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O'Sullivan, Christine Ann. "Electromechanical changes in ischaemic heart disease". Thesis, Imperial College London, 2006. http://hdl.handle.net/10044/1/8251.
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In coronary artery disease,. resting electrical and mechanical function of the left ventricle may vary according to different presentations. Stress or exercise in these patients results in electrical disturbances, which may havc mechanical consequences. The objectives ofthis thesis were: I) to assess the effect of the presence and location of Q wave myocardial infarction on left ventricular segmental mechanical function and identify patterns ofdisturbances. 2) to study the acute implications of induction of localised myocardial infarction at the proximal ventricular septum on ventricular performance. 3) to determine the effect of pharmacological stress on left and right ventricular behaviour in patients with coronary artery disease. AIl patients were studied by Doppler echocardiography using conventional measurements, as well as detailed assessment of long axis function and 12 lead surface EeG's. The foHowing groups ofpatients were studied: a). 72 patients with old Q wave MI; 35 anterior and 37 inferior. b) 54 patients with old anterior MI; 39 Q wave and 15 non-Q wave MI. c) 20 symptomatic patients with hypertrophic obstructive cardiomyopathy before and after non-surgical septal reduction therapy. d) . 27 patients with coronary artery disease, at rest and during dobutamine stress to assess left ventricular fune:tion. e) 33 patients with triple coronary artery disease at rest and at peak dobutamine stress to assess right ventricular function. The normal septal Q wave was' absent in 94% of anterior and 8% of inferior MI patients. Long axis amplitude and shortening and lengthening velocities were globaIly reduced in anterior and inferior myocardial infarction and the onset of shortening and lengthening were delayed by 30-40ms and 20-30 ms respectively in the two patient groups. Post ejection ~hortening was localised to the septum in the majority of patients with anterior myocardial infarction, but was generalised in patients with inferior infarction. 1) The normal septal Q wave was absent in 10% of control subjects and in 46% of patients with non-Q wave myocardial infarction. Q wave anterior MI was associated with a scarred septum and dilated LV cavity. Long axis amplitude was not different from normal in non-Q wave-infarction, but its onset ofshortening and lengthening was delayed by 20ms. Post ejection shortening occurred more frequently in Q wave infarction (76%) compared with non-Q wave infarction (21 %). These .abnormalities were localised to the left rand septal sites in non-Q wave infarction in contrast to their global distribution in Q wave infarction. . 2) Induction of localised upper septal myocardial infarction with alcohol resulted in broadening of the QRS (by 35ms), RBBB in 80% of patients, development of reduced septal long axis amplitude, and accentuated post ejection shortening at the septal long axis site. 3) In contrast to controls, dobutamine stress results in progressive broadening of QRS duration and prolongation of the QTc interval in patients with coronary artery disease, with corresponding reductions in long axis amplitude of motion and peak lengthening .velocity. 4) In patients with triple vessel coronary disease, dobutamine stress results in right ventricular long axis ischaemic disturbances similar to those seen on the left. Failure ofright ventricular long axis amplitude to increase by 2 mm was 88% specific for detecting right ventricular ischaemic dysfunction, which also correlated with the attenuated cardiac output at peak stress r= 0.56, p
2
Claesson, Maria. "Women's hearts : ischaemic heart disease and stress management in women". Doctoral thesis, Umeå : Department of Public Health and Clinical Medicine, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-725.
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Horan, P. G. "Unravelling the genetic basis of ischaemic heart disease". Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426746.
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Byrne, Conor James. "Ischaemic and pharmacological preconditioning of the uraemic heart". Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8831.
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The incidence and mortality from cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) far exceeds that seen in the general population. Whilst a number of risk factors and associations have been identified in patients with CKD that may contribute to the increased risk of CVD, our understanding of the underlying pathophysiology remains poor. It has previously been reported that uraemic animals sustain larger myocardial infarcts and that this ‘reduced ischaemia tolerance’ may in part explain the excess mortality from CVD seen in CKD patients. The aim of this work was to establish an in vivo model of uraemic myocardial infarction in order to further explore the pathophysiology of uraemic CVD with particular focus on ameliorating myocardial ischaemia-reperfusion injury using ischaemic and pharmacological preconditioning. An increase in myocardial infarct size was demonstrated in the sub-total nephrectomy model of chronic uraemia, confirming previous reports in the literature. However, infarct size was not found to be increased in adenine diet induced renal failure. In addition, it was demonstrated for the first time, that the techniques of ischaemic preconditioning (IPC) and remote ischaemic preconditioning (RIPC) are both efficacious and not attenuated by chronic uraemia induced by sub-total nephrectomy or adenine diet (IPC only). Investigations were undertaken using an agent (a HIF stabiliser, FG4497) to induce pharmacological preconditioning in both animals with renal insufficiency and those without. These studies demonstrate that stabilisation of hypoxia inducible factor (HIF) may be a promising strategy to induce pharmacological preconditioning. It is hoped that this work may lay the foundations for future investigations to determine why sub-totally nephrectomised rats have larger infarcts whilst those with adenine induced renal failure, with a substantially greater degree of renal dysfunction, do not. Moreover, it is hoped that; by demonstrating that uraemia 3 does not prevent or attenuate the myocardial protection afforded by ischaemic preconditioning, the recruitment of patients with CKD will be encouraged to clinical trials of both ischaemic preconditioning and other therapies to limit myocardial infarction.
5
Awad, Wael Ibrahim Issa. "Ischaemic preconditioning in the neonatal rat heart". Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391636.
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O'Kane, Peter Danny. "The role of nitric oxide in ischaemic heart disease". Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420333.
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Mackie, Eileen Elizabeth. "Exercise and haemostasis in health and ischaemic heart disease". Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433574.
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Teece, Stewart. "The assessment of ischaemic heart disease in the emergency department". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499952.
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Wright, Robert Anthony. "Hyperinsulinaemia, insulin resistance and endogenous fibrinolysis in ischaemic heart disease". Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21618.
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The work presented in this thesis has explored the hypotheses that disturbances of insulin and of endogenous fibrinolysis are a feature of patients with established ischaemic heart disease and investigated the potential manipulation of these by an inhibitor of the angiotensin converting enzyme. The possibility that the presence of either a previous myocardial infarction or of heart failure might influence the development of hyperinsulinaemia was studied. Only patients with heart failure showed fasting hyperinsulinaemia, whereas the increased insulin response to an oral glucose load in those with heart failure or previous myocardial infarction was similar, and greater than the response in patients with stable angina. Hyperinsulinaemia has been previously associated with impaired peripheral muscle glucose uptake and metabolism and might contribute to the development of muscular fatigue on exertion in patients with previous myocardial infarction or with heart failure. Amongst patients with ischaemic heart disease who had a normal fasting plasma glucose, one fifth had impaired glucose tolerance on formal testing and this group exhibited significantly greater fasting and stimulated hyperinsulinaemia. Including all patients, there was an inverse relationship between left ventricular ejection fraction and fasting plasma insulin concentration. Impaired endogenous fibrinolysis has been associated with an adverse prognosis in patients with ischaemic heart disease. The effect of captopril upon tissue-type plasminogen activator and on plasminogen activator inhibitor type 1 was investigated in patients with recent uncomplicated myocardial infarction. Captopril caused a significant reduction in antigen levels of both type plasminogen activator and on plasminogen activator inhibitor type 1. This may help to explain the reduction in acute coronary syndromes that has been associated with the use of captopril following acute myocardial infarction.
10
See, Hoe Louise. "Mechanisms and Clinical Utility of Sustained Ligand-Activated Preconditioning". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/365566.
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Ischaemic heart disease (IHD) remains a leading cause of global morbidity and mortality, with persistent prevalence in Western populations, and a growing incidence in the developing world. Myocardial ischaemic injury is alleviated through surgical intervention, detrimentally exposing the heart to reperfusion injury. This inevitable and paradoxical injury has driven a field of cardioprotective research aimed at limiting cell death, enhancing standard reperfusion protocols and improving long-term patient outcomes from ischaemia/reperfusion (I/R) injury. Despite promising laboratory results, clinical translation of cardioprotective interventions remains an unrealised goal. Notably, age, co-morbidities and chronic pharmacotherapy negatively influence the efficacy of cardioprotective interventions aimed at limiting I/R injury. Thus, effective interventions that reduce myocardial I/R injury in the settings of ageing and disease are fundamental. Based upon this fundamental premise, this doctoral project investigates a novel opioid therapy termed sustained ligand-activated preconditioning (SLP). Previous work demonstrated that SLP is superior to conventional cardioprotection through engagement of alternative signalling pathways, and exhibits potent and prolonged efficacy in young to aged hearts. Studies executed in this doctorate aimed to further delineate the specific mechanisms involved in generation of the protected SLP phenotype, and determine the clinical utility of SLP using other relevant models of disease and chronic pharmacotherapy.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Bell, Derek. "The acute inflammatory response to myocardial infarction". Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/26295.
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Workman, A. J. "A study of adenosine triphosphate-sensitive potassium channels in rat hearts". Thesis, De Montfort University, 1996. http://hdl.handle.net/2086/4147.
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Moore, Ann Lavinia. "Beta-adrenergic receptor antagonists and exercise radionuclide angiocardiography in patients with proven coronary artery disease". Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361290.
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Elfawal, Mohammed Amin. "A pathological study of sudden coronary death in Glasgow". Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254218.
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Spriggs, David Arthur. "Risk factors for stroke : a case-controlled study". Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308766.
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Pell, Theresa Jane. "The involvement of ATP-sensitive potassium channels in novel forms of myocardial protection". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314289.
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Shaw, Linda Anne. "The influence of platelet derived factors and cholesterol on arrhythmogenesis". Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260369.
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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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Edwards, Natalie. "Myocardial Work Assessment by Non-Invasive Pressure-Strain Relations". Thesis, Griffith University, 2021. http://hdl.handle.net/10072/404458.
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Background. Left ventricular (LV) dysfunction, which is the inability of the LV to pump blood effectively, constitutes the final common pathway for a host of cardiac disorders. The morbidity, mortality and healthcare cost associated with heart failure make the detection and prevention an attractive option before irreversible myocardial damage occurs. Initial diagnosis of LV dysfunction is through echocardiography, which, predominately relies on two-dimensional ejection fraction (EF) however, is fraught with limitation. Global longitudinal strain (GLS) is an established method for subclinical diagnosis of heart disease, however, is sensitive to changes in afterload leading to misinterpretation of true contractile function. Myocardial work (MW) is a recent echocardiographic modality derived from non-invasive LV pressure-strain loops and addresses the afterload limitation of GLS.
Aims. The thesis investigates the use of MW against conventional echocardiographic parameters in hypertensive heart disease, ischaemic and non-ischaemic cardiomyopathy and ischaemic heart disease. It is hypothesised that MW indices will be more sensitive than GLS and provide a new dimension in the clinical evaluation of LV dysfunction.
Methods. Patients enrolled in the CATHARSIS research program performed at The Prince Charles Hospital who have comprehensive echocardiographic studies followed by invasive coronary angiography will be investigated. All echocardiographic measurements were performed in according to the current echocardiographic guidelines. GLS and MW analysis was calculated utilising speckle tracking echocardiography via vendor specific modules (EchoPAC Version 202, GE Vingmed Ultrasound, Norway). MW was derived from derived from non-invasive LV pressurestrain loops indexed to brachial systolic blood pressure. MW indices obtained include: Global myocardial work index (GWI) – a global representation of MW; Constructive MW (CW) – the sum of positive work due to myocardial shortening during systole and negative work due to lengthening during isovolumic relaxation; Wasted MW (WW) – energy loss by myocardial lengthening in systole and shortening in isovolumic relaxation; Myocardial work efficiency (GWE) – derived from the percentage ratio of CW to the sum of CW and WW.
Results. The first research paper demonstrated that patients with early-stage hypertensive heart disease have seemingly normal EF and GLS, however, MW revealed that the LV is functioning at a higher energy level to overcome the resistance of higher arterial pressures. If there is a long-term and sustained increase in MW caused by hypertension, eventual remodelling of the myocardium will occur with heart failure the major consequence. MW provides an ability to detect increased work of the heart in order to prevent the sequalae of events through modification of therapy. Coexistent with low EF and GLS, patients with ischaemic and nonischaemic cardiomyopathy have significantly lower levels of MW which was due to a combination of decreased CW along with increase WW. This is indicative of LV remodelling characterised by ventricular dilatation and contractile dysfunction. The second research paper demonstrated the ability of MW to identify patients with single and multi-vessel coronary artery disease (CAD). This was possible despite the absence of visually detectable regional wall motion abnormalities and no prior history of ischaemic heart disease. In patients with CAD, GWI along with CW were both reduced while WW was increased reflecting the metabolic adaptation of the myocardium in the presence of CAD. The third research paper facilitated the delineation of patients with a false-positive from a true-positive exercise stress echocardiogram, despite normal resting LV systolic function and the absence of visually detectable resting regional wall motion abnormalities. This was possible despite single or multi-vessel CAD. Patients with a positive exercise stress echo and significant CAD on coronary angiography had a reduction in GLS and GWI from a combination of reduced CW and increased WW. The fourth research paper demonstrated the contractile reserve response to exercise and revealed a compromised contractile reserve assessed by myocardial deformation and work. Interestingly, as a result of more significant coronary lesions, patients that were treated using surgical bypass demonstrated a greater deterioration in MW indices at peak exercise compared to those that could be managed using percutaneous options.
Conclusions. The work contained within this thesis has contributed to the diagnostic capabilities of ultrasound in the subclinical diagnosis of LV dysfunction. MW provides a more detailed assessment of intrinsic myocardial function and is an additional technique to assist in the detection of early cardiovascular disease under different loading conditions. This may be important in the future evaluation of patients with heart failure, hypertension and those with ischaemic heart disease where the EF is normal or at the lower limit of normal.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School Allied Health Sciences
Griffith Health
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Swann, Ian D. "Studies of the kallikrein-kinin system in normal and ischaemic rat hearts". Thesis, University of Essex, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236512.
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Spence, M. S. "Family based investigation of the genetic basis of ischaemic heart disease". Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268983.
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Chia, Stanley. "Endothelial function and endogenous fibrinolysis in inflammation and ischaemic heart disease". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29061.
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In a series of studies, we explored the effects of inflammation on endothelial vasomotion and fibrinolytic capacity using an in vivo forearm model of systemic and local inflammation. Systemic inflammation stimulated by typhoid vaccination had no major effect on vasomotor tone. However, tumour necrosis factor-α induced local vascular inflammation was associated with impaired resistance vessel endothelium-dependent vasodilatation, possibly through the development of acute arterial injury. Both systemic and local inflammation were found to augment the acute release of endothelial tissue plasminogen activator. In addition, intra-arterial tumour necrosis factor-α administration resulted in a unique profile of substantial and sustained local increase in endogenous tissue plasminogen activator. We extended these investigations and assessed the role of endogenous fibrinolysis and endothelial dysfunction in the pathogenesis of prothrombotic conditions such as hyperhomocysteinaemia and coronary stent thrombosis or in-stent restenosis using this forearm model of endothelial function assessment. In patients with recent myocardial infarction, elevation of plasma homocysteine concentration was associated with impaired endothelium-dependent vasodilatation but not endogenous fibrinolysis. This vasomotor dysfunction was not rectified by vitamin supplementation. We also assessed three critical aspects of vascular function in patients who have undergone percutaneous coronary intervention and found no evidence that endothelial vasomotor, fibrinolytic or platelet function play a major role in the pathogenesis of acute stent thrombosis or in-stent restenosis. We conclude that there is complex interaction between inflammation, endothelial endogenous fibrinolysis. Modulating cytokine actions and their interaction with fibrinolysis may be critical in the prevention of thrombotic coronary occlusion and myocardial ischaemia as well as in the future development of anti-thrombotic therapies.
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McCance, Alastai J. "Systemic and cardiac noradrenaline kinetics in ischaemic heart disease in man". Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235891.
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Siva, Anjana. "The genetic basis of hyperhomocysteinaemia in patients with ischaemic heart disease". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619625.
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Zhang, Huajun. "Functional characterisation of cardiac progenitors from patients with ischaemic heart disease". Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:3b8a7199-c077-436c-bb89-cd354efe4414.
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Ischaemic heart disease (IHD) is the leading cause of death worldwide. Currently, even optimal medical therapies do not attenuate deterioration of the left ventricular (LV) function completely. Stem cell therapies, and recently cardiac stem cell therapies, have emerged as potential novel treatments for IHD. However, clinical evidence from randomised controlled studies has shown mixed results. Thus understanding what patient-related factors may affect the therapeutic performance of the cells may help improving treatment outcomes. The studies described in this thesis aim to understand how cardiac progenitor cells (CPCs) can re-vascularise ischaemic myocardium and promote functional repair of the heart. Resident CPCs were isolated and expanded from the right atrial appendage of 68 patients following the ‘cardiosphere’ method (cardiosphere-derived cells or CDCs). They resemble mesenchymal progenitors as they lack the expression of endothelial and haematopoietic cell surface markers but express mesenchymal progenitor cell markers (e.g. CD105, CD90). Cell function was evaluated by support of angiogenesis, mesenchymal lineage differentiation potential in vitro, and improvement in heart function in vivo. Notably in vitro, CDC from different patients differed in their angiogenic supportive and differentiation potentials. In a rodent model of myocardial infarction (MI), transplantation of CDC reduced infarct size significantly (p<0.05). However, only those CDCs with a robust pro-angiogenic ability in vitro improved vessel density and heart systolic function (p<0.05) in vivo. A multiple regression model, which accounted for 51% of the variability observed, identified New York Heart Association (NYHA) class, smoking, hypertension, type of ischaemic disease and diseased vessel as independent predictors of angiogenesis. In addition, gene expression analyses revealed that differential gene expression of several extracellular matrix components (e.g. CUX1, COL1A2, BMP1 genes and microRNA-29b) could explain the differences observed in CDC’s vascular supportive function. In summary, this is the first description of variability in the pro-angiogenic and differentiation potential of CDCs and its correlation with their therapeutic potential. This study indicates that patient stratification may need to be included in the design of future trials to improve the efficacy of cell-based therapies.
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Smith, Felicity Barbara. "Role of fibrinogen and fibrin D-dimer in peripheral arterial disease". Thesis, University of Glasgow, 1998. http://theses.gla.ac.uk/30947/.
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This thesis is composed of two studies. The principal aim of the first study, the Sites of Atheroma Study, was to determine whether plasma fibrinogen, fibrin D-dimer and other haemostatic factors (von Willebrand Factor and plasminogen activator inhibitor - type I) were related to the angiographic site and severity of atherosclerosis in the arteries of the lower limb. The principal aim of the second study, the Prognostic Study of Intermittent Claudication, was to determine whether plasma fibrinogen, fibrin D-dimer and other haemostatic factors (von Willebrand Factor and tissue plasminogen activator), were related to the future incidence of atherothrombotic events, and deterioration of peripheral arterial disease in subjects with intermittent claudication. The study samples in both studies consisted of men and women with ischaemic symptoms in the lower limb referred to the Peripheral Vascular Clinic, Royal Infirmary of Edinburgh. In the Sites of Atheroma Study, 192 patients referred for angiography were categorised by site and severity of peripheral atherosclerosis using the Bollinger angiographic scoring system. A clinical examination was conducted on each patient including the administration of a questionnaire and taking of a blood sample for the measurement of haemostatic factors. In the Prognostic Study, 607 patients with intermittent claudication who had had a comprehensive examination at baseline, including measurement of haemostatic factors, were followed up over six years to determine the incidence of fatal and non-fatal ischaemic heart disease and stroke and deterioration of peripheral arterial disease. Follow-up data were obtained from hospital records, general practitioners, self-administered questionnaires, the Information and Statistics division of the Common Services Agency and the Scottish National Health Service Central Registry. Results from the Sites of Atheroma Study indicated that 34 (17.7%) patients had predominantly aorto-iliac disease, 85 (44.3%) had femoro-popliteal disease and 73 (38.0%) had dual-site disease. There were no significant differences in the mean levels of the haemostatic factors between patients with disease affecting different sites. An independent relationship was found between nephelometric fibrinogen and between fibrin D-dimer and disease severity only in the femoro-popliteal arteries. On multiple regression, fibrinogen remained independently associated with disease severity in the femoro-popliteal arteries, when life-time smoking or current smoking were taken into account. There was no influence of current smoking on the association between fibrin D-dimer and disease severity but, on inclusion of life-time smoking, the association became non-significant. In the Prognostic Study of Intermittent Claudication, a total of 210 (34.6%) patients died during the six year follow-up period. Of these 90 (42.9%) died from ischaemic heart disease, 29 (13.8%) from stroke and 27 (12.9%) from other vascular causes, including cardiac arrhythmias and ruptured aneurysm. Ninety three (15.3%) patients had a non-fatal myocardial infarction and 79 (13.0%) had a fatal or non-fatal stroke. Forty five (7.4%) patients underwent investigations for peripheral arterial disease and 64 (10.5%) patients progressed to severe chronic leg ischaemia. A total of 203 (33.4%) patients did not have a vascular event or show any deterioration of limb ischaemia. Baseline median levels of plasma fibrinogen, fibrin D-dimer and von Willebrand Factor were significantly higher in patients who died from ischaemic heart disease compared to those who had no vascular events. Tissue plasminogen activator antigen levels were significantly elevated in patients who suffered a stroke. All the relationships between the haemostatic factors and vascular events became weaker and statistically non-significant in analysis adjusting for cardiovascular risk factors and baseline ischaemic heart disease. von Willebrand Factor levels were significantly raised in claudicants who developed severe chronic leg ischaemia (rest pain, ulceration and gangrene). In multivariate analyses adjusting for life-time smoking, fibrinogen became significantly associated with the risk of vascular intervention, and von Willebrand Factor was associated with the risk of severe chronic leg ischaemia. In conclusion, these results indicate that there may be a stronger relationship between chronic smoking and increased fibrin turnover than coagulation in symptomatic peripheral arterial disease. Increased coagulation and fibrinolytic activity may also contribute to thrombosis or progression of atherosclerosis in the coronary and cerebral arteries in claudicants. The effect that fibrinogen, fibrin D-dimer and other haemostatic factors may have on the progression of peripheral arterial disease was mostly independent of cigarette smoking.
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Woodhouse, Peter Robert. "Seasonal variation of cardiovascular disease risk factors in older adults". Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295672.
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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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Tearse, Rachel Stephanie Houston. "Depressive symptoms in ischaemic heart disease in the Western Isles of Scotland". Thesis, UHI Millennium Institute, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417574.
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Russell, Jake S. "Diabetic Modulation of Caveolar Proteins, Infarct Tolerance and Ischaemic Preconditioning". Thesis, Griffith University, 2019. http://hdl.handle.net/10072/387692.
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Ischaemic heart disease (IHD) remains a leading cause of death worldwide and clinical therapies to improve cardiac outcomes following associated acute myocardial infarction (AMI) remain elusive. Subjecting the heart to transient pharmacological or ischaemic conditioning stimuli prior to or immediately following prolonged ischaemia potently protects hearts from ischaemia-reperfusion (I-R) injury in experimental models; however, this is generally ineffective in the clinical setting, where among other factors, patients suffer one or more co-morbidities. Indeed, multi-morbidity is now dominant in those with IHD. Increasingly common diabetes is a major risk factor for AMI, and not only doubles the risk of AMI but may also worsen cardiac injury and impair or negate normally protective conditioning stimuli. However, effects of diabetes on ischaemic tolerance and cardioprotection are highly variable in both humans and animal models, complicating strategic development of protective therapies. Diabetic disease duration and progression may play critical roles in governing myocardial I-R tolerance, and cardiac outcomes may differ in type 1 diabetes (T1D) vs. more widespread type 2 diabetes (T2D).
Changes in I-R tolerance and cardioprotection with diabetes likely involves multiple mechanisms, including disruption of membrane structure and function and depletion of membranous caveolins. These proteins, together with cavins, play critical structural and functional roles in membrane signalling domains, known as caveolae, and appear essential for cardioprotective conditioning and other responses. Emerging evidence indicates caveolin proteins may be sensitive to hyperglycaemia and hyperlipidaemia; however, studies are limited to acute in vitro and T1D models, with effects in relevant chronic models of diabetes warranting further study. While little is known about the regulation of caveolins, they may be depleted with saturated fat vs. increased with the omega-3 fatty acid, α-linolenic acid (ALA). Studies also indicate differential modulation via pharmacological interventions and hyperglycaemic conditions, indicating restoration of caveolins under diabetic conditions may be possible. However, whether such changes are capable of improving outcomes following infarction is unknown. Studies undertaken in the course of this doctoral project therefore aimed to characterise caveolar protein expression, I-R tolerance and cardioprotection in in vitro and in vivo models of T1D and T2D, and to test whether ALA supplementation might improve cardiac outcomes.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Snaith, Christine D. "The use of amino acids to improve the production of high energy phosphates in the ischaemic myocardium". Thesis, Keele University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277152.
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Cullen, James Henry Stuart. "Magnetic resonance imaging in the assessment of myocardial perfusion in ischaemic heart disease". Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29594.
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Five normal volunteers and twenty patients with angiographically proven IHD underwent rest/stress MRI examinations and myocardial scintigraphy for comparison. Five patients had coronary angioplasty and repeat MRI studies three months later. Five patients with Syndrome X were also studied with MRI. MPRI was significantly reduced in patients compared with normals (2.02 0.7 (mean SD), vs 4.21 1.16, p<0.02), with a significant negative correlation of MPRI with percent diameter stenosis of individual coronary lesions (r=-0.81, p< 0.01). MPRI in regions supplied by non-flow limiting lesions (<40% diameter stenosis) was significantly higher than regions supplied by stenoses of 'intermediate' (>40 % to 59%) severity, (2.80 0.77 and 1.93 0.38, p<0.02). Furthermore, MPRI predicted the functional status of the patients reasonably well after revascularisation in this small group. The sensitivity and specificity of quantitative MRI for the detection of global IHD in patients was comparable to thallium-201 scintigraphy (0.89 and 1.0 (sens/spec) vs 0.89 and 1.00) but both were superior to qualitative MRI (0.79 and 0.94). For identifying a significant coronary lesion the sensitivity of quantitative MRI was superior to both qualitative MRI and scintigraphy (0.82, 0.43, 0.75 respectively). The specificity of quantitative MRI was poorer than scintigraphy but similar to qualitative MRI (0.84, 0.89, 0.84). Finally, MPRI in patients with Syndrome X was reduced vs controls (2.17 0.72, p<0.01). Quantitative MRI perfusion studies can provide functional information to detect IHD in patients and assess adequacy of revascularisation. Furthermore, it may be able to provide insight into the mechanism of ischaemia in patients with Syndrome X.
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Sridhara, Bangalore Sitaramiah. "Clinical evaluation of '9'9'mTc tetrofosmin in the detection of ischaemic heart disease". Thesis, University of Surrey, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259561.
Pełny tekst źródła
34
Willems, Laura E., i n/a. "Adenosine and Ischaemia in Young To Aged Hearts". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061011.163451.
Pełny tekst źródłaStreszczenie:
Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.
35
Willems, Laura E. "Adenosine and Ischaemia in Young To Aged Hearts". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365196.
Pełny tekst źródłaStreszczenie:
Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
36
Ridge, Charlotte. "Elemental concentrations in blood from diabetic and non-diabetic coronary artery bypass patients using neutron activation analysis and proton induced X-ray emission analyses". Thesis, University of Surrey, 2001. http://epubs.surrey.ac.uk/843100/.
Pełny tekst źródłaStreszczenie:
Diabetes is one of the fastest growing diseases today, affecting over a million people in the UK. Numerous medical complications, such as heart disease, are regularly associated with diabetes. Despite advances in methods of diagnosis and treatment there is still a need for greater understanding of these diseases. This will include research directed towards the influence of specific treatments and reasons for the high incidence of diabetes and heart disease in 'at risk' populations. Changes in elemental status are associated as the cause or effect of various diseased states. Elemental imbalance in diabetics can result in impaired glucose tolerance and insulin resistance and in sufferers of heart disease elemental changes impair heart rate and elasticity of blood vessels. In the UK 10,000 patients with Ischaemic Heart Disease undergo coronary artery bypass grafting (CABG) surgery each year. Elemental analysis has been carried out on blood samples collected from a group of patients admitted to hospital for bypass surgery. Proton Induced X-ray Emission (PIXE) and Instrumental Neutron Activation Analysis (INAA) have been applied as complementary analytical tools for determining elemental concentrations. Differences have been examined between CABG patients with and without diabetes. Both experimental methods have been used to investigate elemental levels in whole blood, erythrocytes and plasma. Elemental concentration varied according to the blood constituent and reflected short and long-term influences on elemental homeostasis. Plasma was found to concentrate Na, Mg and Ca the highest using both experimental techniques. All blood samples were collected and prepared at St. George's Hospital, Tooting in the UK. An additional study was conducted to investigate the influence of the bypass operation on the patient's elemental status. Whole blood was obtained at pre (1h before operation), post (1-2 hours after operation) and recovery (24 hours after completion of the operation) stages of bypass surgery. Differences between the three phases were observed, individual variations have been plotted so rates of change can be seen and evaluated with the particular medical history. Concentrations of Na, Mg, Al, P, S, Cl, K, Ca and Fe in whole blood were determined. The two measurement techniques found different concentrations however results showed a general trend that post operative concentrations were elevated compared to pre operative values. Analysis of blood drawn during the recovery phase, 24 hours after the surgery, found that concentration were typically approaching pre operative levels. Both PIXE and INAA found concentrations of Na, Mg and Al peaked post operation and then decreased in the recovery phase, towards values measured pre surgery. Various factors may be responsible for the elemental changes occurring during surgery including, hormone production, routine administration of intra-operative fluids and contact of blood with non- endothelial surfaces. Hierarchical cluster analysis has been used to confirm differences between elemental levels in pre, post and recovery stages of bypass surgery. The dendograms produced indicate significant distinction between the three stages. The explosive impact of diabetes in the UK resident Asian population is discussed and the influence of diabetogenic agents introduced. Examination of research literature revealed that betel nut has been implicated as a causative agent in several medical conditions. Samples of Betel nut and six associated chewing materials widely used in Asian communities has been collected and prepared for analysis. Instrumental neutron activation analysis has been used to determine the concentration of Na, Mg, Al, Cl, Ca, V, Mn, Cu and Br in the samples by means of short-lived radionuclides.
37
Groves, Peter H. "The influence of exogenous nitric oxide on the pathophysiology of angioplasty injury". Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308763.
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Robertson, D. N. "A study of blood platelets in experimental myocardial ischaemia". Thesis, Robert Gordon University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377585.
Pełny tekst źródła
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Schwarz, Konstantin. "The effects of inorganic nitrate and nitrite on the heart : metabolic efficiency and therapeutic potential for ischaemic heart disease". Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=229509.
Pełny tekst źródła
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Yasin, Mohammed. "Non-regenerative benefits of adult bone marrow derived stem cells for myocardial protection". Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8701.
Pełny tekst źródłaStreszczenie:
Ischaemic heart disease is the most common cause of mortality in the western hemisphere and it is rapidly becoming the leading cause of death globally. Moreover, therapeutic interventions by cardiologists and cardiac surgeons frequently subject the heart to acute I/R injury, which in itself can cause mortality. Recent investigations of adult stem cells have primarily focused on their regenerative potential for chronic ischaemic heart disease. In this thesis, I have investigated the hypothesis that adult bone marrow derived stem cells are cardioprotective in acute regional myocardial I/R injury. In a rat model of left anterior descending coronary artery (LAD) reversible occlusion and reperfusion, I demonstrate that an intravenous bolus of adult bone marrow derived (1) bone marrow mononuclear (BMNNC) and (2) mesenchymal stem cells (MSC) upon reperfusion can attenuate infarct size. This effect is comparable to ischaemic preconditioning (IPC), which is the gold standard for cardioprotection. Next, I demonstrated the mechanisms for adult stem cell cardioprotection are principally anti-apoptotic and depend upon stem cell secreted factors to (1) activate phosphatidylinositide 3-kinase (PI3)/Akt cell survival kinase-signaling pathway (2) inhibit glycogen synthase kinase-3β (3) inhibit p38MAPK (4) inhibit nuclear translocation of p65NF-κB. 7 Proteomic analysis of myocardium subjected to I/R and treated with either BMMNC or BMMNC derived supernatant (BMS) upon reperfusion demonstrated higher expression of a whole host of pro-survival proteins. These were notably (1) 14-3-3-ε protein (2) anti-oxidant peroxiredoxin-6 (3) heat shock protein (HSP) αB-crystallin, HSP72, HSP tumour necrosis factor receptor-1 associated protein, and HSP ischaemia responsive protein-94 (4) glycolytic protein glyceraldehyde-3-phosphate dehydrogenase (5) mitochondrial aconitase and mitochondrial voltage-dependent anionselective channel protein-1. Thereafter, I investigated the mobilization of endogenous bone marrow stem cells and trafficking to the ischaemic myocardium by stromal cell derived factor-1 (SDF-1) /chemokine, receptor type 4 (CXCR4) signaling. I demonstrate high up-regulated expression of CXCR4 and CD26 in BMMNC following IPC, which might have a role in IPC-mediated cardioprotection. Finally, and in concordance with this finding I demonstrate that both IPC and an exogenous MSC bolus upon reperfusion can synergize to abolish acute myocardial I/R injury.
41
Arnold, J. R. "Evolving non-invasive techniques for the assessment of myocardial perfusion in ischaemic heart disease". Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543046.
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Lock, Rachel. "The quantitative assessment of ischaemic heart disease : a study of the Leeds Exercise Test". Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/34138.
Pełny tekst źródłaStreszczenie:
Elamin, Mary, Smith Linden, 1980 suggested that the rate of development of ST segment depression with increasing heart rate during a standardised exercise test could predict the number of coronary arteries (0, 1, 2 or 3) seen to be ocluded on the coronary arteriogram. Several attempts to repeat this "Leeds exercise test" had been unsuccessful possibly through inadequate adherence to the Leeds protocol. The work described in this thesis is a further attempt to replicate the Leeds test as precisely as possible after a period of instruction at Leeds. A Leeds test and coronary arteriography were performed on 49 patients at Groby Road Hospital, Leicester. Results of identical exercise ECGs analysed at Leeds and Leicester were compared to ensure the same methods were used and highlight potential causes of disparate results through differences in method. Results of arteriograms assessed at both centres and on two occasions at Leicester were compared to test the reproducibility of the arteriogram and so its value as an index of coronary disease. A computer assisted method of measuring the exercise ECG was developed. The results of coronary arteriography and exercise testing were correlated to assess the Leeds test for the prediction of coronary disease severity. The following main reasons why the Leeds' results have not been repeated at any other centre are proposed: 1. There has been sufficient deviation from the described methods of performing the exercise test and assessing the arteriogram. 2. Patient variables (drug regime and cardiac complications other than coronary disease) may affect the ST/HR slope. 3. There is a large variance associated with the arteriogram result and the estimate of the ST/HR slope. 4. It is questionable that an exact correlation can occur between the results of exercise testing and coronary arteriography. Also, a 3 vessel disease terminology to quantify coronary disease is inadequate. It is recognised that the maximal ST/HR slope is an improved index of myocardial ischaemia which has probably had limited acceptance through being assessed against arteriogram results in terms of 0, 1, 2, and 3 vessel disease. Finally, having highlighted the limitations of exercise testing and coronary arteriography, the potential of nuclear magnetic resonance in the quantitative and qualitative assessment of ischaemic heart disease in the future is addressed.
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Watts, Eric J. "Coagulation changes in long distance runners and their relevance to the prevention of ischaemic heart disease". Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328774.
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Casadei, Barbara. "Some aspects of the parasympathetic control of the cardiovascular system in man". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297082.
Pełny tekst źródła
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Butcher, Anna Louise. "Role of Full and Partial Adenosine Receptor Agonists in the Cardiac Myocyte". Thesis, Griffith University, 2012. http://hdl.handle.net/10072/366145.
Pełny tekst źródłaStreszczenie:
Cardiovascular disease remains one of the largest health burdens facing the westernised world. The ubiquitous nucleoside, adenosine and its accompanying receptors may have beneficial effects in the treatment of ischaemic heart disease. Adenosine is derived from the catabolism of ATP and has long been considered a potent bradycardic and hypotensive compound. For over half a century, adenosine and its analogues have often been considered potential cardioprotective drug targets. These protective effects are mediated via the action of adenosine receptors: ADORA1, ADORA2A, ADORA2B and ADORA3. The main purpose of this thesis was to examine the role and mechanisms of selective adenosine full and partial agonists in the ischaemic-reperfused mouse heart, exploring the potential cellular mechanisms involved in cardiomyocyte cell death, functional parameters and pharmacological manipulation of the recovering heart. The effects of enhancing endogenous adenosine activation through the use of allosteric enhancers are also assessed.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
46
Haider, Agha Waqar. "Continuous electrocardiographic recording in the assessment of ischaemic heart disease : technical problems and clinical role". Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243945.
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Islam, Md Hamidul. "Mathematical Modelling of the Inflammatory Response in Coronary Artery Disease". Thesis, Griffith University, 2017. http://hdl.handle.net/10072/365469.
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Atherosclerosis is a condition whereby fatty material is deposited in the walls of arteries resulting in a thickening of the wall. It is the leading cause of morbidity and mortality in much of the world, including Australia. Some of the clinical manifestations of atherosclerosis include acute ischaemic syndromes such as heart attacks and strokes. Despite continuous eorts over the past four decades, the biology of atherosclerosis and its clinical manifestations are still poorly understood. According to the response-to-injury hypothesis, this disease is initiated by an injury to or dysfunctionality of the inner lining of the artery (the endothelium) and progresses through multiple dynamical cell processes.
Mathematical models that take into account the initiation of atherosclerosis can be used to provide an integrated description of the mechanisms of the formation of an early atherosclerotic lesion. Such models may have signicant utility for designing future clinical and experimental studies, as well as in the development of therapeutic hypotheses and the provision of preventative advice for an individual or group of patients.
This thesis aims to develop models of the cellular dynamics of the process of early atherosclerosis, which will enhance the understanding of the cellular mechanics behind the formation of an early atherosclerotic lesion. In order to address the aims of the thesis, we present increasingly more realistic models.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Markey, Peter. "The prevalence of ischaemic and rheumatic heart disease and risk factors in Aboriginal and non-Aboriginal footballers /". Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09MPM/09mpmm345.pdf.
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McGlinchey, P. G. "An investigation of the genetic basis of ischaemic heart disease using family based tests of association". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273055.
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Atkinson, C. "The effects of isoflavones on some risk factors for breast cancer, osteoporosis, and ischaemic heart disease". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596214.
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To investigate whether phytoestrogens had an antioestrogenic effect, a large double blind, randomised, placebo controlled trial was conducted for approximately one year. Mammographic breast density, hormone levels, menopausal symptoms, cardiovascular risk factors, bone density, and body composition were assessed. When compared with the effects of placebo, 40mg daily dose of isoflavones did not significantly alter mammographic breast density when assessed by several different methods. Mean change in estimated percent density determined from the mammogram comparison data was - 1.35% (SD 5.16) in the isoflavone group, and -1.79% (SD 7.41) in the placebo group. There was also no significant effect on levels of oestradiol, FSH, or LH. Menopausal symptoms, and hot flushes specifically, were not significantly altered by clover isoflavones. Cardiovascular risk factors (blood pressure, blood lipids, and blood clotting factors) were also not significantly altered. However, the isoflavones did affect bone density. Spine bone mineral density (BMD) decreased to a significantly lower extent in the isoflavone group compared with that seen in the placebo group (p<0.01). The effect on BMD was mainly seen in the pre- and peri-menopausal women, and isoflavones also had a significant effect on BMC in this group. Levels of the bone resorption marker, deoxypyridinoline (Dpd) increased in both the isoflavone and placebo pre- and peri-menopausal groups. However, the increase was significantly lower in the isoflavone group compared with placebo (p=0.03), supporting the finding of a beneficial effect of isoflavones on bone as judged by BMD and BMC. Similar trends (not significant) regarding BMC and BMD were seen in the hip in pre-and peri-menopausal women, and there was a significant increase in body fat with the isoflavone supplement in this group (p<0.01).