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Bibliografías temáticas / Myocardial / Tesis

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Tesis sobre el tema "Myocardial"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Egan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction." Thesis, The University of Sydney, 2009. http://hdl.handle.net/2123/5975.

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The vast majority of children undergoing surgical repair of cardiac lesions do spectacularly well. However a significant proportion, ~ 25%, struggle to progress in the early postoperative period and require additional pharmacological and occasionally mechanical circulatory support. All children typically have some degree of postoperative myocardial dysfunction, with the severe spectrum termed the low cardiac output state (LCOS). LCOS is clinically defined as the requirement for new or escalated inotrope therapy, a widened arteriovenous oxygen difference, cardiac arrest or the need for reinstit

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2

Egan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction." Faculty of Medicine, 2009. http://hdl.handle.net/2123/5975.

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Doctor of Philosophy(PhD)<br>The vast majority of children undergoing surgical repair of cardiac lesions do spectacularly well. However a significant proportion, ~ 25%, struggle to progress in the early postoperative period and require additional pharmacological and occasionally mechanical circulatory support. All children typically have some degree of postoperative myocardial dysfunction, with the severe spectrum termed the low cardiac output state (LCOS). LCOS is clinically defined as the requirement for new or escalated inotrope therapy, a widened arteriovenous oxygen difference, cardiac ar

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3

Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.

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4

Zhou, Xiaopeng. "Myocardial T1 Mapping Techniques for Quantification of Myocardial Fibrosis." Cleveland State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=csu1355418392.

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5

Park, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Pyrimidine nucleoside reverse transcriptase inhibitors (NRTIs), one of the primary classes of HIV/AIDS antiretroviral drugs, are known to cause mitochondrial toxicity by inhibiting polymerase gamma during extend

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6

Dwivedi, Girish. "A Comparison between Myocardial Contrast Echocardiography and Radionuclide Myocardial perfusion Imaging in Patients with Acute Myocardial Infarction." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521583.

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7

Treibel, Thomas Alexander. "Aortic stenosis : a myocardial disease : insights from myocardial tissue characterisation." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1574742/.

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Aortic stenosis (AS) is a disease of not just the valve, but also of the myocardium. Patient symptoms and outcome are determined by the myocardial response; a crucial but poorly understood process. Diffuse and focal myocardial fibrosis play a key role. Until recently, both could only be assessed using invasive histology, but now cardiovascular magnetic resonance (CMR) offers late gadolinium enhancement (LGE) and extracellular volume fraction (ECV) techniques. In this thesis, I developed new methods to quantify ECV by synthetic ECV and cardiac CT. I then explored myocardial remodelling and fibr

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8

White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.

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Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The causes of stunning are not fully elucidated, however two major hypotheses currently exist; firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free radical (OFR) that may occu

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9

Singh, Hardial. "Quantitative assessment of myocardial ischaemia with thallium-201 myocardial perfusion imaging." Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/19297.

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10

Frostfeldt, Gunnar. "Coagulation Inhibition and Development of Myocardial Damage in ST-Elevation Myocardial Infarction." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5322-8/.

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11

Hayat, Sajad Ahmed. "Myocardial Contrast Echocardiography to Interrogate the Myocardial Microcirculation in Ischaemic Heart Disease." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521584.

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12

Hickman, Thomas Michael. "Can myocardial contrast echocardiography detect myocardial viability in patients with ischaemic cardiomyopathy?" Thesis, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542948.

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13

Filippone, Scott M. "Inhibition of mTOR Signaling Protects Against Myocardial Reperfusion Injury, Acute Myocardial Infarction." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3847.

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Acute myocardial infarction (AMI) is the leading cause of death worldwide. Currently, the best method of treating cardiac ischemia is early reperfusion which, itself, induces myocardial damage. The mTOR complex is a key regulator of cardioprotection against cell stressors. We hypothesized that reperfusion therapy with Rapamycin, a potent mTOR inhibitor, would reduce infarct size in adult mouse hearts. Rapamycin was administered at the onset of reperfusion following 30 min in situ LAD ligation. After 24 hours of reperfusion, myocardial infarct size and apoptosis were significantly reduced in ra

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14

Shenje, Lincoln Takura. "Studies assessing cardiac myocyte renewal and myocardial repair in the adult mammalian myocardium." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29896.

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The initial aims of this thesis were to investigate whether the myocardium contains resident progenitor cells that contribute to myocardial renewal and whether extra-cardiac bone marrow derived cells contribute to myocardial regeneration. I reveal that the myocardium has the capacity to produce humoral factors that enable extra-cardiac progenitors to survive in vitro though this was insufficient to induce cardiac differentiation. I have shown that the myocardium has the capacity to produce a heterogeneous population of cells in vitro, some of which express cardiac related markers but do not ad

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15

Tähepõld, Peeter. "Myocardial protection by hyperoxia /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-247-7.

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16

Meyer, Theo Egbert. "Regional nonischaemic myocardial performance." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305481.

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17

PATTONERI, PAOLO. "Left ventricular myocardial performance." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1163.

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Recentemente Tei e collaboratori, hanno proposto un nuovo indice Doppler-derivato in grado di valutare simultaneamente la funzione sistolica e diastolica. Questo indice di performance cardiaca (MPI), definito come la somma del tempo di contrazione isovolumetrica e tempo di rilasciamento isovolumetrico diviso per il tempo di eiezione ventricolare sinistro, è considerato di facile esecuzione, non dipendente dalla geometria ventricolare, non invasivo, riproducibile e indipendente dalla frequenza cardiaca e dalla pressione arteriosa. L’MPI ha dimostrato di avere un’importante utilità clinica. È i

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18

Von, Oppell Ulrich O. "Myocardial protection during cardiac surgery." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/25887.

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19

Nussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.

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20

Harvey, K. "Ipratropium bromide mediated myocardial injury in in vitro models of myocardial ischaemia/reperfusion." Thesis, Coventry University, 2015. http://curve.coventry.ac.uk/open/items/f03ffc6e-3554-4062-99c2-1c243feb582a/1.

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Ipratropium bromide is a short-acting, non-selective, muscarinic antagonist frequently prescribed for the treatment of Chronic Obstructive Pulmonary Disease (COPD) and as an emergency adjunct therapy for acute asthma. Within the past decade, there has been an accumulating wealth of clinical evidence which indicates that anti-muscarinic drugs, such as ipratropium, are responsible for an increased risk of stroke or, an adverse cardiovascular outcome (including increasing the risk and severity of myocardial infarction (MI)). MI remains the highest risk factor of death for COPD patients due to the

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21

Feger, Sarah [Verfasser]. "Patient satisfaction with coronary CT angiography, myocardial CT perfusion, myocardial perfusion MRI, SPECT myocardial perfusion imaging and conventional coronary angiography / Sarah Feger." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1102196932/34.

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22

Adix, Longlet Nancy J. "Chronic Ventricular Sympathectomy : Effects on Myocardial Metabolism." Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc278768/.

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Chronic ventricular sympathectomy elicits changes in the coronary circulation, myocardial oxygen consumption and size of infarction resulting fromcoronary occlusion. These changes indicate a change occurring in the basic metabolism of the heart in response to the removal of its sympathetic nervous input. This hypothesis was tested using two groups of dogs, a shamoperated control and a ventricular sympathectomized group. The sympathectomy procedure was an intrapericardial surgical technique which selectively removes ventricular sympathetic input. Four weeks after surgery, left ventricular tissu

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23

Kragten, Johannes Albertus. "New myocardial marker proteins in acute myocardial infarction quantitative aspects : release patterns of cellular enzymes and proteins in plasma following acute myocardial infarction /." Assen : Maastricht : Dekker & van de Vegt en Van Gorcum ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=6052.

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24

Surányi, Pál. "Relaxation rate-based magnetic resonance imaging quantification of myocardial infarction." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007r/suranyi.pdf.

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25

Marelli, Daniel. "Cell transplantation for myocardial repair." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61231.

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It was hypothesized that skeletal muscle (SKM) satellite cells multiplied in vitro could be used to repair injured heart muscle. The purpose of this study was to test this hypothesis by auto-transplanting SKM satellite cells to a myocardial injury site. Fourteen dogs underwent explanation of the anterior tibialis muscle. Satellite cells were multiplied in vitro and their nuclei were labelled with tritiated thymidine 24 hours prior to implantation. The same dogs were then subjected to a myocardial injury by the application of a cryoprobe. The cells were suspended in serum free growth medium and

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26

McMahon, Aisling Clare. "Myocardial dysfunction in experimental uraemia." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264179.

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27

Chatham, J. C. "Biochemical aspects of myocardial damage." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376900.

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28

Elhdere, Souada Ahmed. "Illness cognitions in myocardial infarction." Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548363.

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29

Kumar, Sanjay. "Pathophysioloqical mechanisms underlying myocardial stunning." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522843.

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30

Saurin, Adrian Thomas. "Protein kinases in myocardial protection." Thesis, King's College London (University of London), 2001. https://kclpure.kcl.ac.uk/portal/en/theses/protein-kinases-in-myocardial-protection(ba5e7b96-cf59-409a-b290-f18fec8be6b1).html.

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31

Williamson, K. L. "Characterisation of myocardial alpha-adrenoceptors." Thesis, Cardiff University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376560.

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32

Elliott, Perry Mark. "Myocardial ischaemia in hypertrophic cardiomyopathy." Thesis, St George's, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391632.

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33

Campbell, Kenneth Lindsay. "The myocardial response to endotoxaemia." Thesis, University of Aberdeen, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338575.

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The sharp fall in systemic vascular resistance in sepsis is well characterised but the specific myocardial response remains a subject of debate. The behaviour of the myocardial adrenergic system is inextricably linked to this myocardial response. Using the controlled in vitro environment of an oxygenated organ bath, atria isolated from male Sprague Dawley rats were used to study the effects of in vivo endotoxin exposure on baseline myocardial force and rate of contraction. The same conditions were used to study adrenergic response. A potential site mediating both baseline and adrenergic mediat

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34

Williams, John. "Marker proteins in myocardial infarction." Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359319.

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35

Yellon, Derek M. "The pathophysiology of myocardial protection." Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760654.

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36

Taghavi, Fouad John. "Post-cardiac arrest myocardial dysfunction." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/18885/.

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One of the major medical advances of the twentieth century is the development of cardiac transplantation. Cardiac transplantation is the definitive treatment for end-stage heart disease. Cardiac transplantation relies on organs procured from Brain Dead Donors (DBD). Donation after Circulatory Death (DCD) organs are being increasingly used for renal, liver and lung transplantation. Hearts from DCD donors have not been utilized as there is a fear that they will have sustained irreversible myocardial injury post cardiac arrest. We have a limited understanding of Post cardiac arrest myocardial dep

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37

Hsing, Jeff M. (Jeff Mindy) 1972. "Quantification of myocardial macromolecular transport." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/9068.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2000.<br>Includes bibliographical references (leaves 66-68).<br>The needs and impacts of drug administration have evolved from a systemic to a local focus. Local drug delivery would allow a higher local drug concentration at lower systemic toxicity than what can be achieved if delivered systemically. One of the tissues of interest for local delivery is the heart, or myocardium. Increasingly, clinicians are looking to direct myocardial delivery for therapy of complex cardiovascular diseas

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38

Ruparelia, Neil. "Monocytes in acute myocardial infarction." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:02ad6ebd-a8c2-4cb6-a1f7-0cdf8cec59ed.

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Acute myocardial infarction (AMI) results in the activation of the innate immune system with monocytes playing critical roles in both the initial inflammation following myocardial ischaemia and subsequent recovery. Monocytes are a heterogeneous cell population and observations from experimental models demonstrate that immediately following myocardial injury, classical inflammatory monocytes, which are highly phagocytic, are recruited to ischaemic myocardium from the bone marrow and spleen and peak at 48 hours. This is followed by the recruitment of non-classical monocytes that are involved in

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39

Zarinabad, Nooralipour Niloufar. "Advanced quantification of myocardial perfusion." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/advanced-quantification-of-myocardial-perfusion(1aa4ae14-3452-4f50-bbfc-f433191f210c).html.

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Ischemic heart disease remains a major global health concern with significant morbidity and mortality issues. Identifying areas of myocardial tissue at risk early on can help guide clinical management and develop appropriate treatment strategies to prevent myocardial infarction, thus improving patient outcomes. Using the latest cardiac magnetic resonance (CMR) imaging techniques, first-pass perfusion imaging allows for a very high spatial resolution, non-invasive and radiation free quantification of myocardial blood flow (MBF). True quantification of very high resolution perfusion images offer

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40

Patel, Vimal. "Myocardial fibrosis in hypertrophic cardiomyopathy." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046437/.

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Hypertrophic cardiomyopathy (HCM) is characterised by myocardial hypertrophy, fibrosis and abnormal vascular pathology and is usually caused by mutations in sarcomeric protein genes. Histological studies and in vivo imaging with cardiac magnetic resonance imaging (CMRI) have shown that myocardial fibrosis is an important entity that contributes to disease progression. However, little is known about the regulation of genes involved in collagen synthesis and metabolism, the pathways that contribute to the development of myocardial fibrosis and whether this is an early pathological process which

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41

Joyeux-Faure, Marie. "Heat stress and myocardial protection." Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE18004.

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42

Kidambi, Ananth. "Myocardial tissue characterisation and functional assessment by magnetic resonance imaging in ST elevation myocardial infarction." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7719/.

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Objectives:- To evaluate myocardial tissue characterisation by cardiovascular magnetic resonance (CMR) to predict functional recovery in reperfused acute myocardial infarction (AMI). Background:- Prognosis following AMI is closely related to recovery of myocardial contractile function. Accurate early prediction of functional recovery may allow for additional therapies in high risk patients, and avoid over-treatment of lower risk patients. Clinical prognostication commonly relies on echocardiographic evaluation of function, which may be misleading acutely. CMR offers a number of ways to refine

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43

Buchanan, Lynne M. "Psychophysiological recovery after acute myocardial infarction /." Thesis, Connect to this title online; UW restricted, 1989. http://hdl.handle.net/1773/7244.

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44

Ti, Yalin. "In Vivo Characterization of Myocardial Tissue Post Myocardial Infarction Using Combined Fluorescence and Diffuse Reflectance Spectroscopy." FIU Digital Commons, 2009. http://digitalcommons.fiu.edu/etd/95.

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Accurately assessing the extent of myocardial tissue injury induced by Myocardial infarction (MI) is critical to the planning and optimization of MI patient management. With this in mind, this study investigated the feasibility of using combined fluorescence and diffuse reflectance spectroscopy to characterize a myocardial infarct at the different stages of its development. An animal study was conducted using twenty male Sprague-Dawley rats with MI. In vivo fluorescence spectra at 337 nm excitation and diffuse reflectance between 400 nm and 900 nm were measured from the heart using a portable

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45

Arstall, Margaret Anne. "Studies in myocardial ischaemia and infarction : effects of N-acetylcysteine on oxidative stress and myocardial salvage /." Title page, contents and summary only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09pha783.pdf.

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46

Bennet, Anna. "Insulin resistance, genetic variation and cytokines : associations to myocardial infarction risk /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-666-9/.

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47

Jager, Tertia de. "Estrogen action in the myocardium modulation of myocardial gene expression and the influence on cardiac hypertrophy /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964433621.

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48

Thiru, Yamuna. "Myocardial function in paediatric meningococcal disease." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251576.

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49

Abunasra, Haitham Juma. "Gene therapy in myocardial ischemia-reperfusion." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404964.

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50

Bhimji, Shabir. "Myocardial ischemic injury in experimental diabetes." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25562.

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The nature and extent of myocardial ischemic injury (Mil) produced either by coronary artery ligation/reperfusion or by injection of isoproterenol (ISO) was studied in the 10-week alloxan-diabetic rabbit. Prior to the induction of ischemic injury, investigation of the left ventricles of the diabetic rabbit after 10-weeks revealed significant magnesium depletion and inhibition of myofibrillar and sarcoplasmic reticulum ATPase activities. In addition, the activity of the lysosomal enzyme, N-acetyl-β-glucosaminidase was significantly increased in diabetic left ventricular homogenates. Ultrastruc

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