with worse heart function, and loss of SIRT3 in the FXN KO mouse resulted in significant decrease in ejection fraction and fractional shortening. Treatment of the FXN/SIRT3 DKO with FXN protein therapy reduced acetylation but was not sufficient to fully rescue heart function. Increasing NAD+ with NR-treatment in the FXN KO lead to increased mitochondrial protein acetylation and did not improve cardiac outcome. Conclusion: I found a strong negative correlation between heart function and mitochondrial protein acetylation. My findings also provide evidence that absence of SIRT3 expression in the FXN KO heart exacerbates features of heart failure, and that SIRT3 expression is necessary to rescue the FXN KO heart. These results suggest that SIRT3 inactivation and abnormal acetylation contribute to the pathophysiology of heart disease in FRDA.
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30

Huang, Yu-Fang. "Study on cardiovascular toxicity of ambient particles in rats with left ventricular dysfunction 1. Decreased left ventricular function in spontaneously hypertensive rats exposed to diesel exhaust particles 2. Establishment of a left ventricle-dysfunction animal model induced by isoproterenol." 2007. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-3007200711402100.

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31

Schmidt, Cristine. "Cardioprotective effects of exercise precoditioning in an experimental model of left ventricular dysfunction secondary to pulmonary arterial hypertension." Dissertação, 2013. https://repositorio-aberto.up.pt/handle/10216/68470.

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32

Schmidt, Cristine. "Cardioprotective effects of exercise precoditioning in an experimental model of left ventricular dysfunction secondary to pulmonary arterial hypertension." Master's thesis, 2013. https://repositorio-aberto.up.pt/handle/10216/68470.

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33

Ahmadie, Roien. "Congenital absence of NOS3 potentiates left ventricular dysfunction in a murine model of diet induced obesity and chronic pressure overload." 2009. http://hdl.handle.net/1993/21391.

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