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Dissertations / Theses on the topic 'Myocardial Infarctio'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

HANTIKAINEN, ESSI MARJATTA. "DIETARY NON ENZYMATIC ANTIOXIDANT CAPACITY AND THE RISK OF CARDIOVASCULAR DISEASES – AN EPIDEMIOLOGICAL APPROACH." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263728.

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ABSTRACT Cardiovascular diseases are the leading cause of premature death and disability in the world. A diet containing high amounts of plant-based foods has been associated with a reduced risk of cardiovascular diseases and the beneficial effect has been attributed to the antioxidants found in the foods. However, findings from randomized controlled trials on the role of antioxidant supplementation have been disappointing, reporting null results or even harmful effects. It has been suggested that antioxidants interact with each other to promote cardiovascular health. Therefore, the Non Enzymatic Antioxidant Capacity (NEAC) assay has been proposed, which measures the antioxidant potential of different dietary sources considering interactions between them. This thesis aimed to further clarify the effect of dietary antioxidants on the risk of cardiovascular diseases, with particular interest in measuring NEAC from diet. The specific aims were to prospectively study whether dietary NEAC is associated with a lower risk of myocardial infarction, stroke and heart failure in subjects free from CVD or cancer. Four studies were conducted using data from two large Swedish cohorts. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). In the Swedish Women’s Lifestyle and Health Cohort (n = 45,882), a higher baseline dietary NEAC was inversely associated with the risk of myocardial infarction (quintile 5 vs. quintile 1: HR: 0.60, 95% CI: 0.45-0.81, p for trend < 0.05) and heart failure (tertile 3 vs. tertile 1: HR: 0.63; 95% CI: 0.43-0.93; p for trend < 0.05) in young to middle aged women, whereas no association was found between dietary NEAC and stroke. In the Swedish National March Cohort (n = 34,543), dietary NEAC was inversely associated with the risk of overall (quartile 4 vs. quartile 1: HR: 0.77, 95% CI: 0.61-0.96; p for trend < 0.05) and non-fatal myocardial infarction (quartile 4 vs. quartile 1: HR: 0.72; 95% CI: 0.56-0.92; p for trend < 0.05), but not with fatal myocardial infarction. The association seemed to further be stronger in women compared to men. To conclude, these findings support the hypothesis that a diet with high NEAC might protect from the development of myocardial infarction and heart failure and that the beneficial effect might be exerted through interactions between antioxidants. Whether this is true for stroke needs to be further investigated. Nevertheless, it is suggested to implement high amounts of antioxidant rich foods and beverages, such as fruits, vegetables, whole grains and tea, in the daily diet to lower the burden of cardiovascular diseases.
ABSTRACT Cardiovascular diseases are the leading cause of premature death and disability in the world. A diet containing high amounts of plant-based foods has been associated with a reduced risk of cardiovascular diseases and the beneficial effect has been attributed to the antioxidants found in the foods. However, findings from randomized controlled trials on the role of antioxidant supplementation have been disappointing, reporting null results or even harmful effects. It has been suggested that antioxidants interact with each other to promote cardiovascular health. Therefore, the Non Enzymatic Antioxidant Capacity (NEAC) assay has been proposed, which measures the antioxidant potential of different dietary sources considering interactions between them. This thesis aimed to further clarify the effect of dietary antioxidants on the risk of cardiovascular diseases, with particular interest in measuring NEAC from diet. The specific aims were to prospectively study whether dietary NEAC is associated with a lower risk of myocardial infarction, stroke and heart failure in subjects free from CVD or cancer. Four studies were conducted using data from two large Swedish cohorts. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). In the Swedish Women’s Lifestyle and Health Cohort (n = 45,882), a higher baseline dietary NEAC was inversely associated with the risk of myocardial infarction (quintile 5 vs. quintile 1: HR: 0.60, 95% CI: 0.45-0.81, p for trend < 0.05) and heart failure (tertile 3 vs. tertile 1: HR: 0.63; 95% CI: 0.43-0.93; p for trend < 0.05) in young to middle aged women, whereas no association was found between dietary NEAC and stroke. In the Swedish National March Cohort (n = 34,543), dietary NEAC was inversely associated with the risk of overall (quartile 4 vs. quartile 1: HR: 0.77, 95% CI: 0.61-0.96; p for trend < 0.05) and non-fatal myocardial infarction (quartile 4 vs. quartile 1: HR: 0.72; 95% CI: 0.56-0.92; p for trend < 0.05), but not with fatal myocardial infarction. The association seemed to further be stronger in women compared to men. To conclude, these findings support the hypothesis that a diet with high NEAC might protect from the development of myocardial infarction and heart failure and that the beneficial effect might be exerted through interactions between antioxidants. Whether this is true for stroke needs to be further investigated. Nevertheless, it is suggested to implement high amounts of antioxidant rich foods and beverages, such as fruits, vegetables, whole grains and tea, in the daily diet to lower the burden of cardiovascular diseases.
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2

Murphy, Megan K. "Fibrin microthreads promote stem cell growth for localized delivery in regenerative therapy." Worcester, Mass. : Worcester Polytechnic Institute, 2008. http://www.wpi.edu/Pubs/ETD/Available/etd-090208-143505/.

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3

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

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4

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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5

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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6

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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7

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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8

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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9

Bouhidel, Jalaleddinne Omar. "Etude de la cardioprotection contre l'infarctus du myocarde au cours de l'obésité expérimentale." Thesis, Paris Est, 2010. http://www.theses.fr/2010PEST0034.

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L'infarctus du myocarde (IDM) est l'une des principales causes de morbi-mortalité dans les pays développés et ce malgré l'amélioration enregistrée ces dernières années dans sa prise en charge thérapeutique. L'obésité est classée comme étant un facteur de risque majeur pour les maladies coronaires par l'American Heart Association, et concerne 14,5 % de la population française (enquête ObEpi-Roche/INSERM, 2009). En utilisant un modèle expérimental d'obésité, la souris ob/ob génétiquement dépourvue en leptine, l'objectif du présent travail de thèse a été d'étudier l'efficacité de stratégies cardioprotectrices comme le postconditionnement (PCD) ischémique ou l'exercice physique chronique contre l'IDM. La première partie de ce travail de thèse a mis en évidence une perte de la cardioprotection par PCD ischémique au cours de l'obésité. L'étude des voies de signalisation aura permis de mettre en évidence l'implication des protéines phosphatases PTEN, MKP3 et PP2C dans l'inefficacité du PCD. La seconde partie de ce travail de thèse a montré un effet cardioprotecteur de l'exercice physique chronique contre l'IDM dans un contexte expérimental d'obésité. Cet effet est associé à une augmentation des défenses enzymatiques antioxydantes, à une amélioration des fonctions mitochondriales, à une activation des voies de signalisation cardioprotectrices RISK et SAFE et enfin à une diminution des protéines phosphatases impliquées dans la régulation négative des acteurs des voies de signalisation cardioprotectrices. La preuve scientifique des bienfaits de l'exercice est aujourd'hui un argument de poids pour poursuivre les efforts entrepris par les pouvoirs publics ces dernières années à travers le Programme National Nutrition Santé pour favoriser la pratique d'une activité physique et sportive et en particulier chez les obèses
Myocardial infarction (MI) remains the leading cause of morbidity and mortality in the developing countries despite significant therapeutic advances over these last years. Obesity is a major risk factor for coronary heart disease according to the American Heart Association and concern 14.5% of the French population (ObEpi-Roche/INSERM survey, 2009). Using the leptin-deficient ob/ob mice, an animal model of obesity, the aim of the present thesis was to investigate the efficacy of cardioprotective strategies such as ischemic postconditioning (PCD) or chronic physical exercise against MI. In the first part of this thesis, we have found that the cardioprotective effects of PCD vanish with obesity. The investigation of the cardioprotective pathways has revealed that protein phosphatases such as PTEN, MKP3 and PP2C are involved in the inability of PCD to protect the heart. The second part of this thesis has demonstrated for the first time a cardioprotective effect of chronic physical exercise against MI in an experimental model of obesity. This effect was associated with increased antioxidant enzymes, improved mitochondrial function, activation of the cardioprotective RISK and SAFE pathways and finally a decrease in the related protein phosphatases levels. The scientific proofs given by this work underlines the “Programme National Nutrition Santé” developed by the French government to encourage all people and especially obese people to observe physical and sport activities
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10

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 cardiologists. Data were collected from the participants during interviews using semi-structured open-ended questioning technique. Data were coded and analyzed using the constant comparative method developed by Glaser and Strauss. Three themes that emerged from the data were: 1) coping behaviours related to risk reduction, 2) coping behaviours related to returning to normal, 3) coping behaviours related to reaching a new normal. The findings supported the need for lifestyle changes involving the use of existing coping behaviours and/or the development of new coping behaviours to meet subjects' basic human needs. Certain unmet basic human needs were identified following an MI which required the development of new coping behaviours to meet them. Nurses are in a unique position to assist MI patients in developing coping behaviours to meet their basic human needs. The descriptions and explanations of coping behaviours identified in this study may serve as a useful guide for nurses to help patients deal with changes in their lives and develop necessary coping behaviours to meet their basic human needs.
Applied Science, Faculty of
Nursing, School of
Graduate
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11

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-worry (worry about worry), rather than health worry. The design was cross-sectional, and consisted of administering self-report questionnaires to a total of 34 post-MI patients (n=17 in each group). The questionnaire measured: pathological worry, meta-worry, anxiety, depression, and thought control strategies. Participants in the Experimental group were found to be significantly younger than the Control group, and a higher proportion were employed. The main results indicated that no differences were found between the two groups in terms of worries relating to their health. However, pathological worry, meta-worry, social worry, anxiety and the use of thought control strategies were significantly higher in the Experimental group, compared with the Control group. Interestingly, none of the participants (N=34) reported symptoms of depression at a clinical level. Further analysis revealed that pathological worry significant correlated with meta-worry and the thought control strategy known as 'Punishment'. In conclusion MI patients who rated worry highly as causal to their MI were also found to be more pathologically worried after their MI than participants who implicated physical factors as causal attributes. However, this pathological worry was not related to worry about health, but was regarded as a coping response that is best understood from a metacognitive model of a generalised anxiety disorder.
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12

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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13

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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14

de, Waha Suzanne, Ingo Eitel, Steffen Desch, Georg Fuernau, Philipp Lurz, Thomas Stiermaier, Stephan Blazek, Gerhard Schuler, and Holger Thiele. "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). Infarct size and MO were measured 15 minutes after gadolinium injection. T2-weighted and contrast-enhanced CMR were used to calculate MSI. In addition, traditional outcome markers such as ST-segment resolution, pre- and post-PCI Thrombolysis In Myocardial Infarction (TIMI)-flow, maximum level of creatine kinase-MB, TIMI-risk score, and left ventricular ejection fraction assessed by echocardiography were determined in all patients. Clinical follow-up was conducted after 19 months (IQR 10 to 27). The primary endpoint was defined as a composite of death, myocardial reinfarction, and congestive heart failure (MACE). Results: In multivariable Cox regression analysis, adjusting for all traditional outcome parameters significantly associated with the primary endpoint in univariable analysis, MSI was identified as an independent predictor for the occurrence of MACE (Hazard ratio 0.94, 95% CI 0.92 to 0.96, P <0.001). Further, C-statistics comparing a model including only traditional outcome markers to a model including CMR parameters on top of traditional outcome markers revealed an incremental prognostic value of CMR parameters (0.74 versus 0.94, P <0.001). Conclusions: CMR parameters such as infarct size, MO, MSI, and LV-EFCMR add incremental prognostic value above traditional outcome markers alone in acute reperfused STEMI.
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15

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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16

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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17

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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18

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 synthesis. Some miRs are cardiospecific, can be detected in plasma after a myocardial infarction and show promise as biomarkers and insights into the mechanisms of myocardial injury. In this work, as part of the Oxford Acute MI (OxAMI) Programme, a cohort of patients recruited at the time of ST elevation MI underwent detailed clinical and microRNA analysis at the time of myocardial infarction. This work was validated using separate discovery and validation cohorts. The source of detected miRs was further analysed in an in-vitro endothelial cell culture model and by measuring miRs released into the venous drainage of the heart, the coronary sinus. In the Discovery Cohort, miRs previously shown to be increased in myocardial infarction (e.g. miR-1, -133a, -499) were detectible in plasma after myocardial infarction, and this was confirmed in the validation cohort. Other miRs with a similar relationship were also identified (e.g. miR-30a, -378a, 125b). Microvascular obstruction was found to be associated with increased infarct size and also with release of microRNAs correlating with infarct size suggesting a link between microvascular obstruction and myocardial necrosis. Analysis of paired coronary artery and coronary sinus samples showed that these miRs increased down the myocardial gradient, suggesting myocardial release. The culmination of this work was to use the experimental findings from circulating plasma, cultured endothelial cells and coronary sinus experiments to design a microRNA panel using a blood sample taken six hours after admission to use in a regression model which was more predictive of final infarct size than troponin alone.
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19

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 using generalized linear interactive modelling (GLIM) and the results were compared with the severity of underlying CAD and the clinical outcome after a mean follow-up period of 18.8 +/- 3. 4 months. At the end of the follow-up period, patients were categorized into those who had no cardiac events, minor and major cardiac events. Multivariate analysis produced an algorithm from three factors found to be most predictive of the severity of CAD. These included ST-segment depression on exercise, total score of rest and exercise regional wall motion and the presence of significant redistribution on thallium-201 imaging. The sensitivity of this algorithm for predicting multiple vessel disease was 42%, with a specificity of 94%, and a predictive accuracy of 69%. However, the total score of regional wall motion abnormalities was the single most predictive factor of major cardiac events with a sensitivity of 94%, a specificity of 57%, and predictive accuracy of 63%. None of the other factors produced additional prognostic information. Therefore, exercise radionuclide ventriculography appears to be the investigation of choice in assessing prognosis after myocardial infarction.
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20

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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21

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 population was evidenced by normal kinetics and uptake into sites of infection and inflammation in vivo. In collaboration with others it was shown that the acute inflammatory response to myocardial infarction may be imaged in man using radiolabelled autologous neutrophils. The time interval from onset of pain to injection of labelled cells was the only factor shown to determine the outcome of imaging and suggests that the stimulus for cell recruitment may be early and transient. Detection of increased neutrophil elastase by radioimmunoassay and the non-peroxide diene conjugated isomer of linoleic acid by high performance liquid chromatography in the plasma of these patients demonstrated increased neutrophil activation and free radical activity in acute myocardial infarction in man. Coronary reperfusion, effected by intravenous thrombolysis, might be thought to be associated with increased neutrophil activation but the results showed a reduction in the intensity of the inflammatory response as assessed by uptake of radiolabelled autologous neutrophils, abolition of the late peak of neutrophil activation and a similar degree of free radical activity between patients treated with and without thrombolysis. This is consistent with a reduction rather than an exaggeration of the inflammatory response and conflicts with current views on 'reperfusion injury'.
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22

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 patients with an AMI from 14-30 days to 7-14 days post discharge to reduce unplanned readmission rates. Bandura’s self- efficacy theory provided the theoretical framework for this project. An evaluation of the QI project was completed by comparing patient readmission rates 6 months before and 6 months after implementation of the early follow-up appointments. Data analysis demonstrated that the readmission rate was not improved in the first 6 months post QI project implementation. Using the plan-do-check-act process, a multifactorial approach was recommended to refine the QI project and address the system-wide readmission rates. The implications of this project for positive social change include providing early analysis of the readmission QI project, which allowed the hospital to restructure the QI approach and improve the plan for preventing readmission.
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23

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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24

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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25

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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26

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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27

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

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28

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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29

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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30

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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31

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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32

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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33

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 by flow cytometry, showed marked inter-individual variation (4-5 fold) in both cases and controls. There was a strong correlation between the ADP and TRAP responses and experimental analysis suggested that this was because the TRAP response is substantially mediated via the ADP receptor.;Expression of the GPIaIIa receptor on the platelet surface showed up to 10-fold variation between subjects. The G837A polymorphism in the GP1a gene had a marked effect on GPIaIIa expression (accounting for about one-fifth of the variation) but did not influence the risk of MI (odd ratio 1.12 (95%CI 0.86-1.46)). Expression of the GPIIbIIIa receptor in both the resting state and after agonist stimulation was not affected by C196T polymorphism in the GPIIIa gene and did not influence risk of MI (odds ratio=0.94 (0.61-1.45)).;Of the emerging risk factors, fibrinogen (p<0.001) and Lp(a) (p = 0.016) were higher in the cases. There were significant effect of the G455A polymorphism in the fibrinogen beta chain gene and the C93T polymorphism in the apolipoprotein (a) gene on fibrinogen and Lp(a) levels, respectively.
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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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35

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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36

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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37

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.
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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38

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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39

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.
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40

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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41

Grimaldi-Bensouda, Lamiae. "Evaluation et application d’une nouvelle méthode systématique cas-référents en pharmaco-épidémiologie. Etudes dans l’infarctus du myocarde." Thesis, Tours, 2009. http://www.theses.fr/2009TOUR3136.

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L’objectif de ce travail est de présenter et évaluer une nouvelle méthode, PGRx,systématique cas-référents en pharmaco-épidémiologie avec son application à l’étudede l’infarctus du myocarde (IDM). Elle se distingue par la collecte systématique etcontinue de cas d’événements dans des centres spécialisés et d’un pool de référenceen médecine générale dont sont tirés les témoins appariés aux cas. L’évaluation durisque d’IDM associé au diclofénac (OR 1.5) et celle du bénéfice associé aux statines(OR 0.75) montrent des résultats similaires à ceux publiés (respectivement OR 1.4 etOR 0.74). Nous montrons que les référents sont un échantillon représentatif de lapopulation française en termes de motif de consultation et valide en termesd’évaluation de facteurs de risque. La concordance entre la mesure de l’exposition parla déclaration du patient et par les prescriptions médicales est excellente pour lesmédicaments cardiovasculaires (95%). Notre travail sur une série d’études montre quela collecte systématique de cas et d’un pool de référence, selon la méthode PGRx, estfaisable, reproductible et valide en termes de résultats et d’indicateurs de qualité
The objective of this work is to present and assess PGRx, a new systematic case-referentsmethod in pharmacoepidemiology and its application on the study of themyocardial infarction (MI). The originality of PGRx is the systematic and on-goingcollect of cases of events in a network of specialized centres and of a pool of referentsin general practice (GP), from which controls are selected by matching to the cases.The assessment of the risk of MI associated with diclofenac (OR 1.5) and of thebenefit on MI associated with statins (OR 0.75) displays similar results than theliterature (respectively OR 1.4 and OR 0.74).We show that the pool of referents is arepresentative sample of the French population in terms of reasons of consulting a GPand valid in terms of risk factors’assessment. Agreement between the measure ofexposure from patients’ self-report and from physician’s report of their prescriptionsis excellent on cardiovascular drugs (95%). Our work, through several studies, showsthat the systematic collect of cases and of a reference pool by the PGRx method isfeasible, reproducible and valid in terms of results and quality indicators
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42

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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43

Cediel, Calderón Germán Eduardo. "Papel de la troponina i como biomarcador pronóstico en pacientes atendidos en los servicios de urgencias sin diagnóstico de síndrome coronario agudo." Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/435687.

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En els últims anys, l'ús generalitzat de la troponina en els serveis d'urgències, ha permès la seva detecció en pacients amb diagnòstics clínics diferents a la síndrome coronària aguda (SCA). L'objectiu d'aquesta tesi va ser establir el valor pronòstic d'una troponina I (cTnI) elevada en el seguiment dels pacients atesos en un servei d'urgències i que no són diagnosticats de SCA, estudiant també, el seu valor pronòstic en els pacients donats d'alta directament des d´urgències. També ens plantegem identificar aquells pacients amb diagnòstic d'infart de miocardi (IM) tipus 2 i injúria miocàrdica no isquèmica i comparar la seva mortalitat i esdeveniments cardiovasculars adversos en el seguiment. Per respondre a aquests objectius es va realitzar un estudi de cohorts observacional i retrospectiu en el qual es van incloure pacients atesos al servei d'urgències de l'Hospital Universitari Joan XXIII als que es va sol·licitar almenys una determinació de cTnI. Es van identificar les variables demogràfiques, clíniques i analítiques de l'episodi agut, així com les troballes electrocardiogràfiques i les principals exploracions cardiològiques realitzades. Hem observat que els pacients amb troponina I elevada no diagnosticats de SCA van tenir pitjor supervivència que els pacients amb SCA i els pacients amb cTnI negativa. A més, la cTnI constitueix un marcador independent associat a mortalitat en el seguiment dels pacients que són donats d'alta directament des d´urgències. Finalment, una alta proporció de pacients atesos en urgències amb cTnI positiva compleixen criteris diagnòstics d'IM tipus 2. Els pacients amb diagnòstic d'IM tipus 2 i injúria miocàrdica no isquèmica es caracteritzen per tenir un perfil clínic similar, una elevada taxa de mortalitat i menor proporció de reingrés per SCA en comparació als pacients amb diagnòstic d'IM tipus 1.
En los últimos años, el uso generalizado de la troponina en los servicios de urgencias (SU), ha permitido su detección en pacientes con diagnósticos clínicos diferentes al síndrome coronario agudo (SCA). El objetivo de esta tesis fue establecer el valor pronóstico de una troponina I (cTnI) elevada en el seguimiento de los pacientes atendidos en un SU y que no son diagnosticados de SCA, estudiando a su vez, su valor pronóstico en los pacientes dados de alta directamente desde urgencias. También nos planteamos identificar a aquellos pacientes con diagnóstico de infarto de miocardio (IM) tipo 2 e injuria miocárdica no isquémica y comparar su mortalidad y eventos cardiovasculares adversos en el seguimiento. Para responder a estos objetivos se realizó un estudio de cohortes observacional y retrospectivo en el que se incluyeron pacientes atendidos en el SU del Hospital Universitario Joan XXIII a quienes se solicitó al menos una determinación de cTnI. Se identificaron las variables demográficas, clínicas y analíticas del episodio agudo, así como los hallazgos electrocardiográficos y las principales exploraciones cardiológicas realizadas. Hemos observado que los pacientes con troponina I elevada no diagnosticados de SCA tuvieron peor supervivencia que los pacientes con SCA y los pacientes con cTnI negativa. Además, la cTnI constituye un marcador independiente asociado a mortalidad en el seguimiento de los pacientes que son dados de alta directamente desde urgencias. Finalmente, una alta proporción de pacientes atendidos en los SU con cTnI positiva cumplen criterios diagnósticos de IM tipo 2. Los pacientes con diagnostico de IM tipo 2 e injuria miocárdica no isquémica se caracterizan por tener un perfil clínico similar, una elevada tasa de mortalidad y menor proporción de reingreso por SCA en comparación a los pacientes con diagnóstico de IM tipo 1.
Recently, the widespread use of troponin in emergency services has allowed its detection in patients who are not diagnosed with acute coronary syndrome (ACS). The aim of this thesis was to establish the prognostic value of an elevated troponin I (cTnI) in follow-up of patients admitted to the emergency department and without ACS, also studying, its prognostic value in patients discharged directly from the emergency department. We also aimed to identify patients with diagnosis of type 2 myocardial infarction and non-ischaemic myocardial injury and to compare their mortality and cardiovascular events at follow-up. In order to respond to these objectives, an observational and retrospective cohort study was carried out, including all patients admitted at the emergency department in the Hospital Universitario Joan XXIII, and who underwent at least one cTnI determination. We identified the demographic, clinical and analytical variables of the acute episode, as well as the electrocardiographic findings and the main cardiological explorations performed. We found that patients with high troponin levels and without ACS had higher rates of mortality than patients with ACS and patients with negative troponin. In addition, cTnI is an independent predictor associated with mortality in follow-up of patients discharged directly from the emergency department. Finally, a high percentage of patients admitted in the emergency department with high levels of cTnI meet diagnostic criteria for type 2 IM. Patients with a final diagnosis of type 2 myocardial infarction and non-ischemic myocardial injury have a comparable clinical profile, higher rates of mortality and lower readmission rates for ACS compared with patients with type 1 myocardial infarction.
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44

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 high-risk populations where these biomarkers are of reduced initial diagnostic value and/or their measurement may result in an unnecessary delay to acute myocardial infarction diagnosis. The primary aim of this thesis is to evaluate the BSPM in these groups, namely those patients with: • Negative cardiac biomarkers at presentation; • ST-segment depression only on ECG at presentation; • Typically 'balanced ischaemia' on ECG, i.e. in left main coronary artery stenosis; • Ventricular Fibrillatory cardiac arrest; and • Extreme Body Mass Index.
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45

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 is excellent, adherence is known to decline within weeks of hospital discharge. This decline in evidence-based medication use was confirmed in a population of patients with coronary artery disease in Ontario (Chapter 3). Furthermore, it was demonstrated that this decline was consistent across all medication classes and subgroups of patients. We developed a protocol (Chapter 4) for a cluster-randomized controlled trial evaluating the impact of repeated reminders sent by mail to the family physician and the patient, starting one month after the STEMI. The fifth chapter highlights the results of the cluster-randomized controlled trial, which demonstrates suboptimal persistence to all 4 of 4 cardiac medication classes at 12-months. There was no significant difference compared to usual care in the use of guideline-recommended medications post-STEMI when participants (and their family physicians) receive repeated postal reminders.
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46

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 behavioural change was then examined. Fourthly, sociodemographic, clinical and psychosocial predictors of health-enhancing behaviours were explored.These health-enhancing behaviours included non-smoking behaviours, normal body mass index (BMI), adequate physical activity, medication adherence and low dietary fat intake. Finally, the study examined relationships between sociodemographic , psychosocial and modifiable lifestyle factors, based on Antonovsky's hypothesis on sense of coherence(SOC), stress and adaptive coping. The study highlights that some modifiable risk factors, for example, being overweight or obese and physical inactivity were more resistant to change following an AMI.This finding, and the relationship between stress and increased dietary fat suggest a need for individualised programs to support the specific needs of AMI patients to change their modifiable cardiac risk factors.
Doctor of Philosophy (PhD)(Health)
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47

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].
"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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48

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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49

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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50

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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