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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 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.
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 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.<br>Applied Science, Faculty of<br>Nursing, School of<br>Graduate
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-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.
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, 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.
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 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.
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 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.
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 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'.
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 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.
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 exercise, eating a meal and circadian rhythms in healthy
volunteers were examined in three experimental studies. Case-control studies
were used for assessing the mechanism and etiology of ischaemic
brain infarction triggered during alcohol intoxication.
Alcohol drinking did not potentiate the effects of physical
exercise on platelet function. Sleeping while under acute intoxication
resulted in a significant activation of platelets, as shown by increased urinary
excretion of a thromboxane metabolite. On the other hand, ingestion
of a moderate dose of red wine seemed to attenuate platelet aggregation
measured ex vivo, irrespective of whether the
wine was consumed with a meal or alone. However, both red wine and
a larger acute dose of alcohol in fruit juice inhibited fibrinolytic
activity.
In a case-control study, platelet count and function were
evaluated in 426 consecutive patients hospitalized on account of
acute brain infarction. Compared with the hospital-based controls,
a higher than normal platelet count was observed immediately after
admission. Heavy drinkers showed both higher and lower than normal
platelet counts more often than the other patients with brain infarction. The
changes in platelet function among the heavy drinkers reflected
their recent drinking habits.
Another case-control study indicated that recent heavy drinking
of alcohol was an independent risk factor for cardiogenic embolism
to the brain. Recent heavy drinking also seemed to predispose subjects
to some other types of ischaemic brain infarction such as artery
to artery embolism due to large-artery atherosclerosis and cryptogenic
stroke, but these observations need to be confirmed in larger studies.
In conclusion, the results show some untoward effects of acute
heavy drinking of alcohol, which could contribute to the onset of
brain infarction either as triggering or as predisposing factors.
On the other hand, drinking of a moderate dose of red wine did not
have any clear untoward effect on healthy human volunteers.
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 should be associated with PFO and ischaemic stroke. Relatively little is known about the risk factors of cryptogenic brain infarction, although this subgroup of stroke is relatively common.
As the present diagnostic methods for detecting PFO have certain limitations, new non-invasive, simple and reliable methods would be useful. Two new methods examined here, the dye dilution method and ear oximetry, were both found to be feasible and to be highly specific and sensitive in relation to the present gold standard, contrast transoesophageal echocardiography.
A case-control study among adult patients with PFO and cryptogenic brain infarction showed the presence of a prothrombotic state, particularly factor V Leiden and prothrombin G2021OA gene mutation, to be associated with an increased risk of stroke, and migraine was also identified as a risk factor. Associations with the classical risk factors for venous thrombosis and Valsalva manoeuvre-like activities at the onset of stroke were also observed. The results lend support to the theory that paradoxical embolism is one of the pathogenic mechanisms behind cryptogenic brain infarction with associated PFO.
In another case-control study among adult patients with cryptogenic brain infarction but without associated PFO, prothrombotic states were not identified as risk factors, except that an association was found between elevated factor VIII activity and stroke. The major independent risk factors for such cryptogenic strokes were current cigarette smoking, hypertension and a low level of high density lipoprotein cholesterol.
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 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.
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.
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).
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 some therapies, such as acetyl salicylic acid and the statins, none of the currently approved medicines for management of either stable or complicated atherosclerosis has inflammation as a primary target. Monocytes, as representatives of the innate immune system, play a major role in the initiation, propagation and progression of atherosclerosis from a stable to an unstable state. Animal study data support a role of monocytes in acute coronary syndromes and in outcome post infarction; however, limited research has been done in humans. In this thesis I describe for the first time in a large cohort of ST elevation myocardial infarction(STEMI) patients followed up for three years that total monocyte count, monocyte subset 1(Mon 1), and monocyte subset 2 (Mon 2) are predictive of major adverse cardiac events (MACE)post STEMI (including death, new diagnosis of heart failure, recurrent acute coronary syndrome). Both the inflammatory function of monocyte subsets (via assessment and quantification of IKK as a surrogate for the NFB inflammatory pathway activation) as well as the phagocytic activity of monocytes were studied in order to describe the mechanism through which monocytes affect their action. There was no significant difference in the NFB pathway activity between those patients who developed an adverse event and those who did not. Also NFB activity was not predictive of MACE. However the phagocytic activity of Mon 1 and Mon 2 were predictive of MACE suggesting that phagocytic activity of monocytes is the mechanism through which monocytes implement their action. Also this supports that the newly described monocytes subset 2 (Mon 2) is predominantly an inflammatory monocyte subset, not reparative as Mon 3. Major adverse cardiac events were driven mainly by heart failure diagnosis and echocardiographic findings. Hence the association between ventricular remodelling and phenotypic and functional characterisation of monocytes subsets was studied in this thesis. Total monocyte count, Mon 1 and Mon 2 were again predictive of negative ventricular remodelling with increase in end systolic indexed volume of > 15% at 6 months follow up echocardiogram post infarction. Subclinical parameters of systolic dysfunction, namely global longitudinal strain and global circumferential strain were also significantly correlated with total monocyte count as well as Mon 1 levels. Given the above, I studied the effect of incorporating total monocyte count in Thrombolysis in Myocardial Infarction (TIMI) STEMI score to predict patient outcome at 30 days post infraction. C- statistics indicated improved prognostication of the TIMI STEMI model after incorporation of the total monocyte count into the model with improved area under the curve from 0.67 (for TIMI STEMI score), to area under the curve of 0.77 (TIMIMon score). This allows individual tailoring of secondary preventative therapy in order to improve patient outcome post infarction. Having described a potential mechanism through which the innate immune system affects outcome in STEMI patients, namely Mon1 and Mon2 through their phagocytic activity, the results from this thesis could be a stepping stone into targeted anti-inflammatory therapy in management of myocardial infarction.
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 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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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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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.<br>Doctor of Philosophy (PhD)(Health)
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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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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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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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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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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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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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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 4.21). The receiver-operating curve (ROC) area under curve (AUC) for NTproBNP was greater than TIMI risk score (0.79 vs. 0.67). CT-1 was raised in death or HF (0.77 vs. 0.73fmol/ml; p=0.001). In multivariate analysis CT-1 (HR 1.5) and NTproBNP (HR2.1) predicted death or HF independently of clinical factors. The ROC AUC for CT-1 was 0.62; NTproBNP was 0.77; AUC for combined markers was 0.84. Myotrophin was raised in patients with death, death or HF and MACE. In Cox analysis myotrophin (HR 5.07) and NTproBNP (HR 7.15) independently predicted death. Myotrophin was better at predicting death or HF (HR 2.35) and MACE (HR 1.69). Median MPO was raised in patients experiencing death, death or MI, death or HF and MACE. In Cox analysis median MPO predicted death (HR 13.05) and death or non-fatal MI (HR 5.07). A multimarker approach with NTproBNP may be useful for risk stratification in AMI patients.
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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 arterial coronària que, si no es resol, produceix finalment necrosi miocàrdica. El benefici del tractament de reperfusió és per tant temps-depenent; el tractament trombolític o mecànic, mitjançant angioplastia primària, redueix la necrosi miocàrdica. Els sistemes sanitaris actuals organitzen xarxes arreu dels territoris per a tractar pacients amb IAMEST dins el període temporal en el qual la reperfusió resulta beneficiosa en reduir la morbi-mortalitat a nivell poblacional. L’objectiu del treball d’aquest doctoral és investigar 1) com la implantació i el desplegament de la xarxa de tractament “Codi IAM” a Catalunya ha repercutit en l’administració del tractament de reperfusió i en la mortalitat per IAMEST en dones i 2) si la implantació de la xarxa de tractament urgent de l’IAMEST, “Codi IAM”, té alguna relació significativa amb el nivell socioeconòmic dels pacients amb IAMEST tractats a la ciutat de Barcelona, tant en quant al tractament com en quant al pronòstic. Els resultats de les anàlisi de la cohort prospectiva “Codi IAM” des del 2010 fins al 2017 mostren els beneficis de l’estandardització dels tractaments per a tota la societat i la seva inclusió en el sistema sanitari de prevenció secundària. Malgrat que tant les dones com els pacients amb menor nivell socioeconòmic presenten temps de tractament més perllongats, ni les dones ni els pacients amb menors rentes tenen pitjor pronòstic que els homes o que els pacients amb rendes més altes. Els resultats d’aquests dos treballs constitueixen una mostra de la importància de la posada en marxa de les xarxes de tractament urgent de l’IAMEST ja que impliquen un avenç en la prevenció de les desigualtats a nivell poblacional. Malgrat aquestes dades encoratjadores, a l’actual treball de tesi doctoral també es posa de manifest que encara hi ha marge de millora per a la detecció precoç, pel diagnòstic i el tractament de l’aterosclerosi, especialment per a les persones menys afavorides de la societat.<br>Las enfermedades isquémicas del corazón son la principal causa de muerte en el mundo y en Europa. El fenómeno etiopatogénico fundamental en la cardiopatía isquémica es la aterosclerosis y la inestabilización de las lesiones aterosclerosas comporta, eventualmente, un síndrome coronario agudo. El infarto de miocardio es una de las complicaciones más frecuentes de la enfermedad isquémica del corazón y se traduce en necrosis miocárdica. El infarto agudo de miocardio con elevación del segmento ST (IAMEST o STEMI) se precipita por la oclusión persistente de un vaso coronario epicárdico. La extensión del daño miocárdico resultante depende del tiempo de oclusión coronaria que, si no se resuelve, produce finalmente necrosis. El beneficio del tratamiento de reperfusión es por tanto tiempo-dependiente; el tratamiento trombolítico o mecánico, mediante angioplastia primaria, reduce la necrosis miocárdica. Los sistemas de sanitarios actuales organizan redes distribuidas en el territorio para tratar pacientes con IAMEST dentro del periodo temporal en el que la reperfusión es beneficiosa en cuanto a disminuir la morbi-mortalidad a nivel poblacional. El objetivo de este trabajo doctoral es investigar 1) como la implantación y el despliegue de la red de tratamiento “Codi IAM” en Cataluña ha repercutido en la administración del tratamiento de reperfusión y en la mortalidad por IAMEST en mujeres y, 2) si la implantación de esta red de tratamiento urgente de IAMEST, “Codi IAM”, guarda alguna relación significativa con el nivel socioeconómico de los pacientes con IAMEST tratados en la ciudad de Barcelona dentro de esta red, tanto en cuanto al tratamiento como en cuanto al pronóstico. Los resultados del análisis de la cohorte prospectiva de “Codi IAM&” desde 2010 hasta 2017 muestran los beneficios de la estandarización de los tratamientos para toda la sociedad y la inclusión de los pacientes en el sistema de prevención secundaria. Pese a que tanto las mujeres como los pacientes con menor nivel socioeconómico presentan tiempos más prolongados hasta el tratamiento, ni las mujeres ni los pacientes de bajo nivel socioeconómico tuvieron peor pronóstico que los hombres o los pacientes con rentas más elevadas. Los resultados de estos dos estudios constituyen una muestra de la importancia de la puesta en marcha de las redes de tratamiento urgente del IAMEST ya que implican un avance alentador en la prevención de las desigualdades a nivel poblacional; sin embargo, también revela que todavía hay margen de mejora para la detección precoz, diagnóstico y el tratamiento de la aterosclerosis, especialmente para las personas menos favorecidas de la sociedad.<br>Ischemic heart disease (IHD) is the leading cause of deaths in the world. In Europe ischemic heart disease is also the leading cause of death in both women and men. The disruption of an atherosclerotic lesion is the most common etiopathogenic finding of this entity. Myocardial infarction is a main complication within the IHD body given the fact that it results in myocardial necrosis. ST-elevation myocardial infarction (STEMI) is precipitated by the persistent occlusion of an epicardial coronary vessel. Limiting myocardial necrosis is based on a timely treatment with reperfusion in which the thrombus that is occluding the coronary artery is retrieved by means of mechanical or lytic-drugs. Benefits of STEMI reperfusion treatment are therefore time-depedent. Health systems have organized networks to treat patients with STEMI within a time window in order to obtain benefits from extensive early reperfusion and decrease complications at population level.
The aim of this work has been to investigate: 1) the benefits for women of a contemporary STEMI network “Codi-IAM&” which treats STEMI patients in the region of Catalonia, and 2) the relationship of socioeconomic status with treatment and prognosis after STEMI treated within this network. The results of the analysis of the prospective cohort of Codi IAM from 2010 to 2017 showed the benefits of the standardization of treatments for all society and the inclusion of citizens into a secondary prevention measures. Neither women nor patients with low socioeconomic status had worse prognosis than men or those with higher income. The results of these two studies constitute an important and encouraging achievement to prevent inequalities, however it also reveals that there is still room to improvement by ameliorating atherosclerosis detection and treatment especially for those who are less advantaged in society.<br>Universitat Autònoma de Barcelona. Programa de Doctorat en Medicina
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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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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 eikonal diffusion equation to simulate the electrophysiology; a continuum mechanical model incorporating a passive mechanical model of Usyk to describe the nonlinear, anisotropic and nearly compressible nature of cardiac tissue; and an active stress model of Guccione to model the contraction of cardiac tissue. Boundary conditions modelling the blood pressure on the heart wall were applied to simulate the cardiac cycle.
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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 compared to wild type (WT) BMCs. However, in the mouse MI model, Glo1 BMCs did not improve cardiac function or vascularity or reduce scar formation compared to WT BMCs and saline treatments.
In conclusion, Glo1 overexpression in BMCs does not confer superior therapeutic efficacy for treating MI under the conditions tested.