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1
Walfridsson, Ulla. "Assessing Symptom Burden and Health-Related Quality of Life in patients living with arrhythmia and ASTA : Arrhythmia-Specific questionnaire in Tachycardia and Arrhythmia." Doctoral thesis, Linköpings universitet, Omvårdnad, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-71873.
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Background: Health-Related Quality of Life (HRQOL) can be negatively affected in patients living with arrhythmias and many patients experience a pronounced symptom burden. The arrhythmia can cause both uncertainty and limitations, including interference with work, reluctance to perform and plan for leisure activities and leading to self-imposed restrictions in daily life situations. There are patients striving to find strategies to manage the arrhythmia and for some this can become the focus in their lives. Treatment options are often a choice between pharmaceuticals and radiofrequency ablation (RFA) where RFA is an option for many arrhythmia-patients to be cured. In the care of arrhythmia-patients it is of great importance to combine objective examinations with patient-reported outcomes (PROs) to achieve patient’s own experiences of treatment efficacy and arrhythmias interference in daily life situations. Aims: The overall aims of this thesis were to assess symptom burden and HRQOL in patients with arrhythmias and to develop and validate an arrhythmia-specific questionnaire, suitable for most arrhythmia-patients. Design and Methods: Studies I and II were single-centre studies including patients referred for RFA, with two different arrhythmia diagnoses. Assessments of patient-reported outcomes (PROs) concerning HRQOL were performed using two questionnaires, SF-36 and EQ-5D (I-II). Further, patients were asked some disease-specific questions (I). Study I describes assessments before the RFA treatment and Study II the follow-up assessments at three and twelve months after RFA. Patients’ scoring of HRQOL was compared to age and gender matched reference groups before and after RFA (I-II). Studies III and IV describe the development and validation of a disease-specific questionnaire ASTA (Arrhythmia-Specific questionnaire in Tachycardia and Arrhythmia) assessing symptom burden and HRQOL. Studies III and IV were multicentre studies. Patients planned for DC-conversion, AF patients seeking emergency care and those with different forms of arrhythmias referred for RFA were included. Results: Patients scored significantly lower HRQOL in seven of SF-36’s eight scales compared to the age and gender matched reference groups before RFA treatment. Frequent arrhythmia attacks had a great negative impact on HRQOL, and female gender and older age were factors contributing to worse HRQOL (I). Treatment with RFA restored the patients’ HRQOL. Most positive effects were seen at three months follow-up. One year after treatment patients and the matched reference group scored their HRQOL to a similar level, assessed with SF-36 and EQ-5D index (II). The validated ASTA questionnaire was found to have good psychometric properties. Construct validity was confirmed with sufficient levels of item-total correlations in the ASTA symptom burden scale and HRQOL scales. The dimensionality of the ASTA HRQOL scale was established with confirmatory factor analysis, supporting a physical and a mental subscale. The internal consistency, demonstrated with Cronbach’s alpha (α), was satisfactory for the ASTA symptom burden scale and the ASTA HRQOL scales, varying from α 0.79 to α 0.91 (III-IV). Conclusions and clinical implications: The studies in this thesis confirmed how negatively affected the arrhythmia-patients can be with a pronounced symptom burden and impaired HRQOL. Treatment with RFA was demonstrated to restore the patients HRQOL to an equal level of that of the matched reference group. PROs are important to take into consideration in the care of arrhythmia-patients, to achieve the patients’ subjective experiences of their daily life situation. To the best of our knowledge ASTA is the first arrhythmia-specific questionnaire assessing symptom burden and HRQOL, suitable for most arrhythmia forms. The newly validated ASTA questionnaire can be an important contribution to assessment of PROs in arrhythmia-patients.
2
Williams, Steven Edwin. "Characterisation and representation of arrhythmia substrates." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/characterisation-and-representation-of-arrhythmia-substrates(b591acfd-9ca4-45a0-a3b0-169128bac9d7).html.
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Cardiac arrhythmias arise from a variety of structural and electrical substrates and range in clinical presentation from asymptomatic to severely disabling or life threatening. Existing techniques for the characterisation of arrhythmia substrates include surface electrocardiography and intracardiac mapping together with ultrasound, computed tomography and magnetic resonance imaging. In this thesis I study a spectrum of arrhythmia characterisation techniques to improve the understanding of complex arrhythmia mechanisms. The role of surface electrocardiography and intra-cardiac contact mapping together with cardiac magnetic resonance imaging are studied in a variety of atrial and ventricular arrhythmias as well as in an animal model of atrial ablation. Arrhythmia characterisation techniques result in large quantities of data that are frequently considered in combination with other modalities and visualised within the 3- dimensional nature of cardiac structures. Since no techniques are currently available to display multiple parameters without loss of fidelity of either parameter, I developed a new system for data representation. Termed Dot Mapping, this system allows two or more datasets to be concurrently displayed by using separate visual entities (colour and dots) for each. The function, development and feasibility of the system are studied. In summary, this thesis explores and develops a number of techniques for assessing arrhythmia substrates, including surface electrocardiography, intra-cardiac mapping and cardiac magnetic resonance imaging. New (and existing) data thus created are displayed using a new data representation technique designed to optimise the co-display of multiple related modalities.
3
Fischer, Lindsey Ann. "How Emotions Affect Respiratory Sinus Arrhythmia." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579276.
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Respiratory sinus arrhythmia (RSA) is a measure of heart rate variability in relation to respiration. The current study investigated how the different induced emotional states (i.e., amusement, anger, disgust, happiness, fear, and sadness) affect RSA. This was done by comparing resting RSA to that occurring while watching short film clips intended to induce emotional states. It was hypothesized that RSA would be lower when negative emotions are induced and higher when positive emotions are induced. A difference between the resting RSA and RSA measured during emotion induction was also anticipated. Results indicated a marginally significant difference in RSA between film clip 1 and resting with eyes open and between film clip 1 and film clip 2. There was also a trend in RSA between male and female participants.
4
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.
5
Kehrle, Florian [Verfasser]. "Inverse simulation for cardiac arrhythmia / Florian Kehrle." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1160593698/34.
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Soto-Freita, Angelica Marie. "Parent Predictors of Infant Respiratory Sinus Arrhythmia." TopSCHOLAR®, 2016. http://digitalcommons.wku.edu/theses/1628.
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The development of emotion regulation skills is an imperative task early in development. Respiratory sinus arrhythmia (RSA), a physiological proxy of regulation, is indicative of one’s regulatory capacity and can be predictive of behavior in later life (Graham, Ablow, & Measelle, 2010; Moore, 2010). Children begin regulating their emotions at a physiological level early in infancy. Infants who are able to properly suppress RSA have higher quality social interactions in childhood (Graziano, Keane, & Calkins, 2007). Previous work has suggested that parents play a role in predicting infant RSA (Conradt & Ablow, 2010). For example, parent marital satisfaction is known to impact infants’ physiological regulation, such that infants whose parents are less satisfied with their marriages have a decreased ability to regulate physiologically (Moore et al., 2009; Porter, Wouden-Miller, Silva, & Porter, 2003). Previous research has found that parent personality impacts parenting strategies (Cummings & Davies, 1994; Prinzie, Stams, Deković, Reijntjes, & Belsky, 2009), however work examining how parent personality interacts with marital satisfaction to predict infant RSA is lacking. Moreover, the majority of previous work assessing the parent predictors of infant RSA focused on mothers (e.g., Moore et al., 2009). There are known differences in the way mothers and fathers interact with their infants, as well as differences in the way fathers and mothers respond to marital dissatisfaction (Forbes, Cohn, Allen, & Lewinsohn, 2004; Karney & Bradbury, 1995). The present study focused on examining how marital satisfaction and parent personality predicts infant RSA with mothers and fathers. The current study involved 38 families (6-month old infants, mothers, and fathers). Parents completed questionnaires measuring marital satisfaction and personality. Mother-infant and fatherinfant dyads participated in a baseline and face-to-face play task (Still Face Paradigm; Tronick, Als, Adamson, Wise, & Brazelton, 1978), where infant physiological regulation was assessed. Results involving mothers did not yield significant findings predicting infant physiological regulation. For fathers, results indicated that parent personality and parent marital satisfaction predicted infant physiological regulation. The current study highlights the importance of examining the roles of both mothers and fathers predicting infant physiological regulation.
7
Labarge, Isaac E. "Neural Network Pruning for ECG Arrhythmia Classification." DigitalCommons@CalPoly, 2020. https://digitalcommons.calpoly.edu/theses/2136.
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Convolutional Neural Networks (CNNs) are a widely accepted means of solving complex classification and detection problems in imaging and speech. However, problem complexity often leads to considerable increases in computation and parameter storage costs. Many successful attempts have been made in effectively reducing these overheads by pruning and compressing large CNNs with only a slight decline in model accuracy. In this study, two pruning methods are implemented and compared on the CIFAR-10 database and an ECG arrhythmia classification task. Each pruning method employs a pruning phase interleaved with a finetuning phase. It is shown that when performing the scale-factor pruning algorithm on ECG, finetuning time can be expedited by 1.4 times over the traditional approach with only 10% of expensive floating-point operations retained, while experiencing no significant impact on accuracy.
8
Goetz, Paul W. "Worry, Respiratory Sinus Arrhythmia, and Health Behaviors." Bowling Green State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1308552215.
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Korhonen, Petri. "Magnetocardiography in assessment of ventricular arrhythmia risk." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/korhonen/.
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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.
11
Glandberger, Oliver, and Daniel Fredriksson. "Neural Network Regularization for Generalized Heart Arrhythmia Classification." Thesis, Blekinge Tekniska Högskola, Institutionen för datavetenskap, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:bth-19731.
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Background: Arrhythmias are a collection of heart conditions that affect almost half of the world’s population and accounted for roughly 32.1% of all deaths in 2015. More importantly, early detection of arrhythmia through electrocardiogram analysis can prevent up to 90% of deaths. Neural networks are a modern and increasingly popular tool of choice for classifying arrhythmias hidden within ECG-data. In the pursuit of achieving increased classification accuracy, some of these neural networks can become quite complex which can result in overfitting. To combat this phenomena, a technique called regularization is typically used. Thesis’ Problem Statement: Practically all of today’s research on utilizing neural networks for arrhythmia detection incorporates some form of regularization. However, most of this research has chosen not to focus on, and experiment with, regularization. In this thesis we measured and compared different regularization techniques in order to improve arrhythmia classification accuracy. Objectives: The main objective of this thesis is to expand upon a baseline neural network model by incorporating various regularization techniques and compare how these new models perform in relation to the baseline model. The regularization techniques used are L1, L2, L1 + L2, and Dropout. Methods: The study used quantitative experimentation in order to gather metrics from all of the models. Information regarding related works and relevant scientific articles were collected from Summon and Google Scholar. Results: The study shows that Dropout generally produces the best results, on average improving performance across all parameters and metrics. The Dropout model with a regularization parameter of 0.1 performed particularly well. Conclusions: The study concludes that there are multiple models which can be considered to have the greatest positive impact on the baseline model. Depending on how much one values the consequences of False Negatives vs. False Positives, there are multiple candidates which can be considered to be the best model. For example, is it worth choosing a model which misses 11 people suffering from arrhythmia but simultaneously catches 1651 mistakenly classified arrhythmia cases?<br>Bakgrund: Arytmier är en samling hjärt-kärlsjukdomar som drabbar nästan hälften av världens befolkning och stod för ungefär 32,1% av alla dödsfall 2015. 90% av dödsfallen som arytmi orsakar kan förhindras om arytmin identifieras tidigare. Neurala nätverk har blivit ett populärt verktyg för att detektera arytmi baserat på ECG-data. I strävan på att uppnå bättre klassificeringsnogrannhet kan dessa nätverk råka ut för problemet ’overfitting’. Overfitting kan dock förebyggas med regulariseringstekniker. Problemställning: Praktiskt taget all forskning som utnyttjar neurala nätverk för att klassifiera arytmi innehåller någon form av regularisering. Dock har majoriteten av denna forsknings inte valt att fokusera och experimentera med regularisering. I den här avhandlingen kommer vi att testa olika regulariseringstekniker för att jämföra hur de förbättrar grundmodellens arytmiklassificeringsförmåga. Mål: Huvudmålet med denna avhandling är att modifiera ett neuralt nätverk som utnyttjar transfer learning för att klassificera arytmi baserat på två-dimensionell ECG-data. Grundmodellen utökades med olika regulariseringstekniker i mån om att jämföra dessa och därmed komma fram till vilken teknik som har störst positiv påverkan. De tekniker som jämfördes är L1, L2, L1 + L2, och Dropout. Metod: Kvantitativa experiment användes för att samla in data kring teknikernas olika prestationer och denna data analyserades och presenterades sedan. En litteraturstudie genomfördes med hjälp av Summon och Google Scholar för att hitta information från relevanta artiklar. Resultat: Forskningen tyder på att generellt sett presterar Dropout bättre än de andra teknikerna. Dropout med parametern 0.1 förbättrade mätvärderna mest. Slutsatser: I specifikt denna kontext presterade Dropout(0.1) bäst. Dock anser vi att falska negativ och falska positiv inte är ekvivalenta. Vissa modeller presterar bättre än andra beroende på hur mycket dessa variabler värderas, och därmed är den bästa modellen subjektiv. Är det till exempel värt att låta 11 personer dö om det innebär att 1651 personer inte kommer att vidare testas i onödan?
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Long, Victor P. III. "Modulation of the Arrhythmia Substrate in Cardiovascular Disease." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1459777728.
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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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Gray, Belinda Ruth. "Clinical and Genetic Studies in Inherited Arrhythmia Syndromes." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15994.
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Inherited arrhythmia syndromes, or “ion channelopathies”, is a term encompassing a number of different diseases including long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), Brugada syndrome (BrS), short QT syndrome (SQTS) and idiopathic ventricular fibrillation (IVF). In inherited arrhythmia syndromes, ventricular arrhythmias originate due to abnormalities with intracellular ion channels, predominantly involving potassium, sodium and calcium handling, due to genetic mutations in genes encoding for channel proteins. The cellular abnormalities in these conditions are typically associated with a structurally normal heart with no evidence of disease macroscopically and the autopsy in the deceased is typically negative. Inherited arrhythmia syndromes are an important cause for sudden cardiac death in the young. There is increasing evidence of genetic and phenotypic heterogeneity amongst inherited arrhythmia syndromes. The yield for genetic testing in inherited arrhythmia syndromes remains at most 60-75% despite significant advances in technology. New genetic testing modalities will provide a significant improvement in the efficacy of genetic testing amongst individuals and families with inherited arrhythmia syndromes. Inherited arrhythmia syndromes can lead to serious cardiac complications including sudden cardiac death. It is possible that there are unidentified clinical, genetic or environmental factors which could predispose patients to higher risk of arrhythmia, including widely available caffeinated energy drinks. The work of this PhD thesis highlights the three critical domains of genetics, risk stratification and triggers for arrhythmia when assessing and managing inherited arrhythmia syndromes. There are a number of unique and important aspects when managing patients and families with inherited arrhythmia syndromes. This includes genetic evaluation, diagnosis, risk stratification, and identification of triggers. The research in this PhD thesis directly addresses a number of these issues and has translational clinical implications for patients and families with inherited arrhythmia syndromes. The ultimate goal of this research is improving assessment and management of these patients and families and prevention of sudden cardiac death.
15
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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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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Kalla, Manish. "Mechanistic insights in the automatic modulation of ventricular arrhythmia." Thesis, University of Oxford, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.714086.
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Kalla, Manish. "Mechanistic insights in the autonomic modulation of ventricular arrhythmia." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:019a87c7-322d-4d0b-befa-0da43378b13f.
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Cardiovascular disease is the leading cause of mortality in the developed world with up to fifty percent of cases being due to sudden cardiac death. Changes in sympatho-vagal balance underpin many cardiovascular conditions including heart failure and myocardial infarction. Neuraxial modulation of the autonomic nervous system is an emerging therapy to prevent ventricular arrhythmias, the main cause of sudden cardiac death. <b>Chapter One</b> reviews our current understanding of how the cardiac autonomic nervous system influences ventricular arrhythmogenesis. A particular focus was on the controversial role of cholinergic receptors and nitric oxide (NO) in parasympathetic protection from ventricular arrhythmias. Tetrahydrobiopterin (BH<sub>4</sub>), a critical cofactor for both tyrosine hydroxylase and NO synthases, and the co-transmitter neuropeptide-Y (NPY) may also influence sympathetic triggering of ventricular arrhythmias. This leads to the specific aims of the thesis which were to determine the mechanisms of the cholinergic antifibrillatory effect, investigate the role of cotransmission in arrhythmogenesis and, the mechanistic role of BH4 in autonomic cardiovascular control. <b>Chapter Two</b> detailed the experimental approach taken to investigate the hypotheses. A novel Langendorff heart preparation was developed with intact autonomic nerves to investigate how the stable analogue of acetylcholine, carbamylcholine (CCh) raises ventricular fibrillation threshold (VFT) and whether exogenous or endogenously released NPY lowers VFT. These actions are further investigated using optical mapping, dye free imaging of ventricular cell monolayers, immunohistochemistry, ELISA assays and measurements of NO metabolite production. To investigate the role of BH4 in the sympathetic control of the heart, an IRES-cre recombinase strategy was used to produce genomic deletion of GCH1 (the gene encoding BH4) in sympathetic neurons. Biopterins and plasma catecholamines were measured using HPLC, and blood pressure and heart rate via tail cuff plethysmography. <b>Chapter 3</b> showed that CCh increased VFT, prolonged action potential duration and flattened the electrical restitution curve. This effect required stimulation of both muscarinic and nicotinic receptors and the generation of nNOS derived NO utilising a cGMP dependent pathway. These observations are in keeping with established evidence demonstrating the obligatory role of the muscarinic receptor and indicate that the role of NO is likely to be via modulation of cholinergic neurotransmission. <b>Chapter 4</b> studied the role of the sympathetic co-transmitter NPY. NPY has been shown to increase ventricular myocyte calcium dynamics. Plasma levels are also increased post myocardial infarction and during heart failure, and correlate with outcomes. Perfusion of NPY decreased VFT via a Y1 receptor dependent mechanism and increased arrhythmic activity in myocyte monolayers. Direct sympathetic stimulation resulted in NPY release and remained pro-arrhythmic despite β-blockade, an effect that could be abolished by combined β-Y<sub>1</sub> receptor blockade. These observations indicated that NPY may be a novel, pro-arrhythmic trigger amenable to therapeutic pharmacological modulation. <b>Chapter 5</b> details the generation and phenotyping of two tissue specific Gch1 knockout mouse models. Whilst one model failed to produce significant lowering of BH<sub>4</sub> in sympatho-adrenal tissue, the other did result in a marked neuro-motor phenotype. A biochemical rescue or alternative genomic modification approach would be required to study the cardiovascular phenotype of sympathetic Gch1 deletion in more detail. <b>Chapter 6</b> is a concluding discussion summarising the main findings of the thesis, placing them in a clinical context and discussing avenues for further research.
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Hibbert, Anita S. "Depression and anxiety : differing relationships to respiratory sinus arrhythmia." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43112.
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Many theoretical models addressing the role of the parasympathetic branch of the
autonomic nervous system in psychopathology predict decreased respiratory sinus
arrhythmia (RSA) in disorders such as depression and anxiety. However, decreased RSA
in depression is not consistently observed across studies. Research on the relationship
between anxiety and RSA has also been mixed, but the results may be more robust than
that of depression. Before the theoretical models can be re-examined based on these
findings, researchers must clarify the nature of these relationships. Specifically, three
things should be determined: a) is there a relationship between RSA and depression; b) is
there a relationship between anxiety and RSA; and c) could comorbid anxiety in
depression be playing a role in the mixed findings to date.
This study was specifically designed to address those three questions. Based on
the empirical literature, we hypothesized that: 1) depression would have a small but
significant relationship to RSA; 2) anxiety would have a significant relationship to RSA
that would be stronger than that of depression to RSA; 3) the anxiety-RSA relationship
would persist when controlling for depression, whereas the depression-RSA relationship
would not persist when controlling for anxiety. Additionally, the Cardiac Sympathetic
Index (CSI) was used to explore the potential relationships that depression and anxiety
may have with sympathetic-related heart rate variability and sympathovagal balance.
One-hundred and twenty-eight physically healthy undergraduate students
completed a questionnaire measure assessing depression and anxiety symptoms. Participants’ ECG recordings were taken both at rest and during a stressful arithmetic task
to obtain measures of RSA and CSI. Regression analysis revealed a significant inverse
relationship between anxiety and RSA, and a marginally significant inverse relationship
between depression and RSA, during the stressful arithmetic task. No significant
relationships were observed at rest, or with CSI. Importantly, the relationship between
anxiety and RSA persisted when controlling for depression, whereas the opposite was not
true: the relationship between depression and RSA is almost eliminated when controlling
for anxiety. These results suggest that some of the positive findings in the depression-
RSA literature may be due to uncontrolled, co-occurring anxiety symptoms.
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Deshmane, Anagha Vishwas. "False arrhythmia alarm suppression using ECG, ABP, and photoplethysmogram." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/54209.
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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2009.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis.<br>Includes bibliographical references (p. 91-93).<br>A signal quality assessment scheme for the photoplethysmogram waveform recorded by a pulse oximeter has been created. The signal quality algorithm uses statistical methods on time-series and spectral analysis to locate high-frequency segments of the photoplethysmogram waveform. A photoplethysmogram pulse onset detector has been implemented for heart rate estimation. Application of the signal quality metric and photoplethysmogram pulse onset detector are demonstrated in an algorithm which suppresses false electrocardiogram critical arrhythmia alarms issued by bedside monitors in hospital intensive care units.<br>by Anagha Vishwas Deshmane.<br>M.Eng.
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Ives, Rachel Ayn. "Respiratory Sinus Arrhythmia as a Function of Cognitive Attention." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297655.
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RSA was assessed from electrocardiographic recordings from 95 individuals between the ages of 18 and 22 at resting, and while they were completing three tasks. The tasks were computerized performance tasks that provided increasing levels of difficulty and memory load. Subjects were asked to respond when the same letter repeated itself either one back, two back, or three back, depending on the task. The number of true positives declined as the tasks became increasingly difficult, and the number of false positives increased between the one back task and the two back task, but decreased between the two back task and the three back task. RSA suppression was greater for individuals with a higher resting RSA. RSA was enhanced during the one back task and suppressed during the two and three back tasks. No correlation was found between resting RSA and RSA suppression versus true or false positive responses during each task. No effect was found between resting RSA and RSA suppression versus positive or negative affect at onset of task. These results suggest that although there is a relationship between resting RSA suppression and cognitive attention during the tasks, it was not exactly as expected. The data also suggest that as the task becomes more difficult, RSA is suppressed to a higher extent.
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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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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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Tie, Hii Hui Clinical School St Vincents UNSW. "Cellular mechanisms of QT prolongation and proarrhythmia induced by non-antiarrhythmic drugs." Awarded by:University of New South Wales. Clinical School - St. Vincents, 2002. http://handle.unsw.edu.au/1959.4/19035.
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A variety of drugs prolong cardiac repolarization (manifested as QT prolongation on ECG), although the major example are the so-called class III antiarrhythmics. However, antiarrhythmic drugs which prolong cardiac repolarization are not harmless, as they may also be proarrhythmic, inducing a potentially fatal arrhythmia known as torsade de pointes (TdP). Recently, it has become apparent that a wide variety of non-antiarrhythmic agents may also, as an entirely undesired side-effect, provoke TdP. TdP is also characteristic of the congenital long QT syndrome, one form of which is caused by mutations in the HERG gene which encodes the major repolarizing potassium channel, IKr. Furthermore, HERG appears to be the main molecular target for drugs which cause QT prolongation. This thesis investigates the cellular mechanism for QT prolongation, proarrhythmia and sudden death associated with several commonly prescribed non-antiarrhythmic drugs. Specifically, we studied the effects of an antimalarial agent, halofantrine, and five psychoactive agents, thioridazine, chlorpromazine, clozapine, amitriptyline and mianserin on the HERG channel. A better understanding of the way these drugs interact with HERG could facilitate the development of safer drugs. We used the whole-cell voltage clamp technique to study currents produced by stable transfection of HERG into Chinese hamster ovary cells (CHO-K1). Our HERG-transfected cells possessed a potassium channel with biophysical properties similar to HERG-transfected cells previously reported (e.g. Xenopus oocytes, human embryonic kidney cells 293) and also to human IKr. HERG currents were potently inhibited by E-4031, a defining pharmacological signature of IKr. Therefore, these cells provide an appropriate model for the study of this important current in isolation. Halofantrine is a widely used antimalarial agent which has been associated with QT prolongation, TdP and sudden death. Halofantrine blocked HERG tail currents potently with an IC50 of 196.9 nM. Channel inhibition was time-, voltage- and use-dependent. Halofantrine did not alter channel activation or deactivation kinetics but inactivation was accelerated and there was a 20 mV hyperpolarizing shift in the mid-activation potential of steady state inactivation. Block increased with increasing depolarizing pulse duration and was enhanced by pulses that render channels inactivated. This is the first report of HERG channel blockade by halofantrine and is the likely cellular mechanism for its proarrhythmic potential. Our data indicate preferential binding of halofantrine to the open and inactivated channel states. Cardiovascular mortality in psychiatric patients is high. Reports of sudden unexplained death in those taking antipsychotic drugs have raised concerns that part of this excess may be due to drug-induced arrhythmias. We found that thioridazine and chlorpromazine blocked HERG channels (IC50 1.07 ????M and 1.47????M respectively) at clinically relevant concentrations and this is likely the cellular mechanism for their ability to prolong QT interval and induce TdP. To date, HERG block by chlorpromazine has not been reported and the state dependence of channel blockade by these phenothiazines has not been studied. Our results indicate that both drugs preferentially bind to closed HERG channels on the basis that block was not time-, voltage- or use-dependent, did not alter channel activation or deactivation kinetics and was unaffected by the depolarizing pulse duration. Clozapine is the prototype of the newer atypical antipsychotic drugs and is more efficacious and better tolerated than the traditional agents. Serious cardiotoxicity have occurred in clozapine-treated patients including sudden death. We found that clozapine produced a tonic block on HERG channels indicating preferential binding to the closed channel state. The IC50 for block was 2.62 ????M. This is close to the therapeutic concentration of the drug (0.6 to 2 ????M) and concentrations above 10 ????M have been reported during overdoses. Although there have been no specific reports of QT prolongation or TdP in clozapine-treated patients, our data raises the possibility of proarrhythmia as another potential explanation for sudden death during clozapine treatment. Amitriptyline, a commonly prescribed tricyclic antidepressant, can induce a variety of cardiac rhythm disturbances. Most reports have attributed these effects to its Na+ channel blocking ability. We found that amitriptyline blocked HERG channels with an IC50 of 10 ????M. Such high concentrations can be achieved during overdoses. Thus HERG channel blockade likely underlies amitriptyline????s QT-prolonging effect. Channel inhibition by amitriptyline exhibited positive voltage- and use-dependence and increased progressively with further prolongation of depolarization during an envelope of tails protocol, indicating preferential binding to an activated (open/inactivated) state of the channel. In contrast to the tricyclics, the tetracyclic antidepressant, mianserin, is much safer and only very rarely associated with cardiac complications. HERG channel blockade by mianserin was the least potent among the 5 psychoactive drugs we studied, with an IC50 of 14.78 ????M, which is 30- to 40-fold higher than therapeutic plasma concentrations of the drug. This probably, in part, accounts for the lack of reports of QT prolongation or TdP with mianserin. Mianserin displayed preferential affinity for an activated state of HERG channels on the basis of voltage-dependent block, a hyperpolarizing shift in the voltage of half-maximal activation and an increase in block at low external potassium concentration. Our results show that HERG block is a common feature of many non-cardiac drugs and that this underlies their potential for QT prolongation and TdP. Although the proarrhythmic risk varies according to potency of HERG block (e.g. mianserin is a weak blocker and does not induce TdP), other factors such as drug metabolism, protein binding and myocardial concentrations are also important since the risk of proarrhythmia during clinical use differ significantly even among the more potent HERG blockers. The preferential binding of these drugs to different channel states together with their diverse chemical structures suggest the presence of multiple distinct binding sites for drugs on HERG channels. There is increasing awareness that many non-antiarrhythmic drugs can prolong the QT interval and provoke TdP. Cardiac safety is now a major issue in new drug development. Our model of HERG K+ channels stably expressed in a mammalian cell line (CHO-K1) provides a useful tool for screening, at the preclinical stage, the proarrhythmic potential of novel drugs intended for human use.
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Lesiuk, Veronika. "Respiratory sinus arrhythmia : interaction of breathing frequency and heart rate changes." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81356.
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Heart rate variability is commonly interpreted as a measure of vagal tone. Changes in heart rate variability and more specifically respiratory sinus arrhythmia (RSA) are however also commonly observed when breathing is altered without changes in heart. This study examined how decreasing vagal tone through a low level (6%MVC) handgrip (HG) contraction and changing breathing frequency, alone or in combination, affected heart rate variability and respiratory sinus arrhythmia. ECG and respiratory recordings were obtained in 16 university students. Results show that decreasing breathing rate did not affect mean heart rate but resulted in a significant increase (p < 0.05) from baseline values in RSA amplitude (%) (SP: 0.11+/-0.07; SP-4: 0.14+/-0.07). On the other hand, under spontaneous breathing conditions sustained handgrip contraction resulted in a small yet significant increase in mean heart rate (SP: 62+/-6 bpm; SP-4: 69+/-11 bpm; p < 0.05) but was not associated with significant changes in RSA amplitude. The slope of the relationship between RSA amplitude and respiratory cycle duration was taken to reflect the vagal responsiveness to respiratory stimulation. A slight downward parallel shift from baseline was observed under sustained HG but significant differences in slope or y-intercept were not observed. These results suggest that indices of heart rate variability and respiratory sinus arrhythmia may be more appropriate indices of cardiac vagal efferent activity modulations by respiration than tonic activity.
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Xu, Weichao. "Real time detection of supraventricular arrhythmias /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?
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徐維超 and Weichao Xu. "Real time detection of supraventricular arrhythmias." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31243848.
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Abrams, Dominic James Richard. "Mechanisms and mapping of arrhythmia rate after the Fontan procedure." Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497623.
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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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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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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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Wolf, Roseanne Marie. "Defining new insight into fatal human arrhythmia: a mathematical analysis." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3013.
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Background: Normal cardiac excitability depends upon the coordinated activity of ion channels and transporters. Mutations in genes encoding ion channels affecting their biophysical properties have been known for over twenty years as a root cause of potentially fatal human electrical rhythm disturbance (arrhythmias). More recently, defects in ion channel associated protein (e.g. adapter, regulatory, cytoskeletal proteins) have been shown to cause arrhythmia. Mathematical modeling is ideally suited to integrate large volumes of cellular and in vivo data from human patients and animal disease models with the over goal of determining cellular mechanisms for these atypical human cardiac diseases that involve complex defects in ion channel membrane targeting and/or regulation. Methods and Results: Computational models of ventricular, atrial, and sinoatrial cells were used to determine the mechanism for increased susceptibility to arrhythmias and sudden death in human patients with inherited defects in ankyrin-based targeting pathways. The loss of ankyrin-B was first incorporated into detailed models of the ventricular myocyte to identify the cellular mechanism for arrhythmias in human patients with loos-of-function mutations in ANK2 (encodes ankyrin-B). Mathematical modeling was used to identify the cellular pathway responsible for abnormal Ca2+ handling and cardiac arrhythmias in ventricular cells. A multi-scalar computational model of ankyrin-B deficiency in atrial and sinoatrial cells and tissue was then developed to determine the mechanism for the increased susceptibility to atrial fibrillation in these human patients. Finally, a state-based Markov model of the voltage-gated Na+ channel was incorporated into a ventricular cell model and parameter estimation was performed to determine the mechanism for a new class of human arrhythmia variants that confer susceptibility to arrhythmia by interfering with a regulatory complex comprised of a second member of the ankyrin family, ankyrin-G. Conclusions: Ca2+ accumulation was observed at baseline in the ankyrin-B deficient ventricular model, with pro-arrhythmic spontaneous release and afterdepolarizations in the presence of simulated â-adrenergic stimulation, consistent with the finding of catecholaminergic-induced arrhythmias in human patients. The simulations demonstrated that loss of membrane Na+/Ca2+ exchanger and Na+-K+-ATPase contributed to Ca2+ overload and afterdepolarizations, with loss of Na+/Ca2+ exchanger as the dominant mechanism. In the atrial model of ankyrin-B deficiency, the loss of the L-type Ca2+ channel targeting was identified as the dominant mechanism for the initiation of atrial fibrillation. Finally, the simulations showed that human variants affecting ankyrin-G dependent regulation of NaV1.5 results in arrhythmia by mimicking the phosphorylation of the channel. Most importantly, mathematical modeling has been used to the molecular mechanism underlying human arrhythmia syndromes.
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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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Betts, Timothy Rider. "Atrial architecture and electrical activation." Thesis, University of Southampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288446.
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Martin, Claire Adriana. "Mechanisms of arrhythmogenesis in a murine model of Brugada syndrome." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648347.
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Liu, Pak-yin Anthony, and 廖柏賢. "Genetic counseling in sudden arrhythmia death syndrome : the science and the art." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196059.
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Background: Sudden arrhythmia death syndrome (SADS) is a genotypically and
phenotypically heterogeneous condition that might produce fatal ventricular arrhythmia in otherwise healthy individuals. Congenital long QT syndrome (LQTS) is the most common type of SADS with a frequency of 1 in 2500 individuals. Up to 13 genes have been shown to be associated with LQTS and genetic testing has a role in disease diagnosis, prognostication, treatment guidance, cascade testing, and reproductive counseling. Interdisciplinary care is the standard but such service is unavailable in Hong Kong.
Objectives: In this study, we aim to evaluate the clinical characteristics of a local cohort of pediatric patients with LQTS, establish the practicability of a model on interdisciplinary delivery of care for SADS, and explore the process of genetic counseling in Chinese families with LQTS from the perspective of discourse analysis. Method: Pediatric patients with LQTS and their families were recruited from the Department of Paediatric Cardiology, Queen Mary Hospital between 1 January 2011 and 31 December 2012. With informed consent, patients underwent genetic testing for 6 LQTS genes (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2, KCNJ2). Clinical characteristics were documented and the process of pre-test and post-test counseling was videotaped and transcribed. Data was mapped and analyzed for discourse strategies in the focal themes of uncertainty management in risk communication. Results: 19 patients were identified, 9 were male, with the corrected QT interval (QTc) ranging from 460-619ms. Mode of presentation included syncope (n=9), ventricular tachycardia (n=2), convulsion (n=1) and as incidental finding (n=7). Pathogenic mutations were identified in 9 patients (LQT1=3, LQT2=4, LQT3=1, LQT5=1), likely pathogenic mutations in 2 (LQT2), unclassified variants in 2, and no mutation in 6. Patients with pathogenic and likely pathogenic mutations had significantly longer mean QTc than those without such mutations (p=0.046). Three mutations, all in the LQT2 genes, represented novel mutations. All 3 patients with mutations in the pore-looping forming domains of the KCNH2 (LQT2) channel had personal or family histories of malignant arrhythmia or sudden cardiac death compatible with previously reported genotype-phenotype correlation. Eight families involving 18 family members underwent cascade testing, and family mutations were identified in 10 individuals from 6 families. Autosomal dominant transmission was the likely mode of inheritance in these 6 families. Counseling sessions involved the joint input from clinical geneticist, genetic counsellor and pediatric cardiologist. Discourse analysis on 2 counseling sessions of a selected family with unclassified variants revealed increased uncertainty after genetic testing in the index patient and family members. Strategies used to mitigate uncertainty included abstraction, generalization and categorization. Conclusion: Genetic testing was crucial in the comprehensive assessment of patients with congenital LQTS, and we demonstrated a feasible model to delivery interdisciplinary care for patients with SADS in Hong Kong. The process of genetic counseling is highly complex and deserves further examination.<br>published_or_final_version<br>Paediatrics and Adolescent Medicine<br>Master<br>Master of Medical Sciences
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Matthews, Gareth David Kingsley. "The rate-dependence of pro-arrhythmic properties in murine SCN5A+/- hearts modeling the Brugada syndrome." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648741.
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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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Scott, Adrienne S. "Comparison of respiratory sinus arrhythmia integration in athletes and non-athletes." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33924.
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A comparison of heart rate viability and respiratory sinus arrhythmia (RSA) characteristics was performed in 20 athletes and 12 age-matched sedentary controls (CTRL) (22 +/- 2.4 yrs). More specifically, this study examined the role of regular physical activity on the breathing frequency (BF)---RSA amplitude response curve comparing varsity swimmers (SW) to endurance runners (RU) to test the hypothesis that a locomotor-respiratory entrainment resulting from the water-immersion breathing pattern of swimmers would alter their respiratory related cardiac vagal integrative response. Spectral power components of HRV were computed from R-R interval sequences. Five-minute recordings were performed with subjects breathing either at their spontaneous breathing rate, at four breathing cycles less (M4) and four cycles more (P4) than spontaneous. Amplitude and phase of RSA were computed from the sinusoid fitted to the instantaneous heart rate within each breath while the gain of the RSA response was obtained from the slope of the RSA amplitude versus BF. (Abstract shortened by UMI.)
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Petchdee, Soontaree. "Arrhythmia mechanisms in acute ischaemia and chronic infarction in rabbit heart." Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/1327/.
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In this thesis, a method for studying the electrophysiological consequences of acute regional ischaemia in rabbit heart was established using a combination of a novel snare technique and optical mapping. The purpose of this approach was to discover the mechanistic link between acute coronary infarction and the occurrence of arrhythmias. The electrophysiology of the epicardial surface of isolated hearts was examined using the voltage sensitive dye RH237 and optical action potentials were recorded from a 13x13mm area of left ventricular epicardium using a 16x16 element Hamamatsu photodiode array. Contraction motion artefacts were practically eliminated with blebbistatin (5µM). An alternative mechanical uncoupler, BDM, was found to be not suitable for the study of arrhythmic behaviour associated with ischaemia. After occlusion of the left coronary artery, a progressive reduction in action potential duration (APD), and slowing of upstroke was observed in an area of the left ventricle anterior surface, accompanied by ECG S-T segment elevation. These effects were reversed when the coronary artery occlusion was released. Ligation (duration 12-15mins) caused a decrease in APD50 (APD at 50% repolarisation), in the zone of reduced perfusion, from 141±5.2ms to 53.3±9.3ms (mean±SEM, n=10 hearts, P<0.001). After ligation was reversed and full perfusion restored, APD50 returned to normal values (149±7.0ms, n.s.). Trise (action potential rise time from 10-90% depolarisation) increased from 7.2±1.0ms to 15.8±2.8ms (P<0.01). In the non-infarcted area of myocardium, no significant changes in APD50 (147±7.0ms vs. 147±8.1ms) or Trise (6.4±0.4ms vs 8.8±1.4ms) were observed during occlusion. T-wave alternans behaviour was observed frequently during local ischaemia and associated with alternans of optical action potentials (OAPs) in the ischaemic border zone (BZ) and in ischaemic zone (IZ). T-wave alternans amplitude was not maintained during local ischaemia but OAPs continued to show alternating behaviour. Arrhythmias (VT and VF) were common when conduction block occurred at the interface between the normal and ischaemic zone, but arrhythmias were absent when conduction into the IZ was retained. This observation suggests that the conduction block was the crucial precipitating event for the generation of arrhythmias. Acute local ischaemia was also imposed in a heart with an existing infarct scar to examine the effects of pre-existing ischaemic damage. The incidence of arrhythmias was similar to that observed in the absence of an infarct scar indicating that pre-existing damage did not predispose the heart to arrhythmias. Global ischaemic challenges, both low flow and zero flow produced similar reductions in APD and rise time and were followed by arrhythmias, but the associated changes in the ECG were complex and could not be easily interpreted. Significant temporal variability in electrophysiology was observed in global ischaemia, but absent in the local ischaemic challenge. The underlying mechanisms of these temporal flucuations in cardiac electrophysiology may be dictated by either cellular metabolism or fluctuations in coronary flow. Long-term local ischaemia (~60mins) did not reveal a second phase of arrhythmias after 40-45mins as observed in other animal models, and nor were there signs of significant further electrophysiological changes as a consequence of the additional period of local ischaemia.
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Condy, Emma Elizabeth. "Respiratory Sinus Arrhythmia and Restricted Repetitive Behaviors in Autism Spectrum Disorder." Thesis, Virginia Tech, 2016. http://hdl.handle.net/10919/78124.
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In addition to social communication deficits, restricted repetitive behaviors (RRBs) are a key diagnostic feature of autism spectrum disorder (ASD). Two theories regarding the etiology of RRBs in ASD have been proposed: the hyper-arousal theory, and the hypo-arousal theory. Both of these theories posit the autonomic nervous system (ANS) as being dysfunctional in ASD, resulting in the occurrence of RRBs. Many studies investigating ANS activity in ASD have focused solely on its relation to social functioning. The few that have addressed RRBs have had inconclusive findings. Not only do the current theories and studies simplify ANS activity to a measure of baseline arousal levels through vague measures such as heart rate (HR) and skin conductance response (SCR), but the literature has also framed the theories as mutually exclusive. This study used respiratory sinus arrhythmia (RSA) patterns in children with and without an ASD diagnosis as an indicator of ANS functioning to analyze its relationship to the manifestation of RRBs. Baseline RSA and RSA reactivity were found to predict RRB severity and exploratory analyses revealed that these measures were associated with specific subgroups of RRBs. These results are discussed in regards to the current behavioral literature on RRBs and the benefits of finding biomarkers for these behaviors.<br>Master of Science
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Bernhardt, Madison Nicole. "Reinterpretation of Genetic Variants from a Cohort of Pediatric Arrhythmia Patients." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523624250940948.
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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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Raphisak, Pisut. "Study of the Kalman filter for arrhythmia detection with intracardiac electrograms." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=1098.
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Thesis (M.S.)--West Virginia University, 1999.<br>Title from document title page. Document formatted into pages; contains viii, 143 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. [80]-85).
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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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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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Hörnsten, Rolf. "Cardiac arrhythmias and heart rate variability in familial amyloidotic polyneuropathy : a clinical study before and after liver transplantation /." Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1407.
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Lopes, Philippe. "The relationships between respiratory sinus arrhythmia and coronary heart disease risk factors." Thesis, University of Ulster, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287137.
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Fiore, Paul Vincent. "Interaction of cocaine and sprint-training on ventricular arrhythmia in the rat /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487588939087915.
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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