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Dissertations / Theses on the topic 'Infarction'

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1

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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2

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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3

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

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Acute myocardial infarction (AMI) results in the activation of the innate immune system with monocytes playing critical roles in both the initial inflammation following myocardial ischaemia and subsequent recovery. Monocytes are a heterogeneous cell population and observations from experimental models demonstrate that immediately following myocardial injury, classical inflammatory monocytes, which are highly phagocytic, are recruited to ischaemic myocardium from the bone marrow and spleen and peak at 48 hours. This is followed by the recruitment of non-classical monocytes that are involved in
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4

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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5

Dawson, Lynn Gail. "Coping behaviours in myocardial infarction rehabilitation." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/25722.

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This study was designed to discover the coping behaviours used by patients six to twelve months following a myocardial infarction (MI). The conceptualization of coping behaviours was based on the UBC Model for Nursing which directed the researcher to examine coping behaviours used to meet the patients' basic human needs. The specific research question was, "What new or already established coping behaviours have patients utilized after an MI in an attempt to satisfy their basic human needs?" Seven participants who had experienced an MI six to twelve months previously, were recruited from car
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6

Dulku, Amarjit. "Causal attributions, worry and myocardial infarction." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/31333.

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Although previous research has pointed to worry as one of the highest causal attributions reported by MI patients, no studies have primarily investigated the concept of worry in this cohort. This study aimed to determine the prevalence of pathological worry in MI patients who reported worry as a causal factor to their MI (Experimental group), compared to MI patients that did not implicate worry as a causal attribute (Control group). A central hypothesis to this study was that higher pathological worry would be found in the Experimental group, and would be significantly associated with meta-wor
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7

Stuckey, Daniel James. "Stem cell therapy for myocardial infarction." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442996.

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8

Volmink, James Andrew. "The Oxford Myocardial Infarction Incidence Study." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389026.

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9

de, Waha Suzanne, Ingo Eitel, Steffen Desch, et al. "Prognosis after ST-elevation myocardial infarction." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-148644.

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Background: This study aimed to evaluate the incremental prognostic value of infarct size, microvascular obstruction (MO), myocardial salvage index (MSI), and left ventricular ejection fraction (LV-EFCMR) assessed by cardiac magnetic resonance imaging (CMR) in comparison to traditional outcome markers in patients with ST-elevation myocardial infarction (STEMI) reperfused by primary percutaneous intervention (PCI). Methods: STEMI patients reperfused by primary PCI (n = 278) within 12 hours after symptom onset underwent CMR three days after the index event (interquartile range [IQR] two to four)
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10

Chew, Eng Wooi. "Ventricular late potentials in myocardial infarction." Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334467.

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11

McNeill, Albert John. "Thrombolytic therapy in acute myocardial infarction." Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356866.

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12

Graham, Lee Nicholas. "Sympathetic mechanisms following acute myocardial infarction." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403027.

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13

Bowler, John Vaughan. "Cerebral infarction and '9'9Tc'm HMPAO SPECT." Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260983.

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14

Dawkins, Sam. "MicroRNA release in acute myocardial infarction." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:a0a82298-45e5-4f66-b368-446cad9726ae.

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Coronary heart disease (CHD) is the single biggest cause of death in the United Kingdom1. Primary percutaneous coronary intervention (primary PCI) has transformed the early treatment of acute myocardial infarction (MI), improving outcome by rapidly re-opening the occluded coronary artery, with a larger mortality benefit and reduced risk compared with thrombolysis. Despite these advances, and even with the optimal treatment, some patients still sustain substantial myocardial damage leading to mortality and morbidity. MicroRNAs (miRs) are short non-coding RNAs with a role in regulating protein s
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15

Al-Khawaja, Imad Mahmoud Shihadeh. "Noninvasive risk stratification after myocardial infarction." Thesis, University of Surrey, 1988. http://epubs.surrey.ac.uk/847183/.

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In order to identify patients with severe coronary artery disease (CAD) and at a higher risk of future cardiac events after uncomplicated myocardial infarction, 105 consecutive patients were studied prospectively. There were 93 men and 12 women with a mean age of 56 +/- 8.2 years. Treadmill testing, exercise radionuclide ventriculography, thallium-201 myocardial imaging and selective coronary arteriography were performed 6-8 weeks after infarction. Patients were grouped into those who had single and multiple vessel disease. Multiple regression analysis of 18 noninvasive indices was carried out
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16

Hulaga, O. I. "Eplerenone use in acute myocardial infarction." Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19567.

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17

Jackson, Melanie H. "The neutrophil in acute myocardial infarction." Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/19869.

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The aim of this thesis was to determine if the neutrophil played a significant role in acute myocardial infarction in man. Firstly methods for isolating and radiolabelling neutrophils were developed. These, along with measurement of established markers of neutrophil activation and free radical activity were used to assess neutrophil involvement in myocardial infarction in man. The single-step isolation procedure developed provided a simple and easy means of isolating an essentially 'pure' preparation of cells with a minimum of 'handling'. That this method resulted in isolation of a viable cell
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18

Abraham, Sherin. "Preventing Acute Myocardial Infarction Readmission Rates." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7579.

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Unplanned readmissions to the hospital are a problem faced by most health care organizations in the United States; hospitals are penalized for such readmissions. The project site identified high readmission rates for patients who were discharged after acute myocardial infarction (AMI), making careful transition home a necessity for post-AMI patients. The focus of this quality improvement (QI) project was implementation of an early follow-up appointment of AMI patients following discharge. The purpose of this project was to evaluate the effectiveness of changing follow-up appointments for patie
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19

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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20

Goosen, Helletje. "Egpare se belewing van hulle huweliksverhouding voor en na 'n miokardiale infarksie." Pretoria : [s.n.], 2001. http://upetd.up.ac.za/thesis/available/etd-11182005-115412/.

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21

Numminen, H. (Heikki). "Actions of alcohol and ischaemic brain infarction." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514257227.

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Abstract Alcohol drinking may exercise both beneficial and untoward effects on the haemostatic and fibrinolytic systems. It may also predispose individuals to arterial thrombosis and trigger embolism in the brain. The aim here is to examine these problems. Methods used for evaluating platelet function were platelet aggregation and associated thromboxane B2 release, shear-induced platelet aggregation, and measurement of urinary prostaglandins. Changes in fibrinolytic system were evaluated by measuring plasminogen activator inhibitor type 1. The combined effects of alcohol drinking, physical ex
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22

Karttunen, V. (Vesa). "Patent foramen ovale and cryptogenic brain infarction." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514267435.

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Abstract Patent foramen ovale (PFO) is a common finding in the general population and is present in approximately one quarter of adults. The potential role of PFO in the pathogenesis of ischaemic brain infarction of unknown aetiology in young adults has been investigated during the past 15 years, and associations with other diseases have been proposed. The most plausible mechanism of stroke associated with PFO is paradoxical embolism, but there is uncertainty about this because a venous source of emboli is seldom identified. If the theory of venous emboli is relevant, prothrombotic states shou
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23

Bell, Derek. "The acute inflammatory response to myocardial infarction." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/26295.

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24

Malaviarachchi, Darshaka. "Dietary iron and risk of myocardial infarction." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0035/MQ66538.pdf.

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25

Hupperts, Raymond Maria Mathieu. "Clinically diagnosed borderzone infarction fact or fiction? /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6959.

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26

Thøgersen, Anna Margrethe. "Risk markers for a first myocardial infarction." Doctoral thesis, Umeå : Public Health and Clinical Medicine, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-603.

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27

Wayman, Nicole Style. "Novel therapeutic approaches to acute myocardial infarction." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397925.

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28

Griselli, Massimo. "C-reactive protein and experimental myocardial infarction." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408605.

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29

Hanley, Mary. "Depression following myocardial infarction : a longitudinal investigation." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388095.

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30

Singh, Ravi Kumar. "Platelet reactivity, polymorphisms and premature myocardial infarction." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29880.

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I have carried out a detailed assessment of platelet function and reactivity in 205 subjects that suffered a premature MI (at a mean age 42.3 +/- 5.7) and 200 age and sex matched controls, to two endogenous platelet agonists adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP). I have further analysed the effect on platelet function of polymorphisms in two platelet receptors (GPIIbIIIa C196T and GPIaIIa G873A), which have been proposed as genetic risk factors for MI. Platelet reactivity to several concentrations of ADP and TRAP, measured as degree of fibrinogen binding b
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31

Haider, Agha W., Max Luna, Sunil Patel, and L. Lee Glenn. "Antibiotic Use and Risk of Myocardial Infarction." Digital Commons @ East Tennessee State University, 1999. https://dc.etsu.edu/etsu-works/7531.

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Excerpt: Dr Meier and colleagues1 present intriguing data that individuals with a first acute myocardial infarction (AMI) were less likely than matched controls to have used tetracycline antibiotics or quinolones in the previous 3 years. The authors raise the possibility that organisms susceptible to these antibiotics may be involved in the pathogenesis of coronary heart disease. However, several methodological limitations lead to other possible explanations for the observed associations.
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32

Agarwal, Udit. "Factors Affecting Ventricular Remodeling Post Myocardial Infarction." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1269627876.

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33

Guo, Xiaolei. "Engineering electrospun scaffolds to treat myocardial infarction." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1343072089.

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34

Thompson, Risa Nakase. "Prediction of trauma responses following myocardial infarction." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=712.

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Thesis (Ph. D.)--West Virginia University, 1999.<br>Title from document title page. Document formatted into pages; contains vi, 79 p. Vita. Includes abstract. Includes bibliographical references (p. 54-69).
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35

Ghattas, Angie. "Monocyte subpopulations in patients following ST-elevation myocardial infarction : implications for post-infarction left ventricular remodelling and clinical outcomes." Thesis, Aston University, 2017. http://publications.aston.ac.uk/30383/.

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Despite improvements in interventional and pharmacological therapy of atherosclerotic disease,it is still the leading cause of death in the developed world. Hence there is a need for further development of effective therapeutic approaches. This requires better understanding of the molecular mechanisms and pathophysiology of the disease. Atherosclerosis has long been identified as having an inflammatory component contributing to its pathogenesis, whilst the available therapy primarily targets hyperlipidaemia and prevention of thrombosis. Acknowledging a pleotropic anti-inflammatory effect to so
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36

Cochrane, Bonnie S. "Effects of an in-hospital cardiovascular risk factor management strategy post acute myocardial infarction /." St. John's, NF : [s.n.], 2001.

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37

Daly, Michael John. "Improving the electrocardiographic diagnosis of acute myocardial infarction." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725747.

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The standard 12-lead ECG remains the cornerstone of immediate clinical triage In patients presenting pre-hospital or to an Emergency Department with acute ischaemic-type chest pain at rest However, this non-invasive test is well known to have poor diagnostic sensitivity for acute coronary artery occlusion. Previous research conducted at the Royal Victoria Hospital Belfast has shown the utility of extended lead systems, i.e. the body surface potential map (BSPM). in improving the diagnostic performance of the ECG in this regard. Despite advances in cardiac biomarkers, there remain a variety of
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38

Schwalm, Jon-David. "Improving Medication Adherence Post-ST-Elevation Myocardial Infarction." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32110.

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ST-segment elevation myocardial infarction (STEMI) is a common presentation of acute myocardial infarction, constituting approximately 30% of all cases. Based on the highest level of evidence for improvement in both morbidity and mortality in these patients, clinical guidelines from around the world support the prolonged use of secondary preventative medications (e.g., acetylsalicylic acid, second antiplatelet [clopidogrel, prasugrel, and ticagrelor], statin, beta-blocker, and angiotensin blocker). While in-hospital and discharge prescription rates for these essential life-saving medications
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39

Salamonson, Yenna, University of Western Sydney, College of Social and Health Sciences, and School of Applied Social and Human Sciences. "Health-enhancing behaviours in first myocardial infarction survivors." THESIS_CSHS_ASH_Salamonson_S.xml, 2002. http://handle.uws.edu.au:8081/1959.7/267.

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The adoption of health behaviours is essential if coronary heart disease patients are to optimise their chance of survival and reduce the likelihood of recurrent coronary events. However, this behavioural change may not ensue following an acute myocardial infarction(AMI). This study on first AMI subjects sought firstly to examine the psychometric properties of five scaled instruments used for assessing health behaviours. Secondly, the study assessed the prevalence of health-enhancing behaviours at the time of the first AMI and 6 months after this event.Thirdly, the magnitude of health behaviou
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40

Salamonson, S. Y. Yenna. "Health-enhancing behaviours in first myocardial infarction survivors /." View thesis View thesis, 2002. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030331.125748/index.html.

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Thesis (Ph.D.) -- University of Western Sydney, [2002].<br>"A thesis submitted to the University of Western Sydney in fulfilment of the requirements for the degree of Doctor of Philosophy (Health) " Bibliography: leaves 180-229, and Appendices.
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41

Råmunddal, Truls Are. "Myocardial metabolism in experimental infarction and heart failure /." Göteborg : Department of Molecular and Clinical Medicine, The Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy Göteborg University, 2008. http://hdl.handle.net/2077/9565.

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42

Carson, W. "Vectorcardiographic and nuclear scintigraphic studies of myocardial infarction." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379961.

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43

McMehan, Stephen Robert. "Body surface electrocardiographic mapping in acute myocardial infarction." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361289.

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44

Walker, Linda Jean Elizabeth. "Nifedipine in the acute phase of myocardial infarction." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357513.

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45

Haycock, Philip Charles. "Lipoprotein(a) and myocardial infarction in South Asians." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607890.

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46

Khan, Sohail Q. "Risk stratification of myocardial infarction using cardiac peptides." Thesis, University of Leicester, 2008. http://hdl.handle.net/2381/29901.

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We investigated the TIMI risk score, Cardiotrophin-1 (CT-1) myotrophin and MPO in combination with NTproBNP at predicting adverse outcome following AMI. We recruited 596 patients with AMI. Patients were TIMI risk scored. The concentrations of CT-1, myotrophin, MPO and NTproBNP were measured using non-competitive immunoassays. All patients were followed-up for death, recurrent MI, heart failure (HF) and MACE (death, MI and need for urgent revascularisation). Mortality was related to higher TIMI score (p=0.029) and NTproBNP levels (<0.0001). NTproBNP was an independent predictor of mortality (OR
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47

Tizon, Marcos Helena. "ST-elevation myocardial infarction: gaps in current knowledge." Doctoral thesis, Universitat Autònoma de Barcelona, 2021. http://hdl.handle.net/10803/672584.

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Les malalties isquèmiques del cor són la causa principal de mortalitat al món i a Europa. El seu mecanisme etiopatogènic fonamental és l’aterosclerosi; la inestabilització d’una lesió aterosclerosa comporta, eventualment, una síndrome coronària aguda. L’infart agut de miocardi és una de les complicacions més freqüents de les malalties isquèmiques del cor i es tradueix en necrosi miocárdica. L’infart agut de miocardi amb elevació del segment ST (IAMEST o STEMI en anglès) es precipita per la oclusió persistent d’un vas coronari epicàrdic. L’extensió del dany miocàrdic depèn del temps d’oclusió a
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48

Zaganides, Alexia. "Evolving probability of survival following acute myocardial infarction." Thesis, University of Sussex, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393249.

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49

MBewu, James. "Computational modelling of cardiac function and myocardial infarction." Master's thesis, University of Cape Town, 2012. http://hdl.handle.net/11427/11611.

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Includes abstract.<br>Includes bibliographical references.<br>Cardiovascular disease is a leading cause of death in South Africa. In particular non-fatal myocardial infarction is a key determinant for future cardiac failure due to adverse remodelling and electrophysiological dysfunction. Computational modelling of the electrophysiology and mechanics of the heart can provide useful insights into the causes of cardiac failure and the efficacy of treatments designed to combat myocardial infarction. A computational model of the healthy and infarcted left ventricle of a rat was developed using the
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50

Gonzalez, Gomez Mayte Lorena. "Methylglyoxal Effects in Cell Therapy for Myocardial Infarction." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38431.

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Methylglyoxal (MG), a highly reactive dicarbonyl accumulates after myocardial infarction (MI), causing adverse remodelling and cardiac dysfunction. We hypothesized that therapy using bone marrow cells (BMCs) overexpressing glyoxalase1 (Glo1), the main enzyme that metabolizes MG, injected into mouse MI model would translate into better survival of transplanted cells and improve their therapeutic effect. We found that Glo1 expression is significantly reduced at 7 days post-MI. Glo1 BMCs exposed to MG in vitro displayed greater angiogenic potential and reduced reactive oxygen species production
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