Relevant bibliographies by topics / Left ventricular trabeculation model

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Academic literature on the topic 'Left ventricular trabeculation model'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Left ventricular trabeculation model"

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Sigvardsen, Per E., Andreas Fuchs, Jørgen T. Kühl, Shoaib Afzal, Lars Køber, Børge G. Nordestgaard, and Klaus F. Kofoed. "Left ventricular trabeculation and major adverse cardiovascular events: the Copenhagen General Population Study." European Heart Journal - Cardiovascular Imaging 22, no. 1 (May 9, 2020): 67–74. http://dx.doi.org/10.1093/ehjci/jeaa110.

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Abstract Aims Prominent left ventricular trabeculations is a phenotypic trait observed in cardiovascular diseases. In the general population, the extent of left ventricular trabeculations is highly variable, yet it is unknown whether increased trabeculation is associated with adverse outcome. Methods and results Left ventricular trabeculated mass (g/m2) was measured with contrast-enhanced cardiac computed tomography in 10 097 individuals from the Copenhagen General Population Study. The primary endpoint was a composite of major adverse cardiovascular events and defined as death, heart failure, myocardial infarction, or stroke. The secondary endpoints were the individual components of the primary endpoint. Cox regression models were adjusted for clinical parameters, medical history, electrocardiographic parameters, and cardiac chamber sizes. The mean trabeculated mass was 19.1 g/m2 (standard deviation 4.9 g/m2). During a median follow-up of 4.0 years (interquartile range 1.5–6.7), 710 major adverse cardiovascular events occurred in 619 individuals. Individuals with a left ventricular trabeculated mass in the highest quartile had a hazard ratio for major adverse cardiovascular events of 1.64 [95% confidence interval (CI) 1.30–2.08; P < 0.001] compared to those in the lowest quartile. Corresponding hazard ratios were 2.08 (95% CI 1.38–3.14; P < 0.001) for death, 2.63 (95% CI 1.61–4.31; P < 0.001) for heart failure, 1.08 (95% CI 0.56–2.08; P = 0.82) for myocardial infarction, and 1.07 (95% CI 0.72–1.57; P = 0.74) for stroke. Conclusion Increased left ventricular trabeculation is independently associated with an increased rate of major adverse cardiovascular events in the general population.
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Breckenridge, Ross A., Robert H. Anderson, and Perry M. Elliott. "Isolated left ventricular non-compaction: the case for abnormal myocardial development." Cardiology in the Young 17, no. 2 (February 26, 2007): 124–29. http://dx.doi.org/10.1017/s1047951107000273.

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Isolated ventricular non-compaction is an increasingly commonly diagnosed myocardial disorder characterised by excessive and prominent trabeculation of the morphologically left, and occasionally the right, ventricle. This is associated with high rates of thromboembolism, cardiac failure, and cardiac arrhythmia. Recent improvements in understanding the embryonic processes underlying ventricular formation have led to the hypothesis that ventricular non-compaction is due to a failure of normal ventriculogenesis, leading to abnormal myocardium which may present clinically many years later. Experimental work in animal models provides several candidate transcription factors and signalling molecules that could, in theory, cause ventricular non-compaction if disrupted.
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Hirono, Keiichi, Yukiko Hata, Nariaki Miyao, Mako Okabe, Shinya Takarada, Hideyuki Nakaoka, Keijiro Ibuki, et al. "Left Ventricular Noncompaction and Congenital Heart Disease Increases the Risk of Congestive Heart Failure." Journal of Clinical Medicine 9, no. 3 (March 13, 2020): 785. http://dx.doi.org/10.3390/jcm9030785.

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Background: Left ventricular noncompaction (LVNC) is a hereditary cardiomyopathy that is associated with high morbidity and mortality rates. Recently, LVNC was classified into several phenotypes including congenital heart disease (CHD). However, although LVNC and CHD are frequently observed, the role and clinical significance of genetics in these cardiomyopathies has not been fully evaluated. Therefore, we aimed to evaluate the impact on the perioperative outcomes of children with concomitant LVNC and CHD using next-generation sequencing (NGS). Methods: From May 2000 to August 2018, 53 Japanese probands with LVNC (25 males and 28 females) were enrolled and we screened 182 cardiomyopathy-associated genes in these patients using NGS. Results: The age at diagnosis of the enrolled patients ranged from 0 to 14 years (median: 0.3 months). A total of 23 patients (43.4%) were diagnosed with heart failure, 14 with heart murmur (26.4%), and 6 with cyanosis (11.3%). During the observation period, 31 patients (58.5%) experienced heart failure and 13 (24.5%) developed arrhythmias such as ventricular tachycardia, supraventricular tachycardia, and atrioventricular block. Moreover, 29 patients (54.7%) had ventricular septal defects (VSDs), 17 (32.1%) had atrial septal defects, 10 had patent ductus arteriosus (PDA), and 7 (13.2%) had Ebstein’s anomaly and double outlet right ventricle. Among the included patients, 30 underwent surgery, 19 underwent biventricular repair, and 2 underwent pulmonary artery banding, bilateral pulmonary artery banding, and PDA ligation. Overall, 30 genetic variants were identified in 28 patients with LVNC and CHD. Eight variants were detected in MYH7 and two in TPM1. Echocardiography showed lower ejection fractions and more thickened trabeculations in the left ventricle in patients with LVNC and CHD than in age-matched patients with VSDs. During follow-up, 4 patients died and the condition of 8 worsened postoperatively. The multivariable proportional hazards model showed that heart failure, LV ejection fraction of < 24%, LV end-diastolic diameter z-score of > 8.56, and noncompacted-to-compacted ratio of the left ventricular apex of > 8.33 at the last visit were risk factors for survival. Conclusions: LVNC and CHD are frequently associated with genetic abnormalities. Knowledge of the association between CHD and LVNC is important for the awareness of clinical implications during the preoperative and postoperative periods to identify the populations who are at an increased risk of additional morbidity.
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Stöllberger, Claudia, and Josef Finsterer. "Trabeculation and left ventricular hypertrabeculation/noncompaction." Journal of the American Society of Echocardiography 17, no. 10 (October 2004): 1120–21. http://dx.doi.org/10.1016/j.echo.2004.06.009.

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D’Silva, Andrew. "Physical Activity–Related Left Ventricular Trabeculation." Journal of the American College of Cardiology 77, no. 5 (February 2021): 662–63. http://dx.doi.org/10.1016/j.jacc.2020.11.054.

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Stöllberger, Claudia, Josef Finsterer, Ferdinand Rudolf Waldenberger, Johann Andreas Hainfellner, and Robert Ullrich. "Intramyocardial hematoma mimicking abnormal left ventricular trabeculation." Journal of the American Society of Echocardiography 14, no. 10 (October 2001): 1030–32. http://dx.doi.org/10.1067/mje.2001.115688.

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McNally, Elizabeth M., and Amit R. Patel. "Cardiac Magnetic Resonance of Left Ventricular Trabeculation." Circulation: Cardiovascular Imaging 4, no. 2 (March 2011): 84–86. http://dx.doi.org/10.1161/circimaging.110.962472.

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Fernández-Golfín, Covadonga, and José Zamorano Gómez. "Left ventricular trabeculation assessment with cardiac magnetic resonance." Journal of Cardiovascular Medicine 11, no. 7 (July 2010): 477. http://dx.doi.org/10.2459/jcm.0b013e32833833bc.

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Shieh, Joseph T. C., John L. Jefferies, and Alvin J. Chin. "Disorders of left ventricular trabeculation/compaction or right ventricular wall formation." American Journal of Medical Genetics Part C: Seminars in Medical Genetics 163, no. 3 (July 10, 2013): 141–43. http://dx.doi.org/10.1002/ajmg.c.31370.

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Gati, Sabiha, Ahmed Merghani, and Sanjay Sharma. "Increased Left Ventricular Trabeculation Does Not Necessarily Equate to Left Ventricular Noncompaction in Athletes." JAMA Internal Medicine 175, no. 3 (March 1, 2015): 461. http://dx.doi.org/10.1001/jamainternmed.2014.7186.

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Dissertations / Theses on the topic "Left ventricular trabeculation model"

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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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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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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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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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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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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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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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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
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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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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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Books on the topic "Left ventricular trabeculation model"

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Szilard, Monika. Novel Non-Surgical Porcine Model of Chronic Left Ventricular Dysfunction: Identification of Myocardial Viability Using Different Diagnostic Techniques (Acta Biomedica Lovaniensia, 242). Leuven Univ Pr, 2001.

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O’Mahony, Constantinos. Hypertrophic cardiomyopathy: prevention of sudden cardiac death. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0354.

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Sudden cardiac death (SCD) secondary to ventricular arrhythmias is the most common mode of death in hypertrophic cardiomyopathy (HCM) and can be effectively prevented with an implantable cardioverter defibrillator (ICD). The risk of SCD in HCM relates to the severity of the phenotype and regular risk stratification is an integral part of routine clinical care. For the primary prevention of SCD, risk stratification involves the assessment of seven readily available clinical parameters (age, maximal left ventricular wall thickness, left atrial diameter, left ventricular outflow tract gradient, non-sustained ventricular tachycardia, unexplained syncope, and family history of SCD) which are used to estimate the risk of SCD within 5 years of clinical evaluation using a statistical risk prediction model (HCM Risk-SCD). The 2014 European Society of Cardiology Guidelines provide a framework to aid clinical decisions and consider patients with a 5-year risk of SCD of less than 4% as low risk and recommend regular assessment while those with a risk of 6% or higher should be considered for an ICD. In patients with an intermediate risk (4% to <6%) ICD implantation may also be considered after taking into account age, co-morbid conditions, socioeconomic factors, and the psychological impact of therapy. Survivors of ventricular fibrillation arrest should receive an ICD for secondary prevention unless their life expectancy is less than 1 year. Following device implantation, patients should be followed up for device- and disease-related complications, particularly heart failure and cerebrovascular disease.
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McQuarrie, Emily P., Hallvard Holdaas, Bengt Fellström, and Alan G. Jardine. Cardiovascular disease. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0285.

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Premature cardiovascular disease is much more common in renal transplant recipients than the general population, although less common than in patients relying on maintenance haemodialysis. Cardiovascular disease in renal transplant recipients differs from the traditional atherosclerotic model. Although ordinary risk factors such as age, gender, diabetes, hypertension, and smoking still apply, others such as left ventricular hypertrophy and uraemic cardiomyopathy are relevant. Transplantation also adds specific risks such as immunosuppressive therapies and acute rejection. Understanding and managing the cardiovascular risk in this population is limited by a lack of large-scale randomized trials. The approach to managing the cardiovascular risk profile of these patients should be multifactorial and start even before transplantation.
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Rowland, Thomas W. Cardiovascular function. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0011.

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The circulatory response to increased metabolic demands of endurance exercise is best explained by a model in which volume of circulatory flow is governed by alterations in peripheral vascular resistance. These dynamics of the cardiovascular response to an acute bout of progressive endurance exercise are similar in children and adults, and, when adjusted for body size, true cardiovascular fitness (ability to generate cardiac output) is no different in healthy, untrained pre- and postpubertal individuals. As in adults, the capacity to eject stroke volume at maximal exercise differentiates levels of physiological fitness (maximal oxygen uptake) between individual children. Stroke volume at exhaustive exercise, in turn, appears to be governed by factors which influence left ventricular diastolic size rather than those which dictate myocardial systolic and diastolic function.
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Sinagra, Gianfranco, Marco Merlo, and Davide Stolfo. Dilated cardiomyopathy: clinical diagnosis and medical management. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0356.

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Dilated cardiomyopathy (DCM) is a relatively rare primary heart muscle disease with genetic or post-inflammatory aetiology that affects relatively young patients with a low-risk co-morbidity profile. Therefore, DCM represents a particular heart failure model with specific characteristics and long-term evolution. The progressively earlier diagnosis derived from systematic familial screening programmes and the current therapeutic strategies have greatly modified the prognosis of DCM with a dramatic reduction of mortality over recent decades. A significant number of DCM patients present an impressive response to pharmacological and non-pharmacological evidence-based therapy in terms of haemodynamic improvement with subsequent left ventricular reverse remodelling, which confer a favourable long-term prognosis. However, in some DCM patients the outcome is still severe. This prognostic heterogeneity is possibly related to the aetiological variety of this disease. Maximal effort towards an early aetiological diagnosis of DCM, by using all diagnostic available tools (including cardiovascular magnetic resonance imaging, endomyocardial biopsy, and genetic testing when indicated), as well as the individualized long-term follow-up appear crucial in improving the prognostic stratification and the clinical management of these patients.
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Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
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Book chapters on the topic "Left ventricular trabeculation model"

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Wu, Jimmy Ming-Tai, Meng-Hsiun Tsai, Sheng-Han Xiao, and Tsu-Yang Wu. "Construct Left Ventricular Hypertrophy Prediction Model Based on Random Forest." In Recent Advances in Intelligent Information Hiding and Multimedia Signal Processing, 142–50. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-03745-1_18.

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Ponnaluri, Aditya V. S., Ilya A. Verzhbinsky, Jeff D. Eldredge, Alan Garfinkel, Daniel B. Ennis, and Luigi E. Perotti. "Model of Left Ventricular Contraction: Validation Criteria and Boundary Conditions." In Functional Imaging and Modeling of the Heart, 294–303. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21949-9_32.

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Rondanina, Emanuele, and Peter Bovendeerd. "A Simple Multi-scale Model to Evaluate Left Ventricular Growth Laws." In Functional Imaging and Modeling of the Heart, 249–57. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21949-9_27.

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Medrano-Gracia, Pau, Brett R. Cowan, David A. Bluemke, J. Paul Finn, João A. C. Lima, Avan Suinesiaputra, and Alistair A. Young. "Large Scale Left Ventricular Shape Atlas Using Automated Model Fitting to Contours." In Functional Imaging and Modeling of the Heart, 433–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-38899-6_51.

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Ubbink, Sander, Peter Bovendeerd, Tammo Delhaas, Theo Arts, and Frans van de Vosse. "Left Ventricular Shear Strain in Model and Experiment: The Role of Myofiber Orientation." In Functional Imaging and Modeling of the Heart, 314–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11494621_32.

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Hooghoudt, T. E. H., C. J. Slager, J. H. C. Reiber, and P. W. Serruys. "Quantitation of Regional Left Ventricular Function Using the Endocardial Landmark Model — Clinical Results." In Angiocardiography, 227–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-662-00820-1_20.

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Kroon, Wilco, Tammo Delhaas, Peter Bovendeerd, and Theo Arts. "Adaptive Reorientation of Cardiac Myofibers: Comparison of Left Ventricular Shear in Model and Experiment." In Functional Imaging and Modeling of the Heart, 58–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01932-6_7.

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Rawles, John. "The Haemodynamics of Atrial Fibrillation: The Development of a Model of Left Ventricular Function." In Atrial Fibrillation, 95–114. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-1898-5_5.

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Carapella, Valentina, Rafel Bordas, Pras Pathmanathan, Jurgen E. Schneider, Peter Kohl, Kevin Burrage, and Vicente Grau. "Effect of Fibre Orientation Optimisation in an Electromechanical Model of Left Ventricular Contraction in Rat." In Functional Imaging and Modeling of the Heart, 46–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-38899-6_6.

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De Craene, Mathieu, Paolo Piro, Nicolas Duchateau, Pascal Allain, and Eric Saloux. "Left Ventricular Shape and Motion Reconstruction Through a Healthy Model for Characterizing Remodeling After Infarction." In Functional Imaging and Modeling of the Heart, 159–67. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21949-9_18.

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Conference papers on the topic "Left ventricular trabeculation model"

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Palladino, J. L., R. L. Zukus, A. Marchidan, and A. Noordergraaf. "Left ventricular model parameters and cardiac rate variability." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091681.

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Tehrani, Saeid, Terry E. Weymouth, and G. B. J. Mancini. "Model generation and partial matching of left ventricular boundaries." In Medical Imaging V: Image Processing, edited by Murray H. Loew. SPIE, 1991. http://dx.doi.org/10.1117/12.45240.

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Madbouly, Abeer. "Left Ventricular Functional Analysis through Model-Driven Object Labeling in Echocardiograms." In 2006 IEEE International Symposium on Industrial Electronics. IEEE, 2006. http://dx.doi.org/10.1109/isie.2006.295650.

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Vaes, Mark, Marcel Rutten, René van de Molengraft, and Frans van de Vosse. "Left Ventricular Assist Device Evaluation With a Model-Controlled Mock Circulation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176372.

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Left-ventricular assist devices (LVADs) have evolved from being a bridge to total heart transplant to forming a bridge to recovery of the heart. With this development, the process of weaning has become more important, and consequently, the operation and control of the LVADs during this process is more important as well. To evaluate the function and the assist properties of LVADs, a mock circulation, featuring the properties of the (diseased) heart and the systemic circulation may prove to be a valuable tool.
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Lim, Einly, Shaun L. Cloherty, John A. Reizes, David G. Mason, Robert F. Salamonsen, Dean M. Karantonis, and Nigel H. Lovell. "A Dynamic Lumped Parameter Model of the Left Ventricular Assisted Circulation." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353208.

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Barochia, AV, Y. Li, J. Su, Y. Fitz, S. Solomon, PQ Eichacker, and X. Cui. "E. coliPneumonia Decreases Left Ventricular Contractility Measures in a Murine Model." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4702.

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Khaledi, Marjan, Roozbeh Abolpour, Mohsen Mohammadi, and Maryam Dehghani. "Data-driven Model Predictive Controller Design for Left Ventricular Assist Devices." In 2021 7th International Conference on Control, Instrumentation and Automation (ICCIA). IEEE, 2021. http://dx.doi.org/10.1109/iccia52082.2021.9403602.

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Bistoquet, Arnaud, and Oskar Skrinjar. "LEFT VENTRICULAR DEFORMATION RECOVERY FROM CINE MRI USING A 4D INCOMPRESSIBLE MODEL." In 2007 4th IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2007. http://dx.doi.org/10.1109/isbi.2007.356822.

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Green, Audrey, and Gary Drzewiecki. "Computational left ventricular heart failure model with patient specific inputs and outputs." In 2015 41st Annual Northeast Biomedical Engineering Conference (NEBEC). IEEE, 2015. http://dx.doi.org/10.1109/nebec.2015.7117167.

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LeFevre and Tavernier. "A Generalised Left Ventricular Dynamic Compliance Model: The Chemo-mechanical Capacitive Transducer." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.595624.

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