Rozprawy doktorskie na temat „Myocardial”
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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.
Pełny tekst źródłaEgan, 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.
Pełny tekst źródłaThe 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 reinstitution of mechanical circulatory support. LCOS is largely responsible for the morbidity and mortality involved in paediatric cardiac surgery. Despite the predictability of LCOS in the initial postoperative hours, the underlying pathophysiology remains unclear. The period of decline in cardiac function that typifies LCOS is temporally associated with the development of oedema in the tissues of the body, including the heart. This relationship between oedema and dysfunction has increasingly become blurred, with a tendency to elevate the temporal association to a causal link. We sought to explore the causes and contributions to myocardial dysfunction in this setting, including the roles of oedema and ischaemia within the heart. In focusing on oedema and ischaemia we also examined the effects of these insults on relevant myocardial membrane proteins, including those that permit rapid water transport – aquaporins (AQPs), and those involved in membrane mechanics – dystrophin, and membrane repair – dysferlin. Experimental settings which enabled the in vitro dissection of these insults and proteins of interest were combined with a clinically accurate in vivo model. This thesis describes a series of thematically linked experiments that examined LCOS, myocardial oedema and the role of various membrane proteins. We performed isolated cardiomyocyte studies, isolated heart studies as well as a clinically relevant large animal (lamb) cardiopulmonary bypass (CPB) model. Across these models we also explored the role of therapeutically protecting myocardial membranes with Poloxamer 188 (P188) and assessed any influence on myocardial function, oedema and membrane proteins. vi The results from these three models suggest that the clinically accepted dogma of a causative link between myocardial oedema and dysfunction overstates the contribution of myocardial oedema to LCOS. We found that ischaemia/reperfusion was of primary importance in causing myocardial dysfunction. Myocardial oedema without ischaemia had a mild and reversible contribution to myocardial dysfunction, but this was minor in comparison to the gross dysfunction attributable to ischaemia. Isolated cardiomyocytes, with induced oedema, functioned well. Whilst ischaemic cardiomyocytes, with less swelling still had severe contractile dysfunction. Isolated hearts, perfused with an oedema inducing crystalloid perfusate developed myocardial oedema and had minimal reversible systolic and diastolic dysfunction. Isolated hearts which experienced global ischaemia had comparable degrees of myocardial oedema, and significantly greater degrees of myocardial dysfunction that increased in severity with increasing duration of ischaemia. In the lamb CPB model, only those lambs which underwent aortic cross clamping and had a period of ischaemia had poor myocardial function. These lambs also had swollen hearts, raised myocardial AQP1 mRNA and reduced membrane dysferlin protein expression. Membrane dystrophin protein expression was not altered, somewhat unexpectedly with CPB with or without ischaemia. Lambs placed on CPB without ischaemia had good myocardial function, minimal oedema and unchanged membrane protein expression during the survival period. In a blinded lamb CPB trial of P188 there were improved haemodynamics and indicies of myocardial function associated with its use. This was also associated with preservation of dysferlin expression and reduced membrane injury. In parallel isolated heart trials of this therapy, there was a reduction in myocardial oedema associated with its use in non-ischaemic experiments. There was also a suggestion of improved diastolic function in ischaemic experiments, but no change in myocardial water content. In conclusion, we have highlighted the primacy of ischaemia/reperfusion over oedema in contributing to LCOS. We have refuted the accepted dogma that myocardial oedema causes significant dysfunction in itself, with important oedema likely to result from ischaemia. We have shown that AQP1 may be involved in the pathogenesis of the capillary leak syndrome. Finally we have hinted at a role for prophylactic P188 in the vii setting of LCOS, possibly highlighting the role of membrane repair in recovery after surgery. Isolated heart trials of P188 further support a non-rheological mechanism of action and also lend support to the causal separation of myocardial oedema and dysfunction. The integral membrane protein dysferlin, rather than dystrophin, is relevant in the setting of LCOS in the current era.
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.
Pełny tekst źródłaLöwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.
Pełny tekst źródłaPark, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.
Pełny tekst źródłaPyrimidine 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 extending mitochondrial DNA replication. Extensive, prolonged use of NRTIs, such as zidovudine (3'-azido-2',3'-deoxythymidine; AZT), is associated with cardiovascular complications, such as dilated cardiomyopathy, the most common form of heart failure in which cardiac fibrosis is seen. Moreover, cardiac fibrosis is part of the pathological response of the heart during the progression of heart failure. Thus, we hypothesized that AZT treatment will contribute to the progression of cardiac fibrosis indirectly. Our study specifically focused on the effects of AZT and the development of cardiac fibrosis in the myocardium of wildtype (WT) and Y955CB transgenic mice (TG). Y955CB TG expresses a dominant negative cardiac specific mutant mitochondrial DNA polymerase gamma and were used to enhance the mtDNA toxic effect of AZT. To estimate fibrosis, myocardial collagen levels in each treatment group were assessed using both the hydroxyproline assay and histological image analysis. WT mice treated with AZT 0.22 mg/day for 35 days revealed no change in the level of hydroxyproline. However, a significant increase in hydroxyproline abundance correlated with histologically detectable fibrosis in vehicle-treated Y955CB TG mice. Interestingly, there was no additional increase in the abundance of collagen in AZT-treated Y955CB mice. Taken together, these data demonstrate that Y955CB TG displays an increase in the collagen level of the heart, concomitant with its documented cardiomyopathy. However AZT treatment was insufficient to increase the abundance of collagen in the heart.
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.
Pełny tekst źródłaTreibel, 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/.
Pełny tekst źródłaWhite, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium". Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.
Pełny tekst źródłaSingh, Hardial. "Quantitative assessment of myocardial ischaemia with thallium-201 myocardial perfusion imaging". Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/19297.
Pełny tekst źródłaFrostfeldt, 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/.
Pełny tekst źródłaHayat, 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.
Pełny tekst źródłaHickman, 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.
Pełny tekst źródłaFilippone, Scott M. "Inhibition of mTOR Signaling Protects Against Myocardial Reperfusion Injury, Acute Myocardial Infarction". VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3847.
Pełny tekst źródłaShenje, 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.
Pełny tekst źródłaTähepõld, Peeter. "Myocardial protection by hyperoxia /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-247-7.
Pełny tekst źródłaMeyer, Theo Egbert. "Regional nonischaemic myocardial performance". Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305481.
Pełny tekst źródłaPATTONERI, PAOLO. "Left ventricular myocardial performance". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1163.
Pełny tekst źródłaRecently, a conceptually new Doppler index that combines the assessment of systolic and diastolic left ventricular (LV) performance was proposed by Tei and co-workers. This Myocardial Performance Index (MPI), which is defined as the sum of isovolumetric contraction time and isovolumetric relaxation time divided by the ejection time, was reported to be simple, non-geometrical, non-invasive, reproducible and independent of the heart rate and blood pressure. The MPI has been shown to have significant clinical utility. It is prolonged in many cardiac diseases even in the absence of clinical signs. Studies have demonstrated that MPI correlates well with invasive measures of both systolic and diastolic function in adults and provides prognostic information about morbidity and mortality in patients with ischemic heart disease, cardiac amyloidosis, dilated cardiomyopathy, primary pulmonary hypertension and detects early LV functional improvement as a result of drug therapy. MPI is also abnormal in individuals without overt cardiac disease who have risk factors such as diabetes mellitus and treated and untreated hypertension. Orem et al. demonstrated progressively more abnormal MPI with increasing degrees of albuminuria in a diabetic population. More recently, the MPI has shown promise in the assessment of right ventricular function in fetus, children and adults with various heart disease. The aim of this thesis was to analyse the LV myocardial performance, applying the MPI in various physiological and pathological conditions to elucidate some aspects of LV myocardial dynamic. In the first study, we demonstrated that LV geometry represents an important determinant of the myocardial performance. In fact, our data demonstrates a correlation between MPI and RWT but not with LVM/BSA. The MPI geometry-dependence must be taken into consideration during the application of the Index for the evaluation of myocardial performance, and when used as a prognostic marker in cardiac disease where the LV geometry could be modified. In the second study the MPI has been confirmed able to identify the earliest abnormalities of cardiac performance at echocardiography in a homogeneous group of uncomplicated asymptomatic type 2 diabetic patients with very short duration of disease with or without hypertension. The MPI increase was mainly due to a prolongation of IRT. A correlation between MPI and the HbA1c value, was found indicating its role as an early marker of metabolic control. Our findings may have important clinical implications. First, this index could provide an easy approach to detect an earliest phase of diabetic cardiomyopathy that precede diastolic dysfunction, and to monitor the natural history of the diabetic disease. Second, MPI could be useful for indirectly assess the metabolic control or suggest an early start of specific pharmacological treatments that may help the clinical course of diabetic cardiomyopathy. Most importantly, whether such abnormalities may be reverted by optimal metabolic control and/or pharmacologic treatments could be determined. Diagnosing pre-clinical diabetic cardiomyopathy early through MPI is not only important but also may turn out to be essential for the appropriate clinical testing of new therapeutic approaches to diabetic disease. Finally, the MPI appears to be a sensitive noninvasive technique for detecting significant subclinical left ventricular dysfunction, in patients with multiple sclerosis treated with low dose of mitoxantrone, an antracenedione antineoplastic agent. Besides, provides important prognostic information for the risk of future cardiotoxicity, beyond other conventional echocardiographic measurements. We expect that MPI may be an adjunctive parameter to the conventional echocardiography in monitoring cardiac side effects and for detecting sub-clinical cardiotoxicity of mitoxantrone. In conclusion, a simple measure of Doppler index, combining systolic and diastolic time interval as an expression of global myocardial performance, correlates with overall cardiac function, seem to be a useful predictor of clinical outcome and could be an adjunctive index for the diagnosis and for the clinical management of patients with many cardiac and systemic disease.
Von, Oppell Ulrich O. "Myocardial protection during cardiac surgery". Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/25887.
Pełny tekst źródłaNussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.
Pełny tekst źródłaHarvey, 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.
Pełny tekst źródłaFeger, 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.
Pełny tekst źródłaAdix, Longlet Nancy J. "Chronic Ventricular Sympathectomy : Effects on Myocardial Metabolism". Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc278768/.
Pełny tekst źródłaKragten, 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.
Pełny tekst źródłaMarelli, Daniel. "Cell transplantation for myocardial repair". Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61231.
Pełny tekst źródłaThere was persistence of the implantation channels in the experimental sites when compared to the controls. Macroscopically, muscle tissue completely surrounded by scar could be seen. Masson trichrome staining showed homogeneous scar in the control site, but not in the test site where a patch of muscle fibres containing intercalated discs (characteristic of myocardial tissue) was observed. In 2 dogs, specimens were taken at 14 weeks post-implantation. Muscle tissue could not be found. Electrically stimulated skeletal muscle regenerates did not show histological evidence of cardiac transformation.
These results support the hypothesis that SKM satellite cells can form neo-myocardium within an appropriate environment. The specimens failed to demonstrate the presence of myocyte nuclei. (Abstract shortened by UMI.)
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.
Pełny tekst źródłaChatham, J. C. "Biochemical aspects of myocardial damage". Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376900.
Pełny tekst źródłaElhdere, Souada Ahmed. "Illness cognitions in myocardial infarction". Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548363.
Pełny tekst źródłaKumar, Sanjay. "Pathophysioloqical mechanisms underlying myocardial stunning". Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522843.
Pełny tekst źródłaSaurin, 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.
Pełny tekst źródłaWilliamson, K. L. "Characterisation of myocardial alpha-adrenoceptors". Thesis, Cardiff University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376560.
Pełny tekst źródłaElliott, 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.
Pełny tekst źródłaCampbell, Kenneth Lindsay. "The myocardial response to endotoxaemia". Thesis, University of Aberdeen, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338575.
Pełny tekst źródłaWilliams, John. "Marker proteins in myocardial infarction". Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359319.
Pełny tekst źródłaYellon, Derek M. "The pathophysiology of myocardial protection". Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760654.
Pełny tekst źródłaTaghavi, Fouad John. "Post-cardiac arrest myocardial dysfunction". Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/18885/.
Pełny tekst źródłaHsing, Jeff M. (Jeff Mindy) 1972. "Quantification of myocardial macromolecular transport". Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/9068.
Pełny tekst źródłaIncludes bibliographical references (leaves 66-68).
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 diseases. Yet, there is little quantitative data on the rates of macromolecular transport inside the myocardium. A porcine model was used in this work as it is most closely similar to humans in size, structure and morphology. Using a technique previously developed in this laboratory to quantify the distribution of macromolecules, the delivery of compounds directly into the myocardium was evaluated. To make quantification generic and not specific for a particular drug or compound, fluorescent-labeled 20kDa and 150kDa dextrans were used to simulate small and large diffusing macromolecules. Diffusion in the myocardium in two directions, transmural and cross-sectional, were investigated to look at diffusion of compounds along and against the myocardium fiber orientation. Fluorescent microscopy was used to quantify concentration profiles, and then the data was fit to a simple diffusion model to calculate diffusivities. This validated the technique developed. The diffusivities of 20kDa dextran in the transmural and cross-sectional direction were calculated to be 9.49 ± 2.71 um2/s and 20.12 ± 4.10 um2/s respectively. The diffusivities for 150kDa were calculated to be 2.39 ± 1.86um 2/s and 3.23 ± 1.76um2/s respectively. The diffusivities of the two macromolecules were statistically different (p < 0.02 for transmural direction and p < 0.01 for cross-section direction). While the diffusion for the larger macromolecule was isotropic, it was not the case for the smaller one. The calculated diffusivity values in the myocardium correlated with previously published data for dextran in the arterial media, suggesting that the transport properties of the myocardium and arterial media may be similar. Applications of quantitative macromolecular transport may include developing novel therapies for cardiovascular diseases in the future.
by Jeff M. Hsing.
S.M.
Ruparelia, Neil. "Monocytes in acute myocardial infarction". Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:02ad6ebd-a8c2-4cb6-a1f7-0cdf8cec59ed.
Pełny tekst źródłaZarinabad, 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.
Pełny tekst źródłaPatel, Vimal. "Myocardial fibrosis in hypertrophic cardiomyopathy". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046437/.
Pełny tekst źródłaJoyeux-Faure, Marie. "Heat stress and myocardial protection". Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE18004.
Pełny tekst źródłaSurányi, 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.
Pełny tekst źródłaKidambi, 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/.
Pełny tekst źródłaBuchanan, Lynne M. "Psychophysiological recovery after acute myocardial infarction /". Thesis, Connect to this title online; UW restricted, 1989. http://hdl.handle.net/1773/7244.
Pełny tekst źródłaTi, 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.
Pełny tekst źródłaArstall, 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.
Pełny tekst źródłaBennet, Anna. "Insulin resistance, genetic variation and cytokines : associations to myocardial infarction risk /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-666-9/.
Pełny tekst źródłaJager, 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.
Pełny tekst źródłaThiru, Yamuna. "Myocardial function in paediatric meningococcal disease". Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251576.
Pełny tekst źródłaAbunasra, Haitham Juma. "Gene therapy in myocardial ischemia-reperfusion". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404964.
Pełny tekst źródłaBhimji, Shabir. "Myocardial ischemic injury in experimental diabetes". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25562.
Pełny tekst źródłaPharmaceutical Sciences, Faculty of
Graduate