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.
Full textEl 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.
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.
Full textLeft 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
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.
Full textAssessment 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
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.
Full textGonzalez, Erick. "Development of a three-dimensional model of left ventricular flow dynamics." FIU Digital Commons, 1994. https://digitalcommons.fiu.edu/etd/3980.
Full textA'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.
Full textNagasawa, 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.
Full textSpotswood, 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.
Full textDissertation (MMedVet(Diagnostic Imaging))--University of Pretoria, 2005.
Companion Animal Clinical Studies
unrestricted
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.
Full textWilson, 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.
Full textNishina, 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.
Full textElliott, 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.
Full textYousef, 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.
Full textBen-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.
Full textHorii, 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.
Full textTowner, 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.
Full textVeerassamy, 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.
Full textBalan, 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.
Full textPierrakos, 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.
Full textMaster of Science
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.
Full textEvani, 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.
Full textLi, 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.
Full textKassem, 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.
Full textIntroduction: 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.
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.
Full textTiivistelmä 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
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.
Full textPh.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
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.
Full text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.
Ketout, Hussin Shaban. "Fusion of Deformable and Biomechanical Models for Tracking Left Ventricular Endocardium by Echocardiography." 2013. http://hdl.handle.net/10222/38669.
Full textXiao, 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.
Full text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.
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.
Full textRationale: 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.
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.
Full textSchmidt, 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.
Full textSchmidt, 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.
Full textAhmadie, 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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