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Dissertations / Theses on the topic 'Cardia arrhythmia'

Author: Grafiati

Published: 7 June 2025

Last updated: 26 June 2025

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1

Rodriguez, Luz-Maria. "New observations on cardiac arrhythmias." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6619.

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2

Ware, James. "Genomic dissection of arrhythmia and cardiac electromechanics." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39405.

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Cardiac arrhythmia is a leading cause of death in the developed world and a final common pathway for many forms of cardiac disease. Rare inherited arrhythmia syndromes contribute to this disease burden, particularly through sudden death in the young. The study of rare syndromes, such as inherited arrhythmia, can also identify genes and pathways important in common diseases. Here, genomic approaches were applied to dissect genetic determinants of cardiac arrhythmia, through gene discovery, variant discovery, and variant annotation. First, whole-exome sequencing was used to identify the genetic basis of an unexplained inherited arrhythmia syndrome. Linkage analysis and conventional sequencing excluded known causative genes in a family with Brugada Syndrome, and whole exome sequencing identifie d a shortlist of five new candidate genes that may lead to a genetic diagnosis in this family and new insights into the pathogenesis of the condition. Following the identification of genes responsible for inherited arrhythmia syndromes, the recognition of specific disease-causing variants in those genes allows for clinical application, including molecular diagnosis, cascade screening and stratified therapy. Here, two high-throughput next-generation sequencing approaches for the detection of variants in these genes were compared, technically evaluated, and optimis ed. This represents the de novo establishment of next-generation sequencing technologies and analysis pathways in our laboratory, and provides a platform for molecular diagnosis and future genotype-phenotype correlation studies. Finally, a novel approach for the functional annotation of non-synonymous variants was developed. This approach, termed 'Paralogous Annotation', identifies functionally important, disease-associated residues across protein families using multiple sequence alignment. Paralogous Annotation was validated here by demonstrating the accurate identification of disease-causing variation in genes that cause long QT syndrome - an important cause of sudden death. This methodology is widely applicable to annotate Mendelian human disease genes.

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3

Kehrle, Florian [Verfasser]. "Inverse simulation for cardiac arrhythmia / Florian Kehrle." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1160593698/34.

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4

Ye, Yanping. "Designing New Drugs to Treat Cardiac Arrhythmia." PDXScholar, 2012. https://pdxscholar.library.pdx.edu/open_access_etds/638.

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Heart failure resulting from different forms of cardiomyopathy is defined as the inability of the heart to pump sufficient blood to meet the body's metabolic demands. It is a major disease burden worldwide and the statistics show that 50% of the people who have the heart failure will eventually die from sudden cardiac death (SCD) associated with an arrhythmia. The central cause of disability and SCD is because of ventricular arrhythmias. Genetic mutations and acquired modifications to RyR2, the calcium release channel from sarcoplasmic reticulum, can increase the pathologic SR Ca2+ leak during diastole, which leads to defects in SR calcium handling and causes ventricular arrhythmias. The mechanism of RyR2 dysfunction includes abnormal phosphorylation, disrupted interaction with regulatory proteins and ions, or altered RyR2 domain interactions. Many pharmacological strategies have shown promising prospects to modulate the RyR2 as a therapy for treating cardiac arrhythmias. Here, we are trying to establish a novel approach to designing new drugs to treat heart failure and cardiac arrhythmias. Previously, we demonstrated that all pharmacological inhibitors of RyR channels are electron donors while all activators of RyR channels are electron acceptors. This was the first demonstration that an exchange of electrons was a common molecular mechanism involved in modifying the function of the RyR. Moreover, we found that there is a strong correlation between the strength of the electron donor/acceptor, and its potency as a channel inhibitor/activator, which could serve as a basis and direction for developing new drugs targeting the RyR. In this study, two new potent RyR inhibitors, 4-methoxy-3-methyl phenol (4-MmC) and the 1,3 dioxole derivative of K201, were synthesized which are derivatives of the known RyR modulators, 4-chloro-3-methyl phenol (4-CmC) and K201. The ability of K201, 1,3 dioxole derivative of K201 and 4-MmC to inhibit the cardiac calcium channel is examined and compared at the single channel level. All of these compounds inhibited the channel activity at low micromolar concentrations or sub-micromolar concentrations.

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5

Lee, Ying-siu Andrew, and 李應紹. "Endogenous opioid peptides and cardiac arrhythmias." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1988. http://hub.hku.hk/bib/B31231275.

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6

Bonilla, Ingrid Marie. "Acquired Electrophysiological Remodeling and Cardiac Arrhythmias." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396024058.

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7

Lee, Ying-siu Andrew. "Endogenous opioid peptides and cardiac arrhythmias /." [Hong Kong] : University of Hong Kong, 1988. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12358812.

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8

Chai, Shin Luen Chai. "Novel Genetic Modifiers in a Monogenic Cardiac Arrhythmia." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1516618028568975.

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9

Zhou, Yuan, and 周嫄. "Ionic mechanisms of chloroform-induced cardiac arrhythmias." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085325.

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10

Sitsapesan, R. "Opioid receptors and ischaemia-induced cardiac arrhythmias." Thesis, University of Strathclyde, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381536.

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11

Campbell, G. "Is intravenous magnesium effective in cardiac arrhythmias?" Interim : Interdisciplinary Journal, Vol 7, Issue 2: Central University of Technology Free State Bloemfontein, 2008. http://hdl.handle.net/11462/385.

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Published Article<br>Magnesium is the second most abundant intracellular cation with many control and regulatory functions. It regulates energy production and utilization and modulates activity of membrane ionic channels. Magnesium has direct control effects on cardiac myocyte ion channels making it useful in certain arrhythmias. Calcium is responsible for pacemaker excitation and for excitation-contraction coupling in myocytes but increased intracellular calcium produces early and late afterdepolarisations initiating arrhythmias. Magnesium regulates calcium channel activity preventing raised intracellular levels. Potassium channel activity is enhanced by magnesium hyperpolarizing the cell reducing arrhythmia generation. Magnesium is effective against long QT Torsade de Pointes. In rapid atrial fibrillation magnesium produces rate control slowing AV nodal conduction. Magnesium prevents digitalis toxicity due to associated hypomagnesemia.

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12

Zhou, Yuan. "Ionic mechanisms of chloroform-induced cardiac arrhythmias." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085325.

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13

Martins, Jose L. M. G. "A Rapid Access Arrhythmia Clinic for the Diagnosis and Management of Incident Atrial Fibrillation and Other Cardiac Arrhythmias : The Imperial College New Atrial Fibrillation Study." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520897.

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14

Zhu, Chenhong. "New insight into models of cardiac caveolae and arrhythmia." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1945.

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Recent studies suggest that cardiomyocyte membrane microdomains, caveolae and transverse tubules, play a key role in cardiac arrhythmia. Mutation of caveolin-encoding genes CAV3, co-expressed with genes of caveolae ion channels, leads to a late persistent sodium currents and delayed repolarization stage, called LQT9 disease. A simplified three-current model is created to largely reduce the well-known Pandit rat ventricular myocyte model. The mathematical tractability of the three-current model allows us to conduct asymptotic analysis and efficiently estimate action potential duration. Improvement in the description of the mechanism for caveolae sodium current is incorporated into the three-current model utilizing a probability density approach for the four-state caveolae neck-channel coupling. The prolongation of action potentials and the formation of potential arrhythmia are shown to arise if caveolae neck open probability varies. A minimal model of the Ca2+ spatial distribution of CICR units illustrates the transverse tubule remodeling in failing myocyte causes dysfunction in the Ca2+ profile. With regards to discrimination of protein localization, which is widely used in biological experiments, the bagging pruned decision tree algorithm is tested to be one of the algorithms with best performance on the large data set, and it succeeds in extracting information to be highly predictive on test data. Parallel computation technique is applied to accelerate the speed of implementation in K-nearest neighbor learning algorithms on big data sets.

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15

Eloff, Benjamin Charles. "ROLE OF GAP JUNCTIONS IN THE GENESIS OF CARDIAC ARRHYTHMIAS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1106579517.

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16

Chung, Andrew H. (Andrew Hyun-Chan). "Programmable stimulator system for study of cardiac arrhythmias." Thesis, Massachusetts Institute of Technology, 1993. http://hdl.handle.net/1721.1/72311.

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17

Finlay, M. "Interactions between activation and repolarisation in predisposition towards cardiac arrhythmia." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1429926/.

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The lethal cardiac arrhythmias ventricular fibrillation (VF) and ventricular tachycardia (VT) are a leading cause of death in heart disease. We hypothesised that dynamic activation and repolarisation interactions will vary according to autonomic tone and the nature of the myocardial substrate as affected by disease states. This hypothesis was tested in a series of human and murine experiments. Incorporation of data from human electrophysiological studies into a linear computer model was able to predict activation dynamics of sequential extrastimuli. This served as a validation of the concept of dynamic interactions between activation and repolarisation in man. A human model of mental stress demonstrated that activation and repolarisation dynamics are altered by intrinsic autonomic stimulation. Specifically, a reduction in activation potential duration and an increase in dispersion of repolarisation occurred at short coupling intervals during stress. A weak increase in conduction velocity and excitability was also observed. Patients with early-stage arrhythmogenic right ventricular cardiomyopathy (ARVC) were seen to exhibit conduction changes prior to the onset of structural disease. This was used to determine potential diagnostic criteria based on surface ECG correlates of intracardiac observations. These criteria are able to distinguish early ARVC from benign right ventricular outflow tract tachycardia. Finally, the mechanism of modulation of tissue level activation dynamics were further studied using a novel thin-tissue slice murine model. Conduction velocity and excitability were modulated by both sympathetic and parasympathetic stimuli, parasympathetic modulation is demonstrated to be dependent on the Gαi2 regulatory pathway at the tissue level. The tissue slice method provides a novel tissue-level platform for the study of cardiac electrophysiology in genetically modified mice. In conclusion, this work demonstrates that modulations of activation and repolarisation dynamics are seen in pro-arrhythmic states, specifically in sympathetically active states and in arrhythmogenic right ventricular cardiomyopathy.

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18

Patel, Nehal Jaymish. "Novel Pathways for the Regulation of Cardiac Fibrosis and Arrhythmia." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1586891209137927.

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19

Schredelseker, Johann [Verfasser]. "Targeting cardiac arrhythmia by enhancing mitochondrial calcium uptake / Johann Schredelseker." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1221960741/34.

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20

Reddy, Mairi Helen. "Beta adrenergic function in acute myocardial ischaemia." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/19257.

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21

Sheikh, Abdul Kadir Siti Hamimah. "Molecular mechanisms for fetal cardiac arrhythmia in intrahepatic cholestasis of pregnancy." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6164.

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Intrahepatic cholestasis in pregnancy (ICP) is characterized by raised serum bile acids which can cause fetal complications, including preterm labour and intrauterine death. The fetal death in ICP is not well understood. In this thesis, the mechanisms of bile-acid induced arrhythmia were studied extensively using in vitro models of the fetal heart. Addition of the bile acid taurocholate (TC) to cardiomyocytes led to a reduction in the rate and amplitude of contraction, dysregulation of beating and desynchronization of intracellular calcium release. The results obtained from both differentiated mouse and human embryonic stem cell-derived cardiomyocytes (ESC-CM) demonstrated that immature cardiomyocytes are more susceptible to TC-induced arrhythmias than more mature cardiomyocytes. Although classical hepatic bile acid transporters such as ntcp, mrp2 and mdr2 are expressed in neonatal rat cardiomyocytes, the results suggest that they are unlikely to play role in TC-induced arrhythmia. They also suggest that the bile acid nuclear receptor FXR is not involved as uptake of radioactively labelled TC into the cells is minimal and that there is no functional involvement of the classical hepatic FXR pathways in neonatal rat cardiomyocytes. Similarly, the membrane bile acid receptor TGR5 showed neither immunoreactivity nor functional effects in cardiomyocytes. TC binds to the muscarinic M2 receptor and serves as a partial agonist of this receptor in terms of receptor activation and its inhibitory effect on cAMP in neonatal rat cardiomyocytes. Inhibition of the M2 muscarinic receptor by antagonist and the knockdown of the receptor with siRNA completely abolished the negative effect of TC on cardiomyocyte contraction, calcium transient amplitude and synchronisation in small cell clusters. In conclusion, immature ESC-CMs are more susceptible to TC and this effect is lost as cells progress to more mature phenotypes. Moreover, the findings suggest the arrhythmogenic effect of TC in neonatal cardiomyocytes is mediated by the muscarinic M2 receptor. This mechanism might serve as a promising new therapeutic target for fetal arrhythmia.

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22

Walton, Shane David. "Engineering an Anti-arrhythmic Calmodulin." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461159861.

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23

Philp, Karen L. "Acute actions of 17#beta# on ischaemia- and drug- induced arrhythmias." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250376.

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24

Connors, Sean P. "Compounds that prolong the cardiac action potential." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670306.

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25

Nicholson, Edwina Gaylene 1960. "Cardiac arrhythmias and acute rejection in human to human cardiac transplantation; an exploratory study." Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/278571.

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An exploratory study design was used to describe the relationship between the degree of acute rejection and the presence of cardiac arrhythmias in cardiac transplant patients. The frequencies and types of cardiac arrhythmias were observed in relationship to the results of endomyocardial biopsy and the serum T cell levels. A retrospective primary review of records was conducted utilizing 42 cardiac transplant recipients with a total of 128 endomyocardial biopsy procedures, the unit of analysis. In general, more cardiac arrhythmias were recorded after endomyocarial biopsy than before and the majority were atrial type arrhythmias, followed by ventricular and junctional arrhythmias. The significant relationships occurred between conduction arrhythmias, both frequency and type, and acute rejection. However, very small numbers of conduction arrhythmias were reported. Previous relationships between cardiac arrhythmias in general and acute rejection were not supported, possibly due to the effects of cyclosporine (Sandimmune).

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26

Wong, C. Y. Macrina. "Health-related quality of life in patients with cardiac arrhythmias." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36887171.

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27

Hussan, Jagir R. "Modelling the influence of ion channel distributions in cardiac arrhythmias." Thesis, University of Auckland, 2012. http://hdl.handle.net/2292/19263.

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Understanding cardiac electrophysiology in general and the role of ion channels in particular, is a problem of practical significance. Limitations on experimental investigations have necessitated the development of theoretical and computer models. In this thesis, a theoretical perspective informed by published experimental observations and computer modelling tools is adopted. Myocyte organisation and distribution of ion channels in the cardiac ventricular tissue greatly influence its mechanical and electrical behaviour. Computer simulations of these systems are computationally-expensive, nontrivial and limit model based investigations. A novel algorithm that substantially reduces the computational expenses under specific conditions is developed. The integration of multiple models to reproduce the cardiac behaviour across spatial and temporal scales, introduces non-trivial computing and the mathematical issues. Using an analytic approach that partially resolves these issues, novel models of the passive cardiac-muscle-tissue, extracellular excitation-propagation and stability of the tissue are developed. A rational approach to model deformation of cellular aggregations is presented together with relevant proofs. A remarkable relationship, that the minimisation of local mean angular distortion and Dirichlet energy are identical (up to a measure) is presented. It is anticipated that the results presented in this thesis will initiate further investigation to expand the proposed models and increase understanding the dynamics and control of the heart.

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28

Boachie-Ansah, G. "Adenyl compounds, adrenoreceptor activation, and acute ischaemia-related cardiac arrhythmias." Thesis, University of Strathclyde, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382268.

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29

Armoundas, Antonis A. 1967. "A novel technique for guiding ablative therapy of cardiac arrhythmias." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85372.

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30

Parikka, Hannu. "Effects of intravenously administered magnesium on propensity to cardiac arrhythmias." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/parikka/.

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31

Stedman, Nicholas F. "The non-invasive localization of cardiac arrhythmias : a theoretical study." Thesis, University of Bath, 1999. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299649.

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32

Fayyazifar, Najmeh. "Deep learning and neural architecture search for cardiac arrhythmias classification." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2022. https://ro.ecu.edu.au/theses/2553.

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Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Among people with CVD, cardiac arrhythmias (changes in the natural rhythm of the heart), are a leading cause of death. The clinical routine for arrhythmia diagnosis includes acquiring an electrocardiogram (ECG) and manually reviewing the ECG trace to identify the arrhythmias. However, due to the varying expertise level of clinicians, accurate diagnosis of arrhythmias with similar visual characteristics (that naturally exists in some different types of arrhythmias) can be challenging for some front-line clinicians. In addition, there is a shortage of trained cardiologists globally, and especially in remote areas of Australia, where patients are sometimes required to wait for weeks or months for a visiting cardiologist. This impacts the timely care of patients living in remote areas. Therefore, developing an AI-based model, that assists clinicians in accurate real-time decision-making, is an essential task. This thesis provides supporting evidence that the problem of delayed and/or inaccurate cardiac arrhythmias diagnosis can be addressed by designing accurate deep learning models through Neural Architecture Search (NAS). These models can automatically differentiate different types of arrhythmias in a timely manner. Many different deep learning models and more specifically, Convolutional Neural Networks (CNNs) have been developed for automatic and accurate cardiac arrhythmias detection. However, these models are heavily hand-crafted which means designing an accurate model for a given task, requires significant trial and error. In this thesis, the process of designing an accurate CNN model for 1-dimensional biomedical data classification is automated by applying NAS techniques. NAS is a recent research paradigm in which the process of designing an accurate model (for a given task) is automated by employing a search algorithm over a pre-defined search space of possible operations in a deep learning model. In this thesis, we developed a CNN model for detection of ‘Atrial Fibrillation’ (AF) among ‘normal sinus rhythm’, ‘noise’, and ‘other arrhythmias. This model is designed by employing a well-known NAS method, Efficient Neural Architecture Search (ENAS) which uses Reinforcement Learning (RL) to perform a search over common operations in a CNN structure. This CNN model outperformed state-of-the-art deep learning models for AF detection while minimizing human intervention in CNN structure design. In order to reduce the high computation time that was required by ENAS (and typically by RL-based NAS), in this thesis, a recent NAS method called DARTS was utilized to design a CNN model for accurate diagnosis of a wider range of cardiac arrhythmias. This method employs Stochastic Gradient Descent (SGD) to perform the search procedure over a continuous and therefore differentiable search space. The search space (operations and building blocks) of DARTS was tailored to implement the search procedure over a public dataset of standard 12-lead ECG recordings containing 111 types of arrhythmias (released by the PhysioNet challenge, 2020). The performance of DARTS was further studied by utilizing it to differentiate two major sub-types of Wide QRS Complex Tachycardia (Ventricular Tachycardia- VT vs Supraventricular Tachycardia- SVT). These sub-types have similar visual characteristics, which makes differentiating between them challenging, even for experienced clinicians. This dataset is a unique collection of Wide Complex Tachycardia (WCT) recordings, collected by our medical collaborator (University of Ottawa heart institute) over the course of 11 years. The DARTS-derived model achieved 91% accuracy, outperforming cardiologists (77% accuracy) and state-of-the-art deep learning models (88% accuracy). Lastly, the efficacy of the original DARTS algorithm for the image classification task is empirically studied. Our experiments showed that the performance of the DARTS search algorithm does not deteriorate over the search course; however, the search procedure can be terminated earlier than what was designated in the original algorithm. In addition, the accuracy of the derived model could be further improved by modifying the original search operations (excluding the zero operation), making it highly valuable in a clinical setting.

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33

Montazeri, Ghahjaverestan Nasim. "Early detection of cardiac arrhythmia based on Bayesian methods from ECG data." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1S061/document.

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L'apnée est une complication fréquente chez les nouveaux-nés prématurés. L'un des problèmes les plus fréquents est l'épisode d'apnée bradycardie dont la répétition influence de manière négative le développement de l'enfant. C'est pourquoi les enfants prématurés sont surveillés en continu par un système de monitoring. Depuis la mise en place de ce système, l'espérance de vie et le pronostic de vie des prématurés ont été considérablement améliorés et ainsi la mortalité réduite. En effet, les avancées technologiques en électronique, informatique et télécommunications ont conduit à l'élaboration de systèmes multivoies de monitoring néonatal de plus en plus performants. L'un des principaux signaux exploités dans ces systèmes est l'électrocardiogramme (ECG). Toutefois, même si l'analyse de l'ECG a évolué au fil des années, l'ensemble des informations qu'il fournit n'est pas encore totalement exploité dans les processus de décision, notamment en monitoring en Unité de Soins Intensifs en Néonatalogie (USIN). L'objectif principal de cette thèse est d'améliorer la prise en compte des dynamiques multi-dimensionnelles en proposant de nouvelles approches basées sur un formalisme bayésien, pour la détection précoce des apnées bradycardies chez le nouveau-né prématuré. Aussi, dans cette thèse, nous proposons deux approches bayésiennes, basées sur les caractéristiques de signaux biologiques en vue de la détection précoce de l'apnée bradycardie des nouveaux-nés prématurés. Tout d'abord avec l'approche de Markov caché, nous proposons deux extensions du Modèle de Markov Caché (MMC) classique. La première, qui s'appelle Modèle de Markov Caché Couplé (MMCC), créé une chaîne de Markov à chaque dimension de l'observation et établit un couplage entre les chaînes. La seconde, qui s'appelle Modèle Semi-Markov Caché Couplé (MSMCC), combine les caractéristiques du modèle de MSMC avec le mécanisme de couplage entre canaux. Pour les deux nouveaux modèles (MMCC et MSMCC), les algorithmes récursifs basées sur la version classique de Forward-Backward sont introduits pour résoudre les problèmes d'apprentissage et d'inférence dans le cas couplé. En plus des modèles de Markov, nous proposons deux approches passées sur les filtres de Kalman pour la détection d'apnée. La première utilise les modifications de la morphologie du complexe QRS et est inspirée du modèle générateur de McSharry, déjà utilisé en couplant avec un filtre de Kalman étendu dans le but de détecter des changements subtils de l'ECG, échantillon par échantillon. La deuxième utilise deux modèles AR (l'un pour le processus normal et l'autre pour le processus de bradycardie). Les modèles AR sont appliqués sur la série RR, alors que le filtre de Kalman suit l'évolution des paramètres du modèle AR et fournit une mesure de probabilité des deux processus concurrents<br>Apnea-bradycardia episodes (breathing pauses associated with a significant fall in heart rate) are the most common disease in preterm infants. Consequences associated with apnea-bradycardia episodes involve a compromise in oxygenation and tissue perfusion, a poor neuromotor prognosis at childhood and a predisposing factor to sudden-death syndrome in preterm newborns. It is therefore important that these episodes are recognized (early detected or predicted if possible), to start an appropriate treatment and to prevent the associated risks. In this thesis, we propose two Bayesian Network (BN) approaches (Markovian and Switching Kalman Filter) for the early detection of apnea bradycardia events on preterm infants, using different features extracted from electrocardiographic (ECG) recordings. Concerning the Markovian approach, we propose new frameworks for two generalizations of the classical Hidden Markov Model (HMM). The first framework, Coupled Hidden Markov Model (CHMM), is accomplished by assigning a Markov chain (channel) to each dimension of observation and establishing a coupling among channels. The second framework, Coupled Hidden semi Markov Model (CHMM), combines the characteristics of Hidden semi Markov Model (HSMM) with the above-mentioned coupling concept. For each framework, we present appropriate recursions in order to use modified Forward-Backward (FB) algorithms to solve the learning and inference problems. The proposed learning algorithm is based on Maximum Likelihood (ML) criteria. Moreover, we propose two new switching Kalman Filter (SKF) based algorithms, called wave-based and R-based, to present an index for bradycardia detection from ECG. The wave-based algorithm is established based on McSarry's dynamical model for ECG beat generation which is used in an Extended Kalman filter algorithm in order to detect subtle changes in ECG sample by sample. We also propose a new SKF algorithm to model normal beats and those with bradycardia by two different AR processes

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34

MALERBA, NATASCIA. "Dissecting the IDDCA (Intellectual Developmental Disorder with Cardiac Arrhythmia) syndrome pathogenic mechanisms." Doctoral thesis, Università degli Studi di Foggia, 2019. http://hdl.handle.net/11369/382262.

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La sindrome genetica rara da disabilità intellettiva e disturbo del ritmo cardiaco (acronimo: IDDCA, MIM # 617173) è una malattia multi-sistemica a trasmissione autosomica recessiva con esordio precoce, associata a varianti patogenetiche nel gene GNB5. Il quadro delle manifestazioni cliniche varia da una forma più grave caratterizzata da ritardo nello sviluppo psicomotorio, disabilità intellettiva, encefalopatia epilettica, anomalie visive e aritmie cardiache (IDDCA), a una forma più lieve associata al ritardo del linguaggio, disturbo da deficit di attenzione, deficit cognitivo, in presenza o assenza di aritmia cardiaca (LADCI). Trattandosi di una sindrome rara, pochi casi sono stati descritti in tutto il mondo, di cui l’ottanta per cento caratterizzati da aritmia cardiaca. Sebbene sia stata stabilita la causa genetica della sindrome, non è ancora chiaro il meccanismo alla base della malattia, rendendo più difficile lo sviluppo di trattamenti mirati per una possibile terapia. Il gene GNB5 codifica per Gβ5, un membro che diverge dalle altre sub-unità beta della famiglia delle proteine G eterotrimeriche. Caratteristica peculiare della proteina GNB5 è la sua capacità di formare complessi proteici con i membri del gruppo R7 dei regolatori della segnalazione cellulare mediata dalle proteine G (R7-RGS), con i quali GNB5 esercita un effetto di regolazione negativa sulla segnalazione cellulare mediata dall’attività dei recettori accoppiati alle proteine G (GPCR), inibendo il rilascio di diversi neurotrasmettitori implicati nell'apprendimento, nel controllo motorio oltre che nella vista. Le peculiari manifestazioni cliniche riscontrate nei pazienti affetti dalla sindrome da IDDCA, riconducibili a convulsioni epilettiche, disabilità intellettiva e bradicardia, possono essere attribuite ad alterazioni dell'eccitabilità cellulare poiché GNB5, insieme al gruppo delle proteine R7-RGS, è un membro cruciale nella modulazione della cinetica di attivazione dei canali del potassio attivati dalle proteine G (GIRK) e di altri canali ionici, implicati nella regolazione della funzione neuronale e cardiaca. Questo è supportato dai dati riportati in letteratura, che identificano GNB5 come parte di un complesso multi-proteico composto da GPCR/GNB5/R7-RGS/GIRK. La nostra ipotesi progettuale è che le principali manifestazioni riscontrate nei pazienti siano causate principalmente dalla destabilizzazione di tali complessi proteici, con conseguente alterazione dell’eccitabilità cellulare. Nel nostro studio dimostriamo come il segnale cellulare mediato dalla proteina GNB5 sia essenziale per il controllo del sistema parasimpatico sulla frequenza cardiaca. Nello specifico, abbiamo ingegnerizzato cellule staminali pluripotenti indotte (hiPSC), in cui abbiamo rimosso il gene GNB5 (hiPSC), sottoposte in seguito al differenziamento cellulare in senso cardiogenico. I nostri risultati preliminari ottenuti dai cardiomiociti derivati dalle linee cellulari di hiPSCKO (iCMKO), mostrano una frequenza cardiaca alterata caratterizzata da una spiccata bradicardia se confrontata con quella dei cardiomiociti di controllo (iCMWT). È interessante notare che, in accordo con l'ipotesi di ipersensibilità muscarinica, l'applicazione di un antagonista dei recettori muscarinici cardiaci o di un bloccante dei canali GIRK, in parte favoriscano un recupero del fenotipo bradicardico associato all’assenza della proteina GNB5. Questi risultati indicano che il nostro modello cellulare "in vitro" è efficace per approfondire le conoscenze sui meccanismi molecolari alla base della sindrome da IDDCA e che pertanto potrebbe essere un buon modello per testare e identificare nuove molecole da utilizzare come punto di partenza per la sperimentazione di un programma finalizzato a una possibile terapia.

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35

McKeown, Paschal Patrick Joseph. "Transoesophageal cardioversion and defibrillation." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334471.

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36

Chen, Zhong. "Quantitative scar assessment using cardiac magnetic resonance imaging to predict ventricular arrhythmia risk and cardiac resynchronisation response." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/quantitative-scar-assessment-using-cardiac-magnetic-resonance-imaging-to-predict-ventricular-arrhythmia-risk-and-cardiac-resynchronisation-response(343ffed2-4f6b-4331-9a44-9a027b231831).html.

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Myocardial fibrosis is associated with ventricular arrhythmia. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) has been the standard approach to visualise regional myocardial fibrosis. T1 mapping is a novel CMR technique that overcomes the inherent limitation of conventional LGE imaging to assess diffuse fibrosis. The incidence of arrhythmia and sudden death continues to be high despite the benefits of cardiac resynchronisation therapy (CRT) in terms of symptomatic improvement and overall mortality. As myocardial scar can have a structural and functional impact on remodeling, there is a need to further elucidate the effect of CRT on electrophysiology and to better select patients for CRT. Prospective clinical studies were conducted to assess the ability of CMR scar quantification to: 1. predict the risk of ventricular arrhythmia in both ischaemic and non-ischaemic cardiomyopathy (ICM, NICM) patients; 2. predict reverse remodeling following CRT in dyssynchronous heart failure patients. Investigative studies were also carried out to: 1. explore CMR scar characterisation using high-resolution 3-dimensional scar image acquisition in heart failure patients; 2. explore clinical utilisation of T1 mapping for myocardial fibrosis quantification; 3. understand the relationship between scar heterogeneity and substrate for ventricular arrhythmia; 4. explore electrical remodeling effect of CRT in dyssynchronous heart failure patients. The present study is the first to demonstrate that non-contrast native T1 is an independent predictor of ventricular arrhythmia in patients with ICM or NICM. It provides confirmation that the extents of scar and grey zone derived from LGE-CMR are independently associated with ventricular arrhythmia. With regards to prediction of CRT remodeling, focal scar burden detected by LGE-CMR is associated with a poor response to CRT, whereas markers of diffuse interstitial fibrosis were not however predictive of CRT response. These findings have important clinical implications, lending support for the use of quantitative myocardial scar quantification in selecting patients for complex device therapy.

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37

Donohoe, Paul Thomas. "Cardiac ion currents in a rat model of renal failure." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324668.

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38

Sandoval, Niño Zulma. "Planning and guidance of ultrasound guided High Intensity Focused Ultrasound cardiac arrhythmia therapy." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1S044/document.

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L'objectif des travaux présentés dans ce document est de développer de nouvelles méthodes de traitement d'images pour améliorer la planification et le guidage d'une thérapie par voie transœsophagienne de la fibrillation auriculaire à l'aide d'Ultrason Focalisé Haute Intensité. Le document est divisé en deux parties : la planification du traitement et le guidage de la thérapie. Pour la planification de la thérapie, l'idée est d'exploiter l'information acquise au stade préopératoire par un scanner X ou IRM afin de retrouver l'anatomie spécifique du patient et à y définir le futur geste thérapeutique. Plus particulièrement, nos différentes contributions ont porté sur une approche multi-atlas de segmentation de l'oreillette gauche et des veines pulmonaires ; le tracé des lignes de lésions sur le volume initial ou segmenté ; et la reconstruction d'un volume adapté à la future navigation transœsophagienne. Pour le guidage de la thérapie, nous proposons une nouvelle approche de recalage qui permet d'aligner les images échographiques peropératoires 2D et l'information 3D CT préopératoire. Dans cette approche, dans un premier temps nous avons sélectionné la mesure de similarité la plus adaptée à notre problématique à l'aide d'une évaluation systématique puis nous avons tiré profit des contraintes imposées à la sonde transœsophagienne par l'anatomie du patient pour simplifier la procédure de recalage. Toutes ces méthodes ont été évaluées sur des fantômes numériques ou physiques et sur des données cliniques<br>The work presented in this document aims at developing new image-processing methods to improve the planning and guidance of transesophageal HIFU atrial fibrillation therapy. This document is divided into two parts, namely therapy planning and therapy guidance. We first propose novel therapy planning methods that exploit high-resolution pre-operative CT or MRI information to extract patient-specific anatomical details and to define future therapeutic procedures. Our specific methodological contributions concern the following: an automatically-refined atlas-based segmentation approach to extract the left atrium and pulmonary veins; the delineation of the lesion lines on the original or segmented volume; and the reconstruction of a volume adapted to future intraoperative transesophageal navigation. Secondly, our proposal of a novel registration approach for use in therapy guidance aligns intraoperative 2D ultrasound with preoperative 3D CT information. This approach first carries out a systematic statistical evaluation to select the best similarity measure for our application and then takes advantage of the geometrical constraints of the transesophageal HIFU probe to simplify the registration process. Our proposed methods have been evaluated on digital and/or physical phantoms and on real clinical data

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39

Hund, Thomas J. "Cardiac Arrhythmia After Myocardial Infarction: Insights From a Dynamic Canine Ventricular Myocyte Model." online version, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1078424440.

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40

Day, Christopher Paul. "The QT interval revisited : implications for arrhythmias and sudden cardiac death." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308764.

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41

ShariÌ„f, Ê¿IsÌ£aÌ„m. "Role of endothelin in experimental models of ischaemia induced cardiac arrhythmias." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249886.

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42

Slabaugh, Jessica L. "The Occurrence of Alternans and Arrhythmias in a Multicellular, Cardiac Preparation." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1353949288.

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43

Suboticki, Jessica L. "The Occurrence of Alternans and Arrhythmias in a Multicellular, Cardiac Preparation." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354023333.

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44

Kirk, Nathan Robert. "An adaptive, preconditioned, electromechanical model for the simulation of cardiac arrhythmias." Thesis, University of Leeds, 2012. http://etheses.whiterose.ac.uk/2865/.

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In this thesis a coupled model of cardiac electromechanical activity is presented, using the finite element method to model both electrophysiology and mechanics within a deforming domain. The efficiency of the electrical model was improved using adaptive mesh refinement and the mechanical system performance was improved with the addition of preconditioning. Unstructured triangular meshes were used throughout. The electrophysiology model uses the ten Tusscher-Panfilov 2006 detailed cellular model, and includes anisotropic diffusion, uses a semi-implicit time stepping scheme, stores data in an efficient sparse storage format and applies a Reverse Cuthill-McKee ordering algorithm to reduce the matrices’ bandwidths. Linear elements were used to approximate the transmembrane voltage and spatial and temporal convergence tests were undertaken. Local mesh adaptivity is added to the electrical component of the model and improvements to the performance and efficiency gained by this technique were investigated. Two different monitor functions were utilised and these demonstrated that by targeting adaptive mesh refinement at the front of the electrical wave significant efficiency and performance benefits could be achieved. The cardiac mechanical model is based on finite deformation elasticity theory, enforces the incompressibility of the tissue and incorporates anisotropic tension to simulate fibre orientation. This uses isoparametric quadratic elements for deformation, linear elements for pressure, was integrated with numerical quadrature and the resulting non-linear system solved with the iterative Newton method. Preconditioning was added to the mechanical component of the model and improvements in the performance of the solver due to this were investigated. An ILUT (Incomplete Lower Upper factorisation with drop Tolerance) preconditioner was implemented and this demonstrated performance improvements of up to 27 times on the meshes tested. The resulting cardiac electromechanical solver was then used to consider how known changes in cardiac electrophysiology, which are manifest in end-stage heart disease, affect the stability of the electrical wave. Specifically, investigations were undertaken into the introduction of fibrotic regions (with different sizes and concentrations) and electrical remodelling caused by end-stage cardiac disease. These were modelled on both static and deforming domains to consider whether deformation can alter the stability of a spiral wave. These simulations demonstrated that fibrotic regions and tissue deformation can have significant disruptive effects on the stability of a re-entrant spiral wave and that remodelling the electrophysiology stabilises the wave.

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45

Mathavan, Neashan Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Parameter optimization in simplified models of cardiac myocytes." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2009. http://handle.unsw.edu.au/1959.4/44709.

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Atrial fibrillation (AF) is a complex, multifaceted arrhythmia. Pathogenesis of AF is associated with multiple aetiologies and the mechanisms by which it is sustained and perpetuated are similarly diverse. In particular, regional heterogeneity in the electrophysiological properties of normal and pathological tissue plays a critical role in the occurrence of AF. Understanding AF in the context of electrophysiological heterogeneity requires cell-specific ionic models of electrical activity which can then be incorporated into models on larger temporal and spatial scales. Biophysically-based models have typically dominated the study of cellular excitability providing detailed and precise descriptions in the form of complex mathematical formulations. However, such models have limited applicability in multidimensional simulations as the computational expense is too prohibitive. Simplified mathematical models of cardiac cell electrical activity are an alternative approach to these traditional biophysically-detailed models. Utilizing this approach enables the embodiment of cellular excitation characteristics at minimal computational cost such that simulations of arrhythmogensis in atrial tissue are conceivable. In this thesis, a simplified, generic mathematical model is proposed that characterizes and reproduces the action potential waveforms of individual cardiac myocytes. It incorporates three time-dependent ionic currents and an additional time-independent leakage current. The formulation of the three time-dependent ionic currents is based on 4-state Markov schemes with state transition rates expressed as nonlinear sigmoidal functions of the membrane potential. Parameters of the generic model were optimized to fit the action potential waveforms of the Beeler-Reuter model, and, experimental recordings from atrial and sinoatrial cells of rabbits. A nonlinear least-squares optimization routine was employed for the parameter fits. The model was successfully fitted to the Beeler-Reuter waveform (RMS error: 1.4999 mV) and action potentials recorded from atrial tissue (RMS error: 1.3398 mV) and cells of the peripheral (RMS error: 2.4821 mV) and central (RMS error: 2.3126 mV) sinoatrial node. Thus, the model presented here is a mathematical framework by which a wide variety of cell-specific AP morphologies can be reproduced. Such a model offers the potential for insights into possible mechanisms that contribute to heterogeneity and/or arrhythmia.

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46

Wu, Ling. "Functional Characterization of SCN5A, The Cardiac Sodium Channel Gene Associated With Cardiac Arrhythmias and Sudden Death." Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1206732295.

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47

Heath, Bronagh M. "Influence of drugs on components of delayed rectifier potassium currents in cardiac muscle." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308691.

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48

Bashir, Yaver. "Management of ventricular arrhythmias in the failing heart : a clinical study." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318809.

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49

Glynn, Patric Joseph. "Integrative Studies on the Role of CaMKII in Cardiac Disease and Arrhythmias." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1429132697.

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50

Metcalf, Robert Glenn. "Strategies for increasing consumption of N-3 polyunsaturated fatty acids and their effects on cardiac arrhythmias in humans." Title page, table of contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phm5885.pdf.

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"October 2003" Bibliography: leaves 190-210. Ch. 1. Literature review -- Ch. 2. A practical approach to increasing intakes of n-3 polyunsaturated fatty acids: use of novel foods enriched with n-3 fats -- Ch. 3. Effects of fatty acids on the incidence of arrhythmias in patients with implanted cardioverter-defibrillators (ICDs) -- Ch. 4. A pilot study to investigate the effects of n-3 fatty acids on inducible, sustained ventricular tachycardia in patients undergoing electrophysiology testing -- Ch. 5. Conclusions and future directions.

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