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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 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.
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.
Full textAbstract:
Doctor of Philosophy(PhD)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 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.
3
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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4
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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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.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 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.
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 fibrosis in patients with severe AS undergoing aortic valve replacement (AVR) using myocardial biopsy, CMR, biomarkers and a wide range of clinical parameters. Prior to AVR, CMR in patients with severe AS revealed important differences in myocardial remodelling between sexes, otherwise missed on echocardiography alone. Given apparently equal valve severity, the myocardial response to AS appeared unexpectedly maladaptive in men compared to women. Intra-operative myocardial biopsy revealed three pattern of fibrosis: endocardial fibrosis, microscars (mainly in the subendomyocardium), and diffuse interstitial fibrosis. Biopsy best captured the transmural gradient of fibrosis and microscars, while on CMR, LGE captured mainly microscars and ECV captured mid-myocardial related functional changes beyond LGE. Combining LGE and ECV allowed better stratification of AS patients. Incidentally, I found that 6% of AS patients older then 65 years had wild-type transthyretin amyloid deposits on cardiac biopsy, which was associated with poor outcome. This is now the basis of a BHF research fellowship. Following AVR, I demonstrated for the first time non-invasively that diffuse fibrosis regresses (focal fibrosis did not), which is accompanied by structural and functional improvements suggesting that human diffuse fibrosis is plastic, measurable by CMR and a potential therapeutic target.
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 occur in a dramatic ‘surge’ at the onset of reperfusion. Treatment of
ischemic myocardium with calcium channel blockers and / or OFR scavengers has been
successfully shown to prevent stunning in various animal models. Whilst much is known
about the physiological and biochemical changes that occur in stunned myocardium, very
little is known about events at the molecular level. Since stunning occurs after only brief (15
minutes low-flow in the rabbit model) ischemia and subsequent reperfusion, we hypothesized
that these molecular events are not predominated by large changes in protein expression and
abundance, yet rather by subtle and / or transient changes to protein post-translational
modifications (PTM). Such changes at the protein level are best analysed using the
technologies encompassed under the term ‘proteomics’.
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 rapamycin-treated mice compared to control. Rapamycin inhibited pro-apoptotic protein Bax and phosphorylation of ribosomal protein S6 (target of mTORC1), while it induced phosphorylation of AKT (target of mTORC2). Rapamycin also induced phosphorylation of ERK, while significantly reduced phosphorylation of p38. Thus, our study shows that reperfusion therapy with Rapamycin provides cardioprotection through induction of the phosphorylation of Akt and ERK.
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 adopt a full cardiac phenotype. When these cells are transplanted into a normal or injured heart they integrate into the myocardium but fail to develop a full mature functional cardiac phenotype. I have set up the frame work for demonstrating and defining the qualitative histological structure of the myocardium using lineage tracing techniques and strengthening the criteria for defining various cell lineages in the heart and therefore demonstrated the deficiencies of seminal studies that claimed that adult stem cells had the capacity to differentiate into cardiomyocytes and secondly that cultured heart explants produce cardiac progenitors. From this work it is clear that more needs to be done to identify the various cell lineages and roles of endogenous cardiac cells. The identification of clusters of perivascular cells expressing cardiac markers using 3 dimensional confocal imaging by two photon molecular excitation provided a different approach for identifying putative cardiac progenitors. This in combination with lineage tracing techniques and cell isolation is now required to identify the role of these interesting perivascular cells in cardiac homeostasis.
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 infatti prolungato in molte malattie cardiache, anche in assenza di segni clinici. Studi hanno dimostrato che l’MPI correla bene con misure invasive di funzione sistolica e diastolica, fornendo informazioni prognostiche su morbilità e mortalità nei pazienti con cardiopatia ischemica, amiloidosi cardiaca, cardiomiopatia dilatativa, ipertensione polmonare primitiva e variazioni di funzione ventricolare sinistra come risultato di terapie farmacologiche. L’MPI risulta essere modificato anche in pazienti asintomatici che presentano fattori di rischio come il diabete mellito e l’ipertensione arteriosa. Orem et al. ha registrato variazioni dell’MPI in una popolazione diabetica con diversi gradi di albuminuria. Più recentemente, l’MPI ha mostrato risultati promettenti nella valutazione della funzione ventricolare prenatale e in bambini e adulti con malattie cardiache congenite. L'obiettivo di questa tesi è quello di analizzare le applicazioni cliniche dell’ MPI in diverse condizioni fisiologiche e patologiche, chiarendo alcuni aspetti della dinamica ventricolare sinistra. Nel primo studio, abbiamo dimostrato che la geometria ventricolare sinistra rappresenta un fattore determinante della performance del miocardio. In realtà, i nostri dati dimostrano una correlazione tra MPI e spessore relativo di parete ma non con la massa indicizzata con la superficie corporea. La dipendenza dell’MPI dalla geometria di camera ventricolare deve essere presa in considerazione durante l'applicazione dell’indice per la valutazione della performance miocardica come marcatore prognostico nella malattia cardiaca in cui la geometria ventricolare può essere modificata. Nel secondo studio l’MPI è stato valutato per l’identificazione delle anomalie cardiache subcliniche in un gruppo omogeneo di pazienti asintomatici con diabete mellito tipo 2, di recente diagnosi, con o senza ipertensione arteriosa. L’incremento dell’MPI è dovuto principalmente ad un prolungamento della IRT. Una correlazione tra MPI e il valore di HbA1c è risultata significativa indicando il suo ruolo come marker precoce di controllo metabolico. I nostri risultati potrebbero avere importanti implicazioni cliniche. In primo luogo, questo indice potrebbe rappresentare un facile approccio per individuare una fase precoce di cardiomiopatia diabetica che preceda la disfunzione diastolica, quindi monitorare la storia naturale della malattia diabetica stessa. In secondo luogo, l’MPI potrebbe essere utile per valutare indirettamente il controllo metabolico o suggerire un rapido avvio di specifici trattamenti farmacologici che possano aiutare il decorso clinico della cardiomiopatia diabetica. Una diagnosi precoce di cardiomiopatia diabetica tramite l’MPI non è solo importante, ma può anche rivelarsi essenziale per testare nuovi approcci terapeutici in corso di malattia diabetica. Infine, nel terzo studio, l’MPI sembra essere una tecnica non invasiva sensibile per l’individuazione sub-clinica di una disfunzione ventricolare sinistra in pazienti con sclerosi multipla trattati con basse dosi di mitoxantrone, un agente antineoplastico della famiglia degli antracenedioni. Tale indice sembra fornire migliori informazioni prognostiche per quanto concerne il rischio di cardiotossicità, rispetto alle misurazioni ecocardiografiche convenzionali. Pensiamo che l’MPI possa essere un parametro aggiuntivo all'ecocardiografia convenzionale nel monitoraggio degli effetti collaterali cardiaci, in grado di individuare una cardiotossicità subclinica da mitoxantrone. In conclusione, una semplice misura Doppler-derivata in grado di esprimere la performance globale del miocardio, è correlata alla complessa funzione cardiaca e sembra essere un indicatore utile di risultati clinici, rappresentando un indice aggiuntivo per la diagnosi e per la gestione clinica dei pazienti con molte malattie non solo cardiache ma anche sistemiche.Recently, 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.
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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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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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 systemic co-morbidities associated with COPD, which includes ischaemic heart disease (IHD). Despite the knowledge that approximately 22% of COPD patients also suffer from underlying IHD, the cardiovascular safety of muscarinic antagonists, such as ipratropium, has not been tested in a non-clinical setting of IHD or MI. In order to address this, the current project was designed to investigate, for the first time, the effects of ipratropium on the myocardium in a non-clinical setting. It was identified that under normoxic conditions, ipratropium did not have a significant effect on cardiac myocyte viability or infarction, from 3 month Sprague Dawley rats. In addition to this, following simulated ischaemia, ipratropium also did not appear to exacerbate myocardial injury. However, when ipratropium was administered in the context of simulated ischaemia followed by reperfusion, there was a significant exacerbation in myocardial injury which was characterised by increases in infarction, apoptosis, necrosis and a loss of resilience of oxidative stress. In order to characterise the mechanism by which ipratropium exerts the observed cardio-toxic effects, it was investigated whether acetylcholine (ACh) or cyclosporin A (CsA) were capable of attenuating the ipratropium induced cardiotoxicity. Both agents showed significant limitation of injury when co-administered with ipratropium indicating that ipratropium exerts its cardio-toxic effect through a mechanism which links muscarinic signalling to the mitochondrial permeability transition pore (mPTP). This supports previously published work where the protective signalling of ACh has been shown to promote the phosphorylation of pro-survival kinases, such as Akt and Erk1/2 and that this provides inhibition of the mPTP. Western blotting was employed to identify whether there was an involvement of the pro-survival kinases Akt and Erk1/2, as well as the stress induced kinase JNK. Ipratropium significantly increased levels of phospho-Akt and phospho-Erk1/2. However, JNK levels appeared to be insignificantly altered in comparison with the control groups. Both ACh and CsA were capable of limiting these increases. Further to this, an aged study was carried out, which showed that, within the aged myocardium, ipratropium is capable of eliciting further injury in comparison with the 3 month age groups. The effect of ipratropium on tolerance of oxidative stress was not significant, but, also, ACh and CsA were shown as unable to protect. Significant levels of JNK were also observed in the aged animals in comparison with the 3 month groups. In combination, the results presented here demonstrate, for the first time, that ipratropium is capable of exacerbating ischaemia/reperfusion injury in in vitro models of myocardial ischaemia/reperfusion. In addition, ACh and CsA are capable of limiting this injury, implying a role for pro-survival kinases and the mPTP in ipratropium induced myocardial injury. In the aged study, ipratropium still exacerbated injury, however, ACh and CsA appeared unable to protect, therefore promoting previous work that cellular signalling is altered in the senescent myocardium. In conclusion, further studies must be carried out in order to fully characterise the cardio-vascular safety profile of ipratropium.
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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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 tissue samples were obtained and rapidly frozen to -80°C. Selected metabolic variables were then compared between the two groups.
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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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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 implanted within the damaged muscle.There 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.)
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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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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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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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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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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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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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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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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 mediated responses is the guanidine nucleotide binding protein (G-protein) linking adrenergic receptor to its effector adenylyl cyclase. The hypothesis that this G-protein may be altered was tested by measuring force and rate in response to G-protein activators and by investigating the cholinergic system, a further G-protein linked receptor on myocardium. A biphasic response to increasing endotoxin exposure was observed not only in adrenergic response but in cholinergic responsiveness. Altered response was noted after endotoxin exposure at the G-protein site of both receptor systems when activated by chorera toxin and by sodium fluoride. Similar deficits in response to direct activation of adenylyl cyclase were not noted. The calcium channel is also G-protein linked and response to increase in extracellular calcium ion concentration was also measured and observed to be impaired after endotoxin exposure. The overall contractile ability of endotoxin exposed atria was assessed using controlled hypothermia combined with increased calcium ion concentration. This technique demonstrated a preserved contractile ability in endotoxin exposed atria. These data were consistent with significant alterations at the G-protein level underlying the myocardial response to endotoxaemia.
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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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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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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 depression due to the lack of a good physiological model of the disease. Objective: To develop a model of in-vivo cardiac arrest and resuscitation in order to characterize the biology of the associated myocardial dysfunction and test potential therapeutic strategies. Methods and Results: We developed a rodent model of post arrest myocardial depression (DCD model) using extracorporeal membrane oxygenation for resuscitation, followed by invasive haemodynamic measurements. In isolated cardiomyocytes, we assessed mechanical load and Ca2+-induced Ca2+ release (CICR) simultaneously using the microcarbon fiber technique and observed reduced function and myofilament calcium sensitivity in the post arrest group. Additionally, in contrast with findings from Langendorff models of ischemia-reperfusion, there is a marked augmentation of CICR in isolated cells. This increase in calcium serves to maintain contraction in the face of myofilament dysfunction and, it seems to be mediated by autophosphorylation of calcium-calmodulin protein kinase II (CAMKII). It is further dependent on ryanodine receptor calcium but not PKA leading us to speculate that it is triggered by adrenergic activation but maintained by CAMKII. Finally, activation of aldehyde-dehydrogenase II by the small molecule Alda-1 dramatically improved whole animal and cellular contractile performance after arrest, and restored CICR to close to normal levels. Conclusions: Cardiac arrest and reperfusion lead to calcium cardiac memory, which support cardiomyocyte contractility in the face of post arrest myofilament calcium sensitivity. Alda-1 mitigates these effects and improves outcome.
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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.Includes 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.
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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 repair and healing, peaking at day 5. The monocyte response in humans following AMI is currently poorly understood. Due to their central role in the pathogenesis of AMI, monocytes are attractive both as potential biomarkers to inform of extent of myocardial injury (and recovery) and also as therapeutic targets with the specific targeting of monocytes in experimental models resulting in reduced infarction size and improved LV remodelling. However, in spite of these promising results and our greater understanding of the pathogenesis of AMI, no immune-modulating therapeutic has been translated into routine clinical practice. We therefore hypothesized that characterisation of the monocyte response to AMI by flow cytometry and gene expression profiling in both experimental models and humans would give novel insights into underlying biological processes and function (both locally in the myocardium and systemically), identify novel therapeutic targets, enable their use as cellular biomarkers of disease, and test conservation between species validating the experimental model for future investigation. Classical inflammatory monocytes were found to significantly increase in the peripheral blood 48 hours following AMI in both mice and humans, with the magnitude of the monocyte response correlating with the extent of myocardial injury in both species. Gene expression profiling of peripheral circulating monocytes following AMI identified a number of candidate genes, biological pathways and upstream regulators that were conserved between species and that could represent novel therapeutic targets. Furthermore, in an experimental model of AMI, leukocytes appeared to have effects beyond the ischaemic myocardium, with leukocyte recruitment in remote myocardium and in kidneys associated with elevated inflammatory markers and endothelial activation.
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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 offers a unique capability to localize and measure subendocardial ischemia. A common technique for calculating MBF from dynamic contrast-enhanced cardiovascular MR (DCE-CMR) is to track a bolus of contrast agent and measure MBF using fully quantitative methods. These methods which are based on central volume principle deconvolve the changes in the concentration of the injected contrast agent in the tissue with the arterial input function (AIF). However deconvolution is inherently a difficult process and therefore numerically unstable with noise contaminated data. The purpose of this study is to enable high spatial resolution voxel-wise quantitative analysis of myocardial perfusion in DCE-CMR, in particular by finding the most favourable quantification algorithm in this context. Voxel-wise quantification has the potential to combine the advantage of visual analysis with the objective and reproducible evaluation made possibly by a true quantitative assessment. Four deconvolution algorithms – Fermi function modelling, deconvolution using B-spline basis, deconvolution using exponential basis and Auto-Regressive Moving Average modelling (ARMA) were tested to calculate voxel-wise perfusion estimates. The algorithms were developed on synthetic data and validated against a true gold-standard using a hardware perfusion phantom and an explanted perfused pig heart. The accuracy of each method was assessed for different levels of spatial resolution. Moreover robustness of each deconvolution algorithm to variation in perfusion modelling parameters was evaluated. Finally, voxel-wise analysis was used to generate high resolution perfusion maps on real data acquired from healthy volunteers and patients with coronary artery disease. Both simulations and maps in the hardware phantom, explanted pig heart data and patient studies showed that voxel-wise quantification of myocardium perfusion is feasible and can be used to detect abnormal regions with high sensitivity in identifying the tissue at risk. In general ARMA and the exponential method showed to be more accurate, on the other hand, Fermi model was the most robust method to noise with highest precision for voxel-wise analysis. Inevitably the choice of quantification method for data analysis boils down to a trade-off between accuracy and precision of the estimation.
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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 ultimately leads to the development of the overt phenotype in genetic mutation carriers. Furthermore, the contribution of fibrosis on myocardial function has been poorly defined. In this thesis, I identified that myocardial genetic expression of collagen is upregulated in patients with HCM and this is paralleled by elevated levels of procollagen in plasma. The genetic expression of transforming growth factor beta (TGF-β) and its downstream mediator connective tissue growth factor was also enhanced in HCM and correlated with collagen I and III RNA levels, suggesting a central role of TGF-β in mediating fibrosis. Plasma markers of collagen synthesis and metabolism were also increased in sarcomeric mutation carriers without hypertrophy, suggesting that fibrosis may be an early process that contributes to the development of the overt phenotype. Plasma levels of procollagen I were higher in patients with non-sustained ventricular tachycardia and focal fibrosis identified by CMRI was associated with impaired systolic deformation. Diffuse fibrosis beyond that seen in healthy controls also correlated with a reduction in systolic function. Together, the findings of this thesis support the hypothesis that myocardial fibrosis is an active process in HCM that precedes clinical phenotype. Myocardial fibrosis is at least in part mediated by the TGF- β pathway and associated with impaired systolic performance and may contribute to arrhythmic risk in HCM.
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Joyeux-Faure, Marie. "Heat stress and myocardial protection." Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE18004.
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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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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 prediction of functional recovery by characterising myocardial tissue, but these have not been extensively evaluated. Methods:- Patients following reperfusion for first-presentation ST-elevation AMI were scanned by CMR acutely, subacutely and in convalescence. Tissue pathologies visible on acute CMR were evaluated for their ability to predict recovery of contractile function. Oedema in the peri-infarct zone, microvascular obstruction (MO) and intramyocardial haemorrhage (IMH) in the infarct zone, and extracellular volume (ECV) of the infarct zone were evaluated. In addition, susceptibility-weighted MR imaging (SW-MRI) was evaluated against the reference standards of T2-weighted and T2* imaging to detect the known prognostic marker of IMH. Results:- Acutely oedematous myocardium demonstrated recovery of function over time (p<0.05), whereas non-oedematous peri-infarct myocardium did not (p>0.05). Recovery of function closely mirrored resolution of oedema. Infarct contractile recovery was attenuated in infarcts that demonstrated MO acutely as compared to those without (p<0.01), and attenuated further in those that demonstrated IMH acutely (p<0.01). SW-MRI had sensitivity 93% and specificity 86% as compared to T2-weighted imaging, with excellent inter-observer reliability and shorter breath-hold times (4 seconds vs. 16 seconds). Infarct ECV had higher accuracy to predict improved wall motion than late gadolinium enhancement imaging (c-statistic 0.80 vs. 0.70, p=0.04). Conclusion:- Tissue characterisation by CMR offers a variety of ways to predict functional outcome following AMI, using both established and novel imaging techniques.
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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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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 fiber-optic spectroscopic system. Spectral acquisition was performed on - (1) the normal heart region; (2) the region immediately surrounding the infarct; and (3) the infarcted region - one, two, three and four weeks into MI development. The spectral data were divided into six subgroups according to the histopathological features associated with various degrees / severities of myocardial tissue injury as well as various stages of myocardial tissue remodeling, post infarction. Various data processing and analysis techniques were employed to recognize the representative spectral features corresponding to various histopathological features associated with myocardial infarction. The identified spectral features were utilized in discriminant analysis to further evaluate their effectiveness in classifying tissue injuries induced by MI. In this study, it was observed that MI induced significant alterations (p < 0.05) in the diffuse reflectance spectra, especially between 450 nm and 600 nm, from myocardial tissue within the infarcted and surrounding regions. In addition, MI induced a significant elevation in fluorescence intensities at 400 and 460 nm from the myocardial tissue from the same regions. The extent of these spectral alterations was related to the duration of the infarction. Using the spectral features identified, an effective tissue injury classification algorithm was developed which produced a satisfactory overall classification result (87.8%). The findings of this research support the concept that optical spectroscopy represents a useful tool to non-invasively determine the in vivo pathophysiological features of a myocardial infarct and its surrounding tissue, thereby providing valuable real-time feedback to surgeons during various surgical interventions for MI.
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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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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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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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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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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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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. Ultrastructural studies revealed significant lipid and glycogen accumulation, dilatation of the sarcoplasmic reticulum and damage to the mitochondria in left ventricles of the diabetic animals.
Administration of ISO to both control and diabetic animals resulted
in atrial tachycardias and ventricular fibrillation. The severity of the arrhythmias and the overall mortality was the same in both groups of animals. Serum analyses revealed significantly greater increases in blood glucose, free fatty acids, total cholesterol and creatine kinase activity in the ISO-treated diabetic animals relative to ISO-treated controls. ISO treatment of both control and diabetic animals produced similar increases in heart weight, left ventricular weight and myocardial water content. Analyses of various subcellular organelle marker enzyme activities indicated a significantly greater decrease in the K⁺ ,Ca²⁺ -stimulated sarcoplasmic reticulum ATPase of ISO-treated diabetic animal hearts. In addition, significantly greater increases in Ca and hydroxyproline and decreases in the levels of ATP were evident in the ISO-treated diabetic animal hearts. Ultra-structural studies revealed significant damage to the mitochondria in both ISO-treated control and diabetic hearts, the magnitude of the damage being greater in the diabetic animals. Mitochondria from both groups of animals showed swelling and fragmentation, myofibrils appeared
as a homogeneous mass and did not show the characteristic Z-lines. Glycogen depletion and lipid accumulation was observed in both groups of animals. In addition, both groups of animals showed amorphous dense bodies in the mitochondria after ISO-treatment. After 40-minutes occlusion of the left circumflex coronary artery followed by 60-minutes of reperfusion, hemodynamic measurements revealed significant decreases in the left ventricular and systemic arterial pressures in the diabetic animals relative to controls. Analyses
of subcellular organelle enzymes from the ischemic tissue revealed that sarcolemmal Na⁺ ,K⁺ -ATPase, mitochondrial ATPase and sarcoplasmic reticulum ATPase activities were decreased after coronary occlusion in both control and diabetic animals. However, upon reperfusion, unlike the control, no recovery of the mitochondrial ATPase was observed in the diabetic animals. In addition, a further depression of both the sarcolemmal and sarcoplasmic reticulum ATPase activities were seen in the diabetic animals compared to controls on reperfusion. Ion measurements revealed a significant accumulation of calcium in both control and diabetic animals, the magnitude of the increase being greater in the diabetic animals. Similarly, both tissue ATP levels and the ability of the mitochondria to generate ATP were depressed in the diabetic animals as compared to controls following coronary artery occlusion and reperfusion. Following coronary artery ligation and reperfusion, the diabetic animals showed a significantly higher incidence of ventricular fibrillation and cardiogenic shock as compared to controls. Ultrastructural studies revealed myocardial
damage to both control and diabetic hearts following coronary artery ligation and reperfusion. However, the diabetic myocardium showed a higher incidence and frequency of hypercontraction bands, an increase in the amorphous dense bodies and slightly greater damage to the mitochondria.
Coronary artery ligation in conscious control, 6 and 12 week-diabetic rats resulted in post-ligation arrhythmias (especially ventricular fibrillation), the incidence of which was much greater in the diabetic animals. The mortality rate of 12-week diabetic rats undergoing coronary ligation was 100% within 1-7 minutes following ligation. No differences in occluded or infarcted zones of the surviving 6-week diabetic and control rats were detected. Analyses of ionic composition revealed a significant magnesium deficiency in the diabetic
hearts as compared to controls.
These data indicate that the diabetic animals show a greater susceptibility
of the myocardium to ischemic injury. Although numerous metabolic and chemical alterations are present in the diabetic myocardium,
it is possible that magnesium deficiency may be a factor determining
the higher incidence of arrhythmias and ischemic injury in diabetic animals.Pharmaceutical Sciences, Faculty of
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