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1
Henderson, Louise M. Rosamond Wayne D. "Alcohol and cardiovascular disease." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,492.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Epidemiology, School of Public Health." Discipline: Epidemiology; Department/School: Public Health.
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Yuyun, Matthew F. "Albuminuria and cardiovascular disease." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440608.
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Gadd, Malin. "Cardiovascular diseases in immigrants in Sweden /." Stockholm : Neurotec, Center for family and community medicine, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-627-1/.
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Hammett, Christopher John Keith. "Inflammatory markers and cardiovascular disease." Thesis, University of Auckland, 2010. http://hdl.handle.net/2292/14345.
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Background: Inflammation is now recognised to play a central part in the initiation, progression and clinical manifestation of atherosclerotic cardiovascular disease. Correspondingly, on a population level, circulating levels of a wide range of inflammatory markers have been shown to be predictive of future cardiovascular events, regardless of whether they are measured in asymptomatic people, patients with stable angina, or patients with acute coronary syndromes. These include both systemic markers of inflammation such as the white blood cell count (WBC), fibrinogen, and C-reactive protein (CRP), and locally produced mediators of inflammation such as the cellular adhesion molecule soluble intercellular adhesion molecule 1 (sICAM-1), the cell-surface protein soluble CD40 ligand (sCD40L), and the metalloproteinase pregnancy associated plasma protein-A (PAPP-A). Investigation of these inflammatory markers has given many useful insights into the mechanisms that underlie the development of atherosclerosis and atherosclerotic clinical events. However, although the association (on a population level) of raised inflammatory markers with increased atherosclerotic events is widely accepted, the clinical utility of these markers (their ability to provide meaningful additional information that will help individualise treatment strategies and lead to better clinical outcomes) remains a subject of vigorous debate. Consequently, the research presented in this thesis has two broad purposes: to determine the value of inflammatory markers in a particular clinical situation (the prediction of restenosis following percutaneous coronary intervention), and to examine whether vascular inflammation is a modifiable risk factor (whether marker levels can be lowered by health interventions such as drug therapy, exercise, or smoking cessation). Methods and results: a. Inflammatory markers and restenosis To investigate whether inflammatory markers are predictive of restenosis following PCI, inflammatory markers (CRP, sICAM-1, sCD40L and PAPP-A) were measured prior to and 48 hours, 1 week and 1 month after elective PCI, and angiographic follow-up was performed at 6 months, in 133 stable angina patients. PCI led to a significant rise in CRP, sCD40L and PAPP-A levels 48 hours post-procedure, but neither pre-PCI nor post-PCI inflammatory marker levels were predictive of restenosis. This lack of association could not be attributed to concurrent use of medications such as statins, thienopyridines or glycoprotein IIb/IIIa inhibitors, since 50% of patients were not on statins and no patients received thienopyridines or glycoprotein IIb/IIIa inhibitors during the study. b. The effects of lipid lowering agents on inflammatory marker levels The effects of lipid-modifying agents on inflammatory marker levels were tested in 215 participants with stable angina randomised to simvastatin or placebo, and a further 100 participants randomised to simvastatin or bezafibrate, over a treatment period of at least 2 years. In addition, the effect of statins on the inflammatory response to PCI was assessed in a subset of 92 patients by comparing inflammatory marker levels before and 48 hours, 1week, and 1 month after PCI in those randomised to simvastatin versus those randomised to placebo. Although simvastatin led to a reduction in CRP levels with long-term therapy, the effect was modest and variable compared to the predictable effect on cholesterol levels. Average CRP levels fell ~5%, compared to a 40% reduction in LDL cholesterol, and CRP levels increased in nearly a quarter of patients on simvastatin. In addition, simvastatin did not lower levels of any other inflammatory marker, and had no appreciable effect on the inflammatory response to PCI. Similarly, bezafibrate therapy did not lower levels of any inflammatory marker. c. The effect of exercise training on inflammatory marker levels. The effects of exercise training on inflammatory markers were assessed in two separate randomised controlled trials. The first trial involved CRP measurement in 63 healthy elderly participants randomised to either 6 months��� exercise training or to a control group. The second trial involved measurement of several inflammatory markers (WBC, fibrinogen, CRP, sCD40L, sICAM-1) in 152 healthy female smokers randomised to either 12 weeks��� exercise training or to a health education (control) group as part of a smoking cessation program. In both trials, exercise led to a significant improvement in fitness but had no effect on inflammatory marker levels. d. The effect of smoking cessation on inflammatory marker levels The smoking cessation trial also investigated the effect of abstinence from smoking on inflammatory marker levels. Forty-eight individuals (35%) achieved 6 weeks verified abstinence from smoking. Abstinence caused a significant decrease in WBC and fibrinogen levels but had no effect on other inflammatory markers (CRP, sICAM-1, and sCD40L). Conclusions: There are several important findings from this research. Firstly, inflammatory markers are not useful in the prediction of restenosis following PCI in stable angina. Secondly, neither simvastatin nor bezafibrate have major antiinflammatory effects in vivo. This brings into question the mechanism(s) by which statins lower CRP, and has implications for recent proposals in the literature advocating the clinical use of CRP to titrate statin therapy. Thirdly, smoking cessation leads to a reduction in WBC and fibrinogen levels (which may reflect changes in pulmonary inflammation), but neither exercise nor smoking cessation are associated with a broad reduction in inflammatory markers linked to cardiovascular risk. It is therefore unlikely the appreciable cardiovascular benefits of these interventions are due in any substantial part to antiinflammatory effects. It remains to be demonstrated whether there are interventions which can reliably lower inflammatory marker levels, whether this decreases cardiovascular risk, and whether measurement of inflammatory markers improves upon current management of cardiovascular disease and leads to actual clinical benefit.
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Hermansson, Jonas. "Shift work and cardiovascular disease." Licentiate thesis, Mittuniversitetet, Institutionen för hälsovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-17466.
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Shift work is a work schedule being the opposite of normal daytime work, often defined as working time outside normal daytime hours (06:00 to 18:00). In recent years, shift work has been associated with an increased risk of numerous chronic conditions including for example cardiovascular disease, some types of cancer, type II diabetes, and the metabolic syndrome. While some studies on the association between shift work and chronic disease have found results supporting it, others have not. Therefore, more research is needed to clarify potential associations.The aim of this thesis was to further study the proposed association between shift work and cardiovascular disease. This was addressed by performing two studies, one analysing if shift workers had an increased risk of ischemic stroke compared to day workers. The other study analysed whether shift workers had an increased risk of short-term mortality (case fatality) after a myocardial infarction compared to day workers. The studies were performed using logistic regression analysis in two different case-control databasesThe findings from the first study indicated that shift workers did not have an increased risk of ischemic stroke. The findings from the second study showed that male shift workers had an increased risk of death within 28 days after a myocardial infarction; the results did not indicate an increased risk for female shift workers. The results from both studies were adjusted for both behavioural and medical risk factors without affecting the results. The findings from this thesis provide new evidence showing that male shift workers have an increased risk of death 28 days after a myocardial infarction, however more research is needed to clarify and characterise any such potential associations.
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Soveri, Inga. "Renal Dysfunction and Cardiovascular Disease." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6941.
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Rosenlund, Mats. "Environmental factors in cardiovascular disease /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-292-6/.
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Shbat, Layla. "Immune modulation in cardiovascular disease." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103617.
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The importance of the adaptive immune response in cardiovascular disease has been increasingly appreciated. However, limited information is available on immune modulation in the context of hypertension and atherosclerosis. In order to fill this knowledge gap, the amount of T regulatory (Treg) cells was determined by flow cytometry on cells from the spleen and the aorta in two murine models, namely angiotensin (Ang) II-induced hypertension (HT) and endothelin-1 (ET-1)-exacerbated high fat diet (HFD)-induced atherosclerosis in apolipoprotein E knockout (apoE-/-). Two groups of mice were studied. In the first study, 12-week old male C57BL/6 mice were infused with Ang II (1 µg/kg/min, s.c.) for 14 days via an osmotic pump or implanted with a dummy pump. In the second study, 8-week old C57BL/6 male transgenic mice with endothelium-restricted preproendothelin-1 (eET-1) overexpression, apoE-/-, eET-1/apoE-/- crosses, and wild type (WT) mice were fed a HFD or a normal diet (ND) for 8 weeks. A trend towards an increase in several T lymphocyte subpopulations including natural (CD4+CD25+Foxp3+) Tregs was observed in the spleen of mice infused with Ang II whereas in aorta natural Tregs tended to decrease. In atherosclerosis, an increase in classical (CD4+CD25+) Tregs was observed in the spleen of eET-1. HFD reduced the Treg content in the spleen of both WT and eET-1. In addition, HFD tended to increase natural Tregs in eET-1/apoE-/- crosses. In aorta, HFD increased classical Tregs and tended to increase natural Tregs in eET-1 whereas it tended to decrease natural Tregs in eET-1/apoE-/- crosses. The lack of significant change in the above studies limits drawing conclusions. However, the results suggest that ET-1 and HFD have an impact on Treg populations in the spleen and aorta. Additional animals and/or refinement in the techniques could lead to more definitive conclusions.Le rôle de la réponse immunitaire adaptative dans l'hypertension et l'athérosclérose commence à être apprécié. Cependant, il n'est pas clair que les lymphocytes T régulateurs (Tregs) jouent un rôle dans ces deux pathologies. Dans le but d'éclaircir le rôle de ces lymphocytes, le contenu en Tregs a été déterminé à l'aide de cytométrie de flux dans la rate et l'aorte de deux modèles murins, l'hypertension induite par l'angiotensine (Ang) II et l'athérosclérose induite par une diète riche en gras (DRG) dans des souris knockout pour l'apolipoprotéine E (apoE-/-) exagérée par la surexpression de l'endothéline (ET)-1. Deux groupes de souris ont été étudiés. Dans le premier groupe, des souris mâles C57BL/6 de 12 semaines ont été infusées ou pas avec de l'Ang II (1 µg/kg/min, s.c.) pendant 2 semaines. Dans le second groupe, des souris mâles C57BL/6 de 8 semaines transgéniques surexprimant l'ET-1 dans les cellules endothéliales (eET-1), apoE-/-, eET-1/apoE-/- et sauvages (WT) ont été nourries avec une DRG ou une diète normale (DN) pendant 8 semaines. Les souris infusées avec l'Ang II présentaient une tendance à l'augmentation de plusieurs sous-populations de lymphocytes T incluant les Tregs naturels (CD4+CD25+Foxp3+) dans la rate. Par contre, au niveau de l'aorte les Tregs naturels tendaient à diminuer. Dans l'étude de l'athérosclérose, une augmentation des Tregs (CD4+CD25+) a été observée dans la rate des souris eET-1. La DRG a réduit le contenu de Tregs dans la rate des souris WT et eET-1 et tendait à accroître les Tregs naturels dans la rate des eET-1/apoE-/-. Au niveau de l'aorte, la DRG a augmenté les Tregs et tendait à accroître les Tregs naturels dans les eET-1 et tendait à diminuer ces lymphocytes dans les eET-1/apoE-/-. Le manque de changements significatifs limite la possibilité de tirer des conclusions. Cependant, les résultats suggèrent que l'ET-1 et la DRG ont un impact sur la population de Tregs dans la rate et l'aorte. Des animaux additionnels et/ou un raffinement des techniques pourraient donner des résultats plus définitifs.
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Jhund, Pardeep S. "Socioeconomic deprivation and cardiovascular disease." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2213/.
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Socioeconomic deprivation (SED) is inversely associated with mortality. The most deprived are at a higher risk of all cause mortality and cardiovascular mortality. However, only limited study of the relationship between SED and non-fatal cardiovascular disease has been previously undertaken. In those studies that have examined the relationship between SED and non-fatal cardiovascular disease, analyses have been limited to one form of cardiovascular disease (CVD), such as myocardial infarction or stroke and often prevalent disease. Furthermore, these studies have often failed to examine the association between SED and CVD whilst adjusting analyses for cardiovascular risk factors which are more prevalent in the most deprived. The aim of this work was to examine the association between SED and a number of cardiovascular outcomes after adjusting for the traditional cardiovascular risk factors of age, sex, smoking, blood pressure, diabetes mellitus and cholesterol. To determine is SED is in fact a risk factor for CVD after adjustment for these other risk factors, the relationship between SED and a number of fatal and non-fatal cardiovascular outcomes was examined. A number of forms of CVD were examined, including all coronary heart disease, myocardial infarction, stroke and heart failure A cohort of over 15,000 men and women who participated in the Renfrew Paisley cohort study was examined. These individuals were enrolled between 1974 and 1976 and underwent comprehensive screening for cardiorespiratory risk factors. They have since been followed for hospitalisations and deaths for 28 years. SED was measured using the Registrar General’s social class system and the Carstairs Morris index of deprivation. Rates of fatal and non-fatal outcomes were calculated, as were a number of composite outcomes. Adjusted analyses using multivariable regression were conducted to account for the risk factors of age, sex, smoking, blood pressure, diabetes and cholesterol. Further adjustment for the risk factors of lung function as measured by forced expiratory volume in 1 second, cardiomegaly on chest x-ray, body mass index, and a history of bronchitis was also made. The association between SED and the risk of recurrent cardiovascular hospitalisations, the burden of cardiovascular disease, as well as mortality and premature mortality was assessed for SED. I found that SED was associated with higher rates of hospitalisation for CVD disease in men and women irrespective of the measure of SED, either social class or the area based score of the Carstairs Morris index. This association persisted after adjustment for the traditional cardiovascular risk factors of age, sex, smoking, systolic blood pressure and diabetes and cholesterol. Further adjustment for lung function, the presence of bronchitis, body mass index and cardiomegaly on a chest x-ray did not explain the relationship between SED and each outcome. This risk was long lasting and persisted to the end of follow up. The strength of association of SED with coronary heart disease, myocardial infarction and stroke and all cause mortality was similar. The risk of a recurrent CVD hospitalisation was not higher in the most deprived after adjustment for CVD risk factors. However, I observed that SED was associated with higher mortality following an admission to hospital with CVD, before and after adjustment for cardiovascular risk factors of age, sex, smoking, systolic blood pressure, cholesterol and diabetes and after adjusting for the year of first developing cardiovascular disease. All cause mortality and cardiovascular mortality was highest in the most deprived. Again this association persisted after adjustment for cardiovascular risk factors. The most deprived also experienced longer hospital stays than the least deprived for a number of cardiovascular diseases including myocardial infarction and stroke. As a result the costs associated with cardiovascular disease admissions to hospital were highest in the most deprived despite their higher risk of dying during follow up. The cost differential was also explained by the finding that the most deprived experienced a higher number of admissions per person. Finally, the population attributable risk associated with SED is comparable to that of other traditional cardiovascular risk factors. In conclusion, I have found that the risk of CVD in the most deprived is higher even after adjustment for a number of cardiovascular risk factors. The numbers of hospitalisations, costs and mortality are also highest in the most deprived. Efforts are required to redress this imbalance. This can be achieved at the level of the individual through health care interventions to reduce the absolute burden of cardiovascular risk factors and to treat disease. However, societal level interventions are also required to tackle this problem as SED exerts complex effects on health that seem to also be independent of risk factors.
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Andersen, Kasper. "Physical Activity and Cardiovascular Disease." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-217309.
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The aim was to investigate associations of fitness and types and levels of physical activity with subsequent risk of cardiovascular disease. Four large-scale longitudinal cohort studies were used. The exposures were different measures related to physical activity and the outcomes were obtained through linkage to the Swedish In-Patient Register. In a cohort of 466 elderly men without pre-existing cardiovascular disease, we found that skeletal muscle morphology was associated with risk of cardiovascular events. A high amount of type I (slow-twitch, oxidative) skeletal muscle fibres was associated with lower risk of cardiovascular events and high amount of type IIx was associated with higher risk of cardiovascular events. This association was only seen among physically active men. Among 39,805 participants in a fundraising event, higher levels of both total and leisure time physical activity were associated with lower risk of heart failure. The associations were strongest for leisure time physical activity. In a cohort of 53,755 participants in the 90 km skiing event Vasaloppet, a higher number of completed races was associated with higher risk of atrial fibrillation and a higher risk of bradyarrhythmias. Further, better relative performance was associated with a higher risk of bradyarrhythmias. Among 1,26 million Swedish 18-year-old men, exercise capacity and muscle strength were independently associated with lower risk of vascular disease. The associations were seen across a range of major vascular disease events (ischemic heart disease, heart failure, stroke and cardiovascular death). Further, high exercise capacity was associated with higher risk of atrial fibrillation and a U-shaped association with bradyarrhythmias was found. Higher muscle strength was associated with lower risk of bradyarrhythmias and lower risk of ventricular arrhythmias. These findings suggest a higher rate of atrial fibrillation with higher levels of physical activity. The higher risk of atrial fibrillation does not appear to lead to a higher risk of stroke. In contrast, we found a strong inverse association of higher exercise capacity and muscle strength with vascular disease. Further, high exercise capacity and muscle strength are related to lower risk of cardiovascular death, including arrhythmia deaths. From a population perspective, the total impact of physical activity on cardiovascular disease is positive.
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Islam, Shahed. "Therapeutic hypothermia in cardiovascular disease." Thesis, Anglia Ruskin University, 2017. http://arro.anglia.ac.uk/704083/.
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Introduction: Historical trials demonstrated clinical benefit of therapeutic hypothermia (TH) in unconscious cardiac arrest survivors. However, recent research raised important unanswered questions about this concept. Cardiac arrest associated mortality and morbidity including psychological trauma for survivors and caregivers remain alarmingly high, warranting further research in this field. TH has also been shown to offer additional protection against reperfusion injury in experimental models of myocardial ischaemia. However, co-administration of TH in conscious patients undergoing treatment for acute myocardial infarction (AMI) is potentially challenging. Methodology: (i) Rhinochill®, a novel intranasal cooling device is compared to Blanketrol for TH induction in unconscious cardiac arrest survivors, investigating efficacy and clinical outcome at hospital discharge. (ii) The emotional burden of cardiac arrest in patients and their caregivers is documented and the impact of simple interventions on quality of life is assessed. (iii) The feasibility of co-administration of TH in conscious patients undergoing emergency treatment of AMI is investigated. Results: (i) Rhinochill® is found to be more efficient in TH induction when measured from the tympanic membrane. However, Rhinochill® did not offer any superior clinical benefit. (ii) Simple psychological interventions are shown to improve quality of life in cardiac arrest survivors. (iii) Co-administration of endovascular cooling is shown to be feasible in conscious patients undergoing AMI treatment with minimum disruption to patient care. Discussion: Delays in TH administration may offset any potential benefit that it can offer in neuroprotection and therefore, earlier targeted brain cooling with more efficient portable devices is worth investigating. Improving quality of life of cardiac arrest survivors has been shown to be cost effective and therefore, investing in resources to better identify and help those at risk is justified. Delivery of TH in conscious heart attack patients is feasible and safe but more efficient endovascular cooling devices are required and these will need to be assessed in larger trials to assess the effect on clinical outcomes.
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Ness, Andrew Robert. "Vitamin C and cardiovascular disease." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627295.
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Gobin, Reeta Rukmini Devi. "Metabolic syndrome and cardiovascular disease." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610102.
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Hermansson, Jonas. "Shift work and cardiovascular disease." Doctoral thesis, Mittuniversitetet, Avdelningen för hälsovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-26219.
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Shift work is often defined as working time outside daytime hours (06:00 to 18:00). In recent years, shift work has been associated with an increased risk of cardiovascular disease (CVD), type II diabetes, and the metabolic syndrome. While some studies support the associations, others do not. Therefore, more research is needed. The aim of this thesis was to further study the association between shift work and CVD. This was addressed by performing four studies, one analysed if shift workers had an increased risk of ischemic stroke, the second study analysed whether shift workers had an increased risk of short-term mortality (case fatality)after a myocardial infarction (MI). The third study analysed if shift work interacts with other risk factors for MI and the fourth study analysed if parental history of CVD interacted with shift work on the risk of MI. The studies were performed using logistic regression analyses and additive interaction analyses in two different case-control databases. Shift workers did not have an increased risk of ischemic stroke. Male shift workers had an increased risk of death within 28 days after a MI. Shift work interacts with some CVD risk factors and interacts with paternal history of CVD and the risk of MI for males. The findings from this thesis provide new evidence showing that shift work is in different ways associated with an increased risk of MI and related mortality, but not with ischemic stroke. However, more research is needed to clarify and characterise these results.Vid tidpunkten för disputationen var följande delarbeten opublicerade: delarbete 3 manuskript, delarbete 4 manuskript
At the time of the doctoral defence the following papers were unpublished: paper 3 manuscript, paper 4 manuscript
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Willeit, Peter. "Natriuretic peptides and cardiovascular disease." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648533.
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Casas, Juan-Pablo. "Mendelian randomisation and cardiovascular disease." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2009. http://researchonline.lshtm.ac.uk/682420/.
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Background and aims: Homocysteine (Hcy), C-reactive protein (CRP), and Lipoprotein- associated phospholipase A2 (Lp-PLA2) have been associated with a high risk of cardiovascular disease. If casual, they are expected to provide additional tools for prevention. Utilising the unique properties of genetic variants (randomly allocated and unmodifiable), they could be used as unconfounded proxies of environmental exposures to investigate disease aetiology, known as Mendelian randomisation. Herein I conduct a series of Mendelian randomisation experiments to: (i) investigate the role of Hyc in stroke; (ii) judge causality of CRP in cardiovascular disease; (iii) investigate the validity of Lp-PLA2 as a therapeutic target in coronary heart disease (CHD) and; (iv) describe how the integration of cis-acting variants and their cognate proteins can be used to dissect causal pathways. Methods: For aim (i), I conducted synthesis research of published and unpublished studies investigating the MTHFR/C677T variant, Hcy and stroke. For aims (ii) to (iv), a series of prospective collaborations conducting de novo genotyping for CRP and PLA2G7 genes, were established using European-based cardiovascular genetic studies of adults. Results: The meta-analyses of studies on MTHFR/C677T-Hcy-Stroke to 2003, showed that subjects with the TT genotype had on average 1.93 µmol/L higher levels of Hcy compared with subjects with CC genotype, and an odds ratio (OR) of stroke of 1.26 (95%Cl: 1.14,1.40). An update analyses to 2008 showed that in both MTHFR-Hcy and MTHFR-stroke associations, studies in Asia had the largest effect, followed by Europe with intermediate effect, and lower or negligible effect in the Americas and Australasia. Analysis on CRP, indicated that subjects homozygous for the T-allele of CRP/+1444C>T variant despite having 0.68 mg/L higher levels of CRP, had no increase in risk of myocardial infarction (OR of 1.01 [95CI: 0.74,1.38]). A tagging- haplotype approach showed a gradual increase on CRP levels by haplotype, but no effect on CHID, diabetes or stroke. Analysis of the seven PLA2G7 tagging-SNPs showed that the best variant (rs1051931) had small to moderate effects on the Lp-PLA2 activity (up to 7% relative differences). No genetic signal with CHD was observed for any PLA2G7 variant, despite some comparisons including up to 8412 CHID cases. A description of the proof of principle, illustrating how to utilise cis-acting variants and their cognate proteins to distinguish causal from non-causal effects among correlated blood proteins was presented, using as an example 6 proteins that have been associated with CHD risk. Conclusions: Genetic evidence reported in this document suggested that the MTHFR effect is more pronounced in geographic regions associated with low folate intake. Genetic studies on CRP presented in this document indicated that CRP is unlikely to be causal in cardiovascular disease. A genetic approach using common variants in PLA2G7 had a reduced ability to confirm or reject Lp-PLA2 as a valid drug target. Finally, integration of cis-acting variants with their cognate proteins seems to be an effective way of dissecting biological pathways.
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Islam, Shahed. "Therapeutic hypothermia in cardiovascular disease." Thesis, Anglia Ruskin University, 2017. https://arro.anglia.ac.uk/id/eprint/704083/1/Islam_2017.pdf.
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Introduction: Historical trials demonstrated clinical benefit of therapeutic hypothermia (TH) in unconscious cardiac arrest survivors. However, recent research raised important unanswered questions about this concept. Cardiac arrest associated mortality and morbidity including psychological trauma for survivors and caregivers remain alarmingly high, warranting further research in this field. TH has also been shown to offer additional protection against reperfusion injury in experimental models of myocardial ischaemia. However, co-administration of TH in conscious patients undergoing treatment for acute myocardial infarction (AMI) is potentially challenging.
Methodology: (i) Rhinochill®, a novel intranasal cooling device is compared to Blanketrol for TH induction in unconscious cardiac arrest survivors, investigating efficacy and clinical outcome at hospital discharge. (ii) The emotional burden of cardiac arrest in patients and their caregivers is documented and the impact of simple interventions on quality of life is assessed. (iii) The feasibility of co-administration of TH in conscious patients undergoing emergency treatment of AMI is investigated.
Results: (i) Rhinochill® is found to be more efficient in TH induction when measured from the tympanic membrane. However, Rhinochill® did not offer any superior clinical benefit. (ii) Simple psychological interventions are shown to improve quality of life in cardiac arrest survivors. (iii) Co-administration of endovascular cooling is shown to be feasible in conscious patients undergoing AMI treatment with minimum disruption to patient care.
Discussion: Delays in TH administration may offset any potential benefit that it can offer in neuroprotection and therefore, earlier targeted brain cooling with more efficient portable devices is worth investigating. Improving quality of life of cardiac arrest survivors has been shown to be cost effective and therefore, investing in resources to better identify and help those at risk is justified. Delivery of TH in conscious heart attack patients is feasible and safe but more efficient endovascular cooling devices are required and these will need to be assessed in larger trials to assess the effect on clinical outcomes.
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Baker, J. E. "Ethnicity and cardiovascular disease prevention." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6524/.
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Background Public health interventions need to both improve health and reduce health inequalities, whilst using limited health care resources efficiently. Well-established ethnic differences in cardiovascular disease (CVD) raise the possibility that CVD prevention policies may not work equally well across ethnic groups. The aim of this thesis was to explore whether there are ethnic differences in the potential impact of two CVD prevention policy choices – the choice between mass and targeted screening for high cardiovascular risk, including the use of area deprivation measures to target screening, and the choice between population and high-risk approaches. Methods Cross-sectional data from the Health Survey for England 2003 and 2004 were used. Three sets of analyses were carried out – first, calculation of ethnic differences in the utility of area deprivation measures to identify individual socioeconomic deprivation; second, investigation of ethnic differences in the cost-effectiveness of mass and targeted screening for high cardiovascular risk; third, analysis of ethnic differences in the potential impact of population and high-risk approaches to CVD prevention. Results Area deprivation measures worked relatively effectively and efficiently at identifying individual socioeconomic deprivation in ethnic minority groups compared to the white group. In ethnic groups at high risk of CVD, cardiovascular risk screening programmes were a relatively cost-effective option, screening programmes targeted at deprived areas were particularly cost-effective, and population approaches were found to be an effective and equitable way of preventing CVD despite potential underestimation of their impact. Discussion This thesis found that ethnic minority groups in the UK are unlikely to be systematically disadvantaged by a range of CVD prevention policies that have been proposed, or implemented, for the general population. Additional CVD prevention policies, in particular those based on the population approach, should be implemented.
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Fry, Catherine Mary. "Vitamin D and cardiovascular disease." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/vitamin-d-and-cardiovascular-disease(68a482b3-7d7f-4cac-a798-1e5ed984d1f9).html.
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Evidence for the association between vitamin D status and cardiovascular disease (CVD) is reviewed. Cross-sectional analysis of data from the CRESSIDA and MARINA trials revealed a strong association between vitamin D status and arterial stiffness. An increase in vitamin D status measured as serum 25-OH-D concentrations after following advice to consume 1-2 portions of oily fish/wk was demonstrated (9.2 nmol/L, 95% CI 4.2, 14.2). The effects of malted milk drinks fortified with vitamin D2 or D3 at 5 and 10 μg/d vs. placebo taken for 4 wk on serum 25-OH-D metabolite concentrations were compared in 8 subjects/group in winter (minimal UVB exposure): mean increments ± SED vs. placebo were 9.4 ± 2.5 and 17.8 ± 2.4 nmol/L in 25-OH-D2 after 5 and 10 μg D2/d and 15.1 ± 4.7 and 22.9 ± 4.6 nmol/L in 25-OH-D3 after 5 and 10 μg D3/d. A total of 41 predominantly normotensive men and post-menopausal women (50-70 y) were randomly allocated to receive 10 μg/d D2 (Rx) or a placebo malted milk drink for 12 wk in winter. The specified primary outcomes of the trial were 24 h ambulatory blood pressure (BP) and flow mediated dilation (FMD) of the brachial artery. The mean increase ± SED in serum 25-OH-D2 on Rx vs. placebo was 22.8 ± 2.0 nmol/L (P < 0.001). The treatment effects (mean changes on Rx vs. placebo with 95% CI) were 0.17% (-1.62, 1.28; P=0.82) for FMD and -4.3 mm Hg (-7.3, -1.2; P=0.007) and -2.8 mm Hg (-5.4, -0.2; P=0.032) for systolic and diastolic BP respectively. This BP lowering effect of vitamin D2 in the winter months and the null finding with regard to FMD need confirmation with a larger sample. A trial of several years duration is required to demonstrate whether the association of PWV with vitamin D status is causal.
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Holmlund, Anders. "Oral health and cardiovascular disease." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8708.
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Tomson, Joseph. "Vitamin D and cardiovascular disease." Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/87895/.
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Cardiovascular disease (CVD) is the leading cause of death worldwide. Vitamin D is important for bones and for other body functions. Whether insufficient vitamin D causes CVD is unclear. Previous trials of vitamin D were unable to evaluate effects on CVD. This thesis will (i) review the literature on vitamin D and CVD; (ii) evaluate the observational associations between plasma 25(OH)D levels and CVD; and (iii) describe the design and results of the BEST-D trial. (i) Associations between baseline 25(OH)D levels and cause-specific mortality were evaluated in the Whitehall Resurvey of survivors undertaken in 1995, and findings included in a meta-analysis of similar studies. (ii) The BEST-D study was a randomised trial in older healthy volunteers of the effects of two doses of vitamin D3 (4000 IU or 2000 IU daily) compared to placebo, on blood 25(OH)D concentrations and CVD risk factors including blood pressure and arterial stiffness. (i) The Whitehall Resurvey of 5409 men with mean age of 77 years, among whom there were 3215 deaths showed an approximately linear (log-log scale) inverse association of plasma 25(OH)D concentrations and both CVD and non-vascular causes of death between 30 to 90 nmol/L. The meta-analysis confirmed the associations of 25(OH)D with CVD mortality. (ii) The BEST-D trial showed marked increases in 25(OH)D blood concentrations but no effects of taking higher doses of vitamin D3 for 12 months on blood pressure or arterial stiffness, compared to placebo. Plasma 25(OH)D is inversely associated with both CVD and non-vascular mortality. No effects were found after oral intake of vitamin D3 on blood pressure or arterial stiffness after 1 year. Randomised trials using adequate doses of vitamin D3 are needed, to evaluate causal effects of taking vitamin D on CVD outcomes.
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LAGUZZI, FEDERICA. "DIETARY HABITS AND CARDIOVASCULAR DISEASE." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/257427.
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BACKGROUND AND AIM: Diet, in particular dietary fats, and cardiovascular disease (CVD) are closely related. Dietary fats might be captured by measuring blood fatty acid profiles. The role of diet as well as the role of blood fatty acid (FA) levels, in CVD aetiology is still uncertain. Aims of this thesis were to investigate in a large cohort of 60-year-old Swedish men and women: 1) The association between self-reported dietary intake, with a specific focus on foods rich in fat, and selected serum cholesterol ester FAs (Project I); 2) The relation between self-reported intake of specific types of dietary fats (primary aim) and fruit and vegetables (secondary aim) and incident of CVD and all-cause mortality (Project II); 3) The relation between serum cholesterol FAs, with a specific focus on polyunsaturated FAs (PUFA)eicosapentaenoic acid (EPA), docosaesaenoic acid (DHA), linoleic (LA) and linolenic (ALA) acid and incident CVD and all-cause mortality (Project III).
METHODS: Data collected between 1997 and 1998 from 4,232 individuals (2,039 men and 2,139 women) aged 60, randomly selected from Stockholm County were used. The participants were followed regarding incident CVD up to 31st December 2012 using national registers yielding 359 incident CVD cases and 595 deaths. From nutritional data, collected by questionnaires, we created: 1) five diet scores reflecting intake of saturated fats in general, and fats from dairy, fish, processed meat and vegetable oils and margarines (Project I, II) 2) binary variables classifying study participants into exposed and unexposed and evaluating 16 specific dietary factors (Project II). Gas chromatography was used to assess 13 FAs in serum cholesterol esters (Project I, III). Association between each diet score and specific FAs was assessed by percentile differences (PD) with 95% confidence intervals (CI) at the 10th, 25th, 50th, 75th, and 90th percentile of each FA across levels of diet scores using quantile regression (Project I). Crude and adjusted Cox proportional hazards models were used to estimate hazard ratios (HR) with 95% CI in the association between specific self-reported dietary fats (diet scores and single dietary items), fruit and vegetables intake (Project II) and serum PUFA (Project III) and incidence of CVD and all-causes mortality.
RESULTS: In men and women combined, fish intake was associated with high serum proportions of EPA (50thPD=31.41, 95% CI= 27.77; 35.05) and DHA (50thPD=10∙51, 95% CI= 9.40; 11.62). Vegetable fat intake was associated with high serum proportion of total PUFA (50thPD 36.34, 95% CI= 22.77;49.92) and low proportion of total SFA (50thPD=11.33, 95%CI= 14.92;7.73). (Project I) In women, an increased risk of CVD was related to high consumption of spread butter or margarine (≥10g/day vs <10g/day), HR=1.49, CI=1.02 ; 2.20, and oily potatoes (≥2 times/week vs <2time/week), HR=2.00, CI=1.11;3.60. In men, an increased risk of early death was related to the consumption of butter (vs margarine), HR=1.28, CI=1.01; 1.62, high consumption of spread butter or margarine, HR=1.57, CI=1.23; 2.02 and egg consumption ≥4 times/week (vs <4times/week), HR=1.53, CI=1.15;2.02. In men, daily intake of fruits (vs <1time/day) was inversely related to early death, HR=0.75, CI=0.60; 0.94. (Project II) High serum EPA and DHA proportions were inversely associated with CVD in women (for EPA HR= 0.79, 95% CI 0.64; 0.97; for DHA HR= 0.74 0.61; 0.89) but not in men. Inverse associations with early death were also noted in men for high serum EPA proportion, HR=0.82, 95% CI 0.71;0.95; and DHA proportion, HR= 0.82, 95%CI= 0.71;0.94, and in women for high serum EPA proportion, HR=0.79, 95%CI= 0.65;0.96, and DHA proportion, HR= 0.78, 95% CI= 0.66;0.93. High serum ALA proprotion was associated with moderately increased of CVD incidence, HR= 1.16, 95% CI=1.02;1.32 in women whereas high serum LA proportion was associated with reduced all-cause mortality in men, HR= 0.73 95% CI=0.64;0.83. (Project III).
CONCLUSION: Based on our results, self-reported intake of fish and vegetable fats was clearly associated with serum PUFA. High intake of specific foods and not fats in general may have negative effects on CVD for women and all-causes mortality for men, whereas fruit may reduce mortality only in men. Similarly serum EPA, DHA and LA were protective for CVD and all-causes mortality with gender difference whereas serum ALA might be associated with increased of CVD in only women.
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Cunningham, R. G. C. "Cardiovascular disease in an end stage renal disease population." Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396856.
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McAllister, David Anthony. "Chronic obstructive pulmonary disease, pulmonary function and cardiovascular disease." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5615.
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Cardiovascular disease is common in Chronic Obstructive Pulmonary Disease (COPD), and forced expiratory volume in one second (FEV1) independently predicts cardiovascular morbidity and mortality. Pathological changes in the systemic vasculature have been proposed as potential mechanisms linking COPD to cardiovascular disease, and patients with COPD may be at increased risk of acute myocardial infarction during acute exacerbations. Notwithstanding causation, FEV1 may be a useful prognostic marker in patients undergoing cardiac surgery. This thesis examined these three aspects of cardiovascular co-morbidity in relation to COPD and FEV1. In 2,241 consecutive cardiac surgery patients, FEV1 was associated with length of hospital stay (p<0.001) and mortality (p<0.001) adjusting for age, sex, height, body mass index, socioeconomic status, smoking, cardiovascular risk factors, chronic pulmonary disease, and type/urgency of surgery. In a survey of Scottish Respiratory Consultants there was no consensus regarding the investigation and management of acute coronary syndrome in exacerbation of COPD. In a case-series of 242 patients with exacerbations 2.5% (95% CI 1.0 to 5.6%) had chest pain, raised serum troponin and serial electrocardiogram changes suggestive of acute coronary syndrome. However, over half reported chest pain, while raised troponin was not associated with chest pain or serial ECG changes. Carotid-radial pulse wave velocity (PWV), aortic distensibility, and aortic calcification were measured to assess the relationship of the systemic vasculature to FEV1 and emphysema severity on CT. In adjusted analyses, emphysema was associated with PWV in patients with COPD (p = 0.006) and, in population based samples, with extent of distal aortic calcification (p=0.02) but not with aortic distensibility (p=0.60). This thesis found that FEV1 was associated with mortality and length of hospital stay in patients undergoing cardiac surgery, and that chest pain and raised troponin were common but unrelated in exacerbation of COPD. In the vascular studies distal but not proximal vascular pathology was associated with FEV1, and if COPD is truly related to systemic arterial disease, the distal arterial tree is implicated.
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Ekblom, Kim. "Oxidants and antioxidants in cardiovascular disease." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33762.
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Eriksson, Maria. "Adipocyte-derived hormones and cardiovascular disease." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36679.
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Obesity is increasing globally and related to major changes in lifestyle. This increase is associated with an increased risk of cardiovascular disease (CVD). Knowledge about adipose tissue as a metabolic-endocrine organ has increased during the last few decades. Adipose tissue produces a number of proteins with increased body weight, many of which are important for food intake and satiety, insulin sensitivity, and vessel integrity, and aberrations have been related to atherosclerosis. Notably, the risk for developing CVD over the course of a lifetime differs between men and women. In Northern Sweden, men have a higher risk for myocardial infarction (MI). However, the incidence is declining in men but not in women. These sex differences could be due to functional and anatomical differences in the fat mass and its functions. The primary aim of this thesis was to evaluate associations between the adipocyte-derived hormones leptin and adiponectin, and fibrinolysis and other variables associated with the metabolic syndrome, and particularly whether these associations differ between men and women. Another aim was to evaluate these associations during physical exercise and pharmacological intervention (i.e. enalapril). Finally, whether leptin and adiponectin predict a first MI or sudden cardiac death with putative sex differences was also investigated. The first study used a cross-sectional design and included 72 men and women recruited from the WHO MONICA project. We found pronounced sex differences in the associations with fibrinolytic variables. Leptin was associated with fibrinolytic factors in men, whereas insulin resistance was strongly associated with all fibrinolytic factors in women. The second study was an experimental observational study with 20 men exposed to strenuous physical exercise. During exercise, leptin levels decreased and adiponectin levels increased, and both were strongly associated with an improved fibrinolytic capacity measured as decreased PAI-1 activity. Changes in insulin sensitivity were not associated with changing adiponectin levels. The third study was a randomised, double-blind, single centre clinical trial including 46 men and 37 women who had an earlier MI. The study duration was one year, and participating subjects were randomised to either placebo or ACE inhibitor (i.e. enalapril). Circulating leptin levels were not associated with enalapril treatment. During the one-year study, changes in leptin levels were associated with changes in circulating levels of tPA mass, PAI-1 mass, and tPA-PAI complex in men, but not vWF. These associations were found in all men and men on placebo treatment. In women on enalapril treatment there was an association between changes in leptin and changes in vWF. In the fourth study, the impact of leptin, adiponectin, and their ratio on future MI risk or sudden cardiac death was tested in a prospective nested casecontrol study within the framework of the WHO MONICA, Västerbotten Intervention Project (VIP), and Västerbotten Mammary Screening Program (MSP). A total 564 cases (first-ever MI or sudden cardiac death) and 1082 matched controls were selected. High leptin, low adiponectin, and a high leptin/adiponectin ratio independently predicted a first-ever MI, possibly with higher risk in men in regards to leptin. The association was found for non-fatal cases with ST-elevation MI. Subjects with low adiponectin levels had their MI earlier than those with high levels. In conclusion, the adipocyte-derived hormones leptin and adiponectin are related to the development of CVD with a sex difference, and fibrinolytic mechanisms could be possible contributors to CVD risk.
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Laugsand, Lars Erik Sande. "Insomnia and risk for cardiovascular disease." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for samfunnsmedisin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-17010.
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Insomni og risiko for hjerte- og karsykdom Forskning som har blitt utført det siste tiåret har gitt resultater som taler for at dårlig søvn og søvnlidelser bidrar til utvikling av hjerte- og karsykdom. Insomni er definert som en subjektiv opplevelse av å ha problemer med innsoving, for tidlig oppvåkning om morgenen og/eller dårlig søvnkvalitet, og insomni ansees for å være den vanligste søvnforstyrrelsen. Forekomsten av minst ett av symptomene kan være så høy som 33% i den generelle befolkningen. Foreløpig er det få studier på sammenhengen mellom insomni og risiko for framtidig hjerte- og karsykdom. Insomni henger sammen med en ugunstig livsstil og utvikling av metabolsk syndrom, som betyr at personer med insomni ofte har høyere blodtrykk, kolesterol og høyere kroppsmasseindeks enn personer uten slike søvnplager. En annen mulighet for sammenhengen er at søvnproblemene bidrar til økt utskillelse av inflammatoriske stoffer i blodet som kan øke risikoen for hjerte- og karsykdom. Om det er en klar sammenheng mellom metabolsk syndrom og inflammasjon, er heller ikke kjent, og spesielt er dette uavklart i yngre aldersgrupper. Studiene i avhandlingen tok utgangspunkt i den andre Helseundersøkelsen i Nord-Trøndelag (HUNT-2) som foregikk i perioden 1995-97. Alle personer over 20 år i fylket ble invitert, og deltakerne fylte ut spørreskjema, gjennomgikk en klinisk undersøkelse, og det ble tatt blodprøver. I spørreskjemaet ble det blant annet spurt om søvnplager. Fra undersøkelsen startet til og med 2008 ble det fortløpende registrert førstegangs hjerteinfarkt eller hjertesvikt, hvor opplysningene enten ble hentet fra sykehusjournaler i Helse-Nord Trøndelag eller fra Dødsårsaksregisteret. I en undergruppe bestående av 10 000 deltakere ble det målt høy-sensitivt C-reaktivt protein (hsCRP) i blod, som er et mål på graden av inflammasjon i kroppen. Resultatene viste at personer med symptomer på insomni hadde en moderat økt risiko for førstegangs hjerteinfarkt og økt risiko for hjertesvikt sammenliknet med personer uten søvnproblemer. Vi fant også at sjansen for å få hjerteinfarkt eller hjertesvikt var høyere jo flere symptomer på insomni som var tilstede samtidig. Vi tok høyde for betydningen av andre faktorer som kunne påvirke resultatene, og i de statistiske analysene justerte vi for forskjeller i alder, kjønn, ekteskapsstatus, utdanningsnivå, skiftarbeid, blodtrykk, kolesterol, diabetes, vekt, fysisk aktivitet, alkohol og røyking. I tillegg justerte vi for symptomer på depresjon og angst, som begge kan medføre søvnplager. De justerte analysene viste at disse mulig konfunderende faktorene ikke påvirket resultatene i nevneverdig grad, noe som styrker sannsynligheten for at våre funn har en underliggende biologisk årsak. I en annen studie fant vi at den positive sammenhengen mellom metabolsk syndrom og hsCRP var like tydelig i alle aldersgrupper. Til tross for at personer med insomni oftere har metabolsk syndrom, fant vi ingen holdepunkter for at personer med insomni har økt utskillelse av hsCRP. Disse funnene taler imot at inflammasjon, indikert av høy hsCRP, kan forklare sammenhengen mellom insomni og framtidig hjerte- og karsykdom. Til tross for at insomni er forbundet med en moderat risikoøkning for hjerte- og karsykdom, er insomni så vanlig i befolkningen at søvnplager kan spille en viktig rolle for hjertehelse. I tillegg er insomni en lett gjenkjennbar og potensielt håndterbar tilstand. I forebygging av hjerte- og karsykdom bør derfor søvnplager tas med i vurderingen. Det kreves mer forskning på området, slik at man får en bedre forståelse av de underliggende mekanismene.
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Dockery, Frances. "Androgens and cardiovascular disease in men." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435055.
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Svenungsson, Elisabet. "Cardiovascular disease in systemic lupus erythematosus /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-501-8.
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Kietselaer, Bas L. J. H. "The Annexin Code revealing cardiovascular disease /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=11598.
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Lawson, Kenneth Daniel. "The Scottish cardiovascular disease policy model." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4695/.
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This thesis is concerned with economic evaluation in the primary prevention of cardiovascular disease. Policymakers are increasingly focussed on reducing the health and economic burden of CVD and to reduce health inequalities. However, the approach to primary prevention suffers from fundamental weaknesses that this research intends to help address. There is general lack of effectiveness and cost effectiveness evidence underpinning current primary prevention interventions. First, there is a policy impetus towards mass screening strategies to target individuals at high risk of developing CVD when more focussed approaches may be more cost effective. Second, clinicians prioritise individuals on the basis of 10-year risk scores, which are strongly driven by age, and not the potential benefits (or costs) from treatment. Third, targeted and population interventions are often still treated as competing approaches, whereas the key issue is how they might best combine. The key premise of this thesis is that the aims of primary prevention are the avoidance of premature morbidity, mortality and to close health inequalities - subject to a budget constraint. A CVD Policy Model was created using the same nine risk factors as used in the ASSIGN 10-year risk score, currently used in clinical practice in Scotland, to estimate life expectancy, quality adjusted life expectancy and lifetime hospital costs. This model can be employed to estimate the cost effectiveness of interventions and the impact on health inequalities. The model performed well in a comprehensive validation process in terms of face validity, internal validity, and external validity. Life expectancy predictions were re-calibrated to contemporary lifetables. This generic modelling approach (i.e. using a wide range of inputs and producing a wide range of outputs) is intended to avoid the need to build bespoke models for different interventions aimed at particular risk factors or to produce particular outputs. In application, the CVD Policy Model is intended to assist clinicians and policymakers to develop a more coherent approach to primary prevention, namely: to design more efficient screening strategies; prioritise individuals for intervention on the basis of potential benefit (rather than risk); and to assess the impact of both individually targeted and population interventions on a consistent basis. Using the model in these ways may enable primary prevention approaches to be more consistent with guidelines from health sector reimbursement agencies, which may result in a more efficient use of scarce resources.
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Leung, Yiu-por, and 梁耀波. "Coping strategies of cardiovascular disease patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31978125.
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Kim, Jin Hee. "Functional genomics of cardiovascular disease risk." Thesis, Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/51769.
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Understanding variability of heath status is highly likely to be an important component of personalized medicine to predict health status of individuals and to promote personal health. Evidences of Genome Wide Association Study and gene expression study indicating that genetic factors affect the risk susceptibility of individuals have suggested adding genetic factors as a component of health status measurements. In order to validate or to predict health risk status with collected personal data such as clinical measurements or genomic data, it is important to have a well-established profile of diseases.
The primary effort of this work was to find genomic evidence relevant to coronary artery disease. Two major methods of genomic analysis, gene expression profiling and GWAS on gene expression, were performed to dissect transcriptional and genotypic fingerprints of coronary artery disease. Blood-informative transcriptional Axes that can be described by 10 covariating transcripts per each Axis were utilized as a crucial measure of gene expression analysis.
This study of the relationship between gene expression variation and various measurements of coronary artery disease delivered compelling results showing strong association between two transcriptional Axes and incident of myocardial infarction. 244 transcripts closely correlated with death by cardiovascular disease related events were also showing clear association with those two transcriptional Axes. These results suggest potential transcripts for use in risk prediction for the advent of myocardial infarction and cardiac death.
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Bloomer, Lisa Danielle Susan. "The Y chromosome in cardiovascular disease." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/27792.
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Men develop coronary artery disease (CAD) approximately 10 years earlier and die of CAD more frequently (2:1) than age-matched women. This sexual dimorphism is even more striking in abdominal aortic aneurysms (AAA) – the ratio of affected men to women is as high as 6:1. A major biological difference between both sexes is the exclusive presence of the Y chromosome in men. Haplogroup I of the Y chromosome increases the risk of CAD by ~50% compared to other Y chromosome lineages. The analysis of ~1940 men from 3 cohorts recruited from the general European population revealed that the association between haplogroup I and CAD is not driven by conventional cardiovascular risk factors BMI, blood pressure, total cholesterol, HDL-C, triglycerides, LDL-C, glucose, aggression (total aggression, physical aggression, verbal aggression, hostility, anger) or sex steroids (testosterone, androstenedione, DHEA-S, estrone, oestradiol). Transcriptomic analysis revealed that none of “Kyoto Encyclopaedia of Genes and Genomes” (KEGG) pathways were differentially regulated in monocytes between men from haplogroup I and all other lineages. In contrast, 30 KEGG pathways showed differential expression between haplogroup I and other lineages of the Y chromosome in transcriptome-wide analysis of macrophages. Of these, 19 pathways were interconnected by common genes of adaptive immunity and the inflammatory response. In gene-centred analysis of the Y chromosome, carriers of haplogroup I also showed significant down-regulation of two X-degenerate male specific Y chromosome genes (PRKY and UTY) in macrophages (P=0.001 and P=0.0001) but not in monocytes (P=0.181, and P=0.611). Meta-analysis of 3 cohorts of British and Irish men revealed that the presence of haplogroup I was not associated with predisposition to AAA. Neither conventional CAD risk factors nor male-associated/sex-specific phenotypes appear to drive the increased risk of CAD in carriers of haplogroup I. Furthermore, these results show that immune system and response to inflammation may mediate the association between Y chromosome and CAD. The absence of association between the Y chromosome and AAA suggest differences in the pathogenesis of sexual dimorphism of AAA and CAD.
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Berrones, Adam J. "LIFESTYLE CONTRIBUTORS TO CARDIOVASCULAR DISEASE RISK." UKnowledge, 2016. http://uknowledge.uky.edu/khp_etds/28.
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Aortic stiffness is an independent risk factor that has prognostic value regarding future cardiovascular disease (CVD) events such as myocardial infarction, strokes, and heart failure. Although death rates due to coronary heart disease have declined in recent years, the leading global killer remains CVD and prevalence is still high. Understanding lifestyle contributors associated with aortic stiffness would provide the public with insight into targeting key health-related behaviors.
The purpose of this observational study was to examine the association of physical activity, physical function, and dietary quality as independent factors contributing to aortic stiffness in apparently healthy middle aged men. Fifty-two men between the ages of 30 and 59 years were recruited to participate in this study, which required two visits to the Exercise Physiology Laboratory. Aortic stiffness was measured by aortic pulse wave velocity (aPWV) and was not associated with total daily step counts (r=-0.06; P=0.70). However, aortic stiffness was inversely associated with physical function, determined with the sitting-rising test score (r=-0.44; P<0.01) and inversely associated with relative muscular strength, determined with peak handgrip strength in both hands normalized to body mass (r=-0.41; P<0.01). Additionally, aortic stiffness was inversely associated with dietary quality, determined with the Healthy Eating Index score (r=0.51; P<0.01).
In conclusion, key health-related behaviors in this study that explained a large percentage of the variation in aortic stiffness were physical function and dietary quality (Adj r²=0.47; SEE=0.634). Hence, optimizing overall musculoskeletal fitness by focusing on strength, balance, coordination, and flexibility in addition to greater adherence to the U.S. Dietary Guidelines are key lifestyle contributors associated with reduced CVD risk in otherwise healthy middle aged men.
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Richards, Jennifer Margaret Jane. "Magnetic resonance imaging in cardiovascular disease." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8079.
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Background Superparamagnetic particles of iron oxide (SPIO) are part of a novel and exciting class of ‘smart’ magnetic resonance imaging (MRI) contrast agents that are taken up by inflammatory cells. Ultrasmall SPIO (USPIO; ~30 nm diameter) can be used to assess cellular tissue inflammation and SPIO (80-150 nm) have the potential to be used to label cells ex vivo for in vivo cell tracking studies. Objectives The aims of the thesis were therefore (i) to develop and validate quantitative MRI methodology for assessing SPIO uptake within tissues, (ii) to demonstrate USPIO accumulation within the aortic wall and its implications in patients with abdominal aortic aneurysms (AAA), and (iii) to develop and apply a Good Manufacturing Practice (GMP) compliant method of SPIO cell labelling in healthy volunteers. Methods Patients with asymptomatic AAA >4.0 cm in diameter were recruited. Imaging sequences were optimised in eight patients using a 3 tesla MRI scanner. Data were analysed using the decay constant for multi echo T2* weighted (T2*W) sequences (T2*) or its inverse (R2*) and the repeatability of these measurements was established. A further twenty-nine patients underwent MRI scanning before and 24- 36 hours after administration of USPIO. T2 and multi echo T2*W sequences were performed and ultrasound-based growth rate data were collected. Operative aortic wall tissue samples were obtained from patients undergoing open surgical aneurysm repair. A GMP compliant protocol was developed for labelling cells with SPIO for clinical cell tracking studies. The effects of SPIO-labelling on cell viability and function were assessed in vitro. A phased-dosing protocol was used to establish the safety of intravenous administration of SPIO-labelled cells in healthy volunteers. The feasibility of imaging cells at a target site in vivo following local or systemic administration was assessed. Tracking of SPIO-labelled cells to a target site was investigated by inducing an iatrogenic inflammatory focus in the skin of the anterior thigh of healthy volunteers, following which autologous SPIO-labelled cells were administered and their accumulation was assessed using MRI scanning and histology of skin biopsies. Results Robust and semi-quantitative data acquisition and image analysis methodology was developed for the assessment of SPIO accumulation in tissues. In patients with AAA, histological analysis of aortic wall tissue samples confirmed USPIO accumulation in areas of cellular inflammation. USPIO-enhanced MRI detected aortic wall inflammation and mural USPIO uptake was associated with a 3-fold higher aneurysm expansion rate. Human mononuclear cells were labelled with SPIO under GMP compliant conditions without affecting cell viability or function. Both local and intravenous administration of SPIO-labelled cells was safe and cells were detectable in vitro and in vivo using a clinical MRI scanner. SPIO-labelled cells tracked to a focal iatrogenic inflammatory focus following intravenous administration in humans and were detectable on MRI scanning and histological examination of skin biopsies. Conclusions SPIO contrast agents have an extensive range of potential clinical applications. USPIO uptake in the wall of AAA appears to identify cellular inflammation and predict accelerated aneurysm expansion. This is therefore a promising investigative tool for stratifying the risk of disease progression in patients with AAA, and may also be considered as a biomarker for response to novel pharmacological agents. The ability to label cells for non-invasive cell tracking studies would facilitate the further development of novel cell-based therapies and would enable assessment of dynamic inflammatory processes through inflammatory cell tracking.
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Leung, Yiu-por. "Coping strategies of cardiovascular disease patients." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19470125.
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Yu, Qianli. "Effects of immunomodulators on cardiovascular disease." Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/290016.
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Cardiovascular disease (CVD) is a genetic and environmental factors involved disease resulting in cardiovascular dysfunction. This study investigated cardiovascular dysfunction induced by immunomodulators including methamphetamine (MA), high salt-fat dietary and retrovirus. The mechanism and potential therapeutic role of T-cell receptor (TCR) peptides in cardiovascular disease were studied. The immune and cardiac function changes due to chronic MA use were evaluated in C57BL/C mice with LP-BM5 retrovirus infection plus MA intraperitoneally injection for 12 weeks. MA treatment significantly decreased T helper 1 (TH1) cytokine production; tumor necrosis factor (TNF-α) and oxidative stress were significantly increased in both uninfected and infected mice; the load independent contractile cardiac function was significantly decreased. The poor dietary intake effects on cardiovascular function were investigated in one-month old C57BL/6J mice fed with two established dietary formulations, high salt (HS) and high fat-high carbohydrate (HFHSC), separately or in combination (HFHS) for 3 months. The HFHSC mice demonstrated significantly increased end-diastolic volume and end-systolic volume (p < 0.01) and a reduction of ventricular stiffness (p < 0.05). The HS mice exhibited arterial hypertension with an increase in maximum end-systolic pressure (p < 0.05) and a decrease of arterial elastance (p < 0.05) corroborated by an increase in heart weight to body weight ratios (p < 0.01) and vascular types I and III collagen. Modulated T-lymphocyte function with a suppressed TH2 subset fashion by TCR peptide vaccination significantly increased collagen I and III mRNA and protein in cardiac cells from naive mice (p < 0.05). The gelatinase MMP-2 and collagenase MMP-13 mRNA expression were significantly decreased (p < 0.05). Meanwhile, the compliance of heart (β and dV/dt min) was significantly increased by T-cell receptor peptide treatment (p < 0.05). LP-BM5 retrovirus-infection induced DCM was improved by TCR peptide treatment. The collagen I & III mRNA and protein levels were significantly increased by TCR peptide treatment in both fibroblast and cardiac cells (p < 0.05). In conclusion, drug use, poor dietary intake and retrovirus-infection as immunomodulation factors induce cardiovascular dysfunction mediated by T-lymphocyte dysregulation. TCR peptide, a selective T-lymphocyte function modulator, may be a promising pharmaco-therapeutic immunomodulator for cardiovascular disease.
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Radavelli, Bagatini Simone. "Diet, cardiovascular disease, and mental health." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2022. https://ro.ecu.edu.au/theses/2548.
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Cardiovascular disease (CVD) is the leading cause of death in Australia and worldwide. Prolonged exposure to stress is a risk factor for mental and physical illnesses, such as CVD. A healthy diet may help alleviate stress levels and improve mental and physical wellbeing. The aim of this thesis was to examine the potential benefits of higher fruit and vegetable (FV) intake on stress, mental and physical health. This thesis includes one scoping review, one study protocol and four epidemiological cross-sectional studies, providing new and exciting evidence for the relationship of higher FV intake with FV types on stress, mental and physical wellbeing.
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O’Lone, Emma. "Cardiovascular disease: priorities and outcomes in end stage kidney disease." Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/22326.
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Introduction End stage kidney disease (ESKD) accounts for 5-10 million deaths annually worldwide. The current treatment modalities for ESKD include dialysis, transplant and supportive care. The leading cause of death for people with ESKD is cardiovascular disease (CVD). CVD is a collective term for disease affecting the heart and blood vessels including coronary, cerebral and peripheral blood vessels. CVD causes significant morbidity and has a substantial impact on quality of life for people with ESKD. Improving cardiovascular outcomes for people living with ESKD is a priority. The escalating incidence of chronic kidney disease, its progression to ESKD and the high burden of cardiovascular disease has generated an increasing amount of research in the ESKD population. The ESKD population have previously been under-represented in clinical trials and current trials in ESKD have infrequently and inconsistently reported CVD outcomes. It is important to standardise outcomes used in research. When outcome reporting is standardised it enables comparisons of findings across trials, populations and eras. It is important that the outcomes reflect patient priorities and are relevant to patients and clinicians for use in shared decision making. The Standardised Outcomes in Nephrology Group (SONG) is an international initiative to establish a set of core outcomes and outcome measures across the spectrum of kidney disease for trials and other forms of research. The SONG-Haemodialysis (SONG - HD) initiative is developing a core outcome set for use in haemodialysis. As part of SONG-HD, CVD (as well as fatigue, vascular access and mortality) has been identified as important to all stakeholders and included in the core outcome set for haemodialysis. This requires appropriate measures of CVD to be identified and used. The first aim of this thesis was to achieve consensus on a CVD outcome measure for use in haemodialysis trials. In approaching this goal I first needed to ascertain the current use of cardiovascular outcomes (Chapter 2) and then determine which ones were important to all stakeholders (Chapter 3). Consensus over which is the most appropriate measure of CVD for use in trials in people on haemodialysis (Chapter 4) will allow improved standardisation of cardiovascular outcome reporting, reducing research wastage and will propel forward cardiovascular research to improve morbidity and mortality in this high risk population. The second aim of this thesis was to further examine some of the prioritised outcomes and to review the patterns and risks of CVD in the ESKD population. The magnitude of risk for cardiac events and cardiac deaths in people with ESKD relative to the general population and the changes over time are not well described. I hypothesised that the magnitude of risk remained high in the ESKD population and that epidemiological improvements seen in CVD outcomes in the general population have not been mirrored in the ESKD population (Chapters 5 and 6). CVD and more specifically cerebrovascular disease can lead to significant cognitive impairment which has a substantial impact on the ability of ESKD patients to understand their disease, interpret education and be involved in shared decision making. The patterns of cognitive deficit in the ESKD population are not well understood and I hypothesised that cognitive deficits in the ESKD population may be different to those found in the general population and may differ by modality of renal replacement therapy. Standardising CVD outcomes, examining the epidemiology of CVD in ESKD and comparing the trends and patterns to the general population can drive hypotheses into potential causative mechanisms and new treatments. I present this thesis as a hybrid of published work, work currently under peer review for publication and work submitted for publication on the theme of priorities and outcomes in ESKD.
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Minh, Hoang Van. "Epidemiology of cardiovascular disease in rural Vietnam." Doctoral thesis, Umeå : Public Health and Clinical Medicine Folkhälsa och klinisk medicin, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-779.
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Li, Wai-sum Rachel, and 李蕙琛. "Effects of abacavir on cardiovascular system." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46330288.
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Johns, David James. "Dietary patterns and cardiovascular disease in severe obesity." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610554.
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Price, Hermione Clare. "Personalised cardiovascular disease risk information as a motivator of behaviour change in individuals at high cardiovascular disease risk." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:3cab4a20-355c-43af-9377-c655e42a4acf.
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Introduction: Cardiovascular disease (CVD) risk assessment is becoming increasingly common in routine clinical practice. Consequently many individuals are likely to be identified as being at increased CVD risk and risk reducing strategies implemented with a view to preventing future CVD. There are many steps along the pathway from CVD risk assessment to the prevention of CVD events. First, CVD risk needs to be accurately estimated using an appropriate CVD risk calculator. Secondly CVD risk information needs to be effectively communicated to the individual identified as being at increased risk. Thirdly, the risk information communicated needs to be capable of motivating behaviour change and finally behaviour change needs to result in a reduction in CVD risk. The evidence base for many of these steps has yet to be fully established. Aims: The overall aims of this work were first to adapt the United Kingdom Prospective Diabetes Study (UKPDS) Risk Engine to better display risk and achievable risk. Secondly to investigate lay perceptions of risk and to develop two interventions designed to reduce CVD risk. The two interventions were a personalised 10-year CVD risk estimate and a brief lifestyle advice intervention. Finally, the capacity of these interventions to increase physical activity and improve CVD risk factors in adults at increased CVD risk was tested. Methods: Three focus groups were held to investigate lay perceptions of risk and to inform the design of the UKPDS Risk Engine interface and a brief lifestyle advice intervention designed to motivate risk reducing behaviours. The two interventions were then tested in a 2x2 factorial randomised controlled trial. Results: The focus group results demonstrated that public interest and understanding of risk was high. In addition participants expressed clear views regarding how risk information and lifestyle advice should be presented. 194 participants at increased 10-year CVD risk (≥ 20%) were recruited from 4 Oxfordshire general practices. Neither a personalised 10-year CVD risk estimate nor a brief lifestyle advice intervention was capable of increasing physical activity or reducing estimated 10-year CVD risk in this group. Conclusions: Whilst public interest in CVD risk appeared to be high this study was unable to demonstrate that a 10-year personalised CVD risk estimate or a brief lifestyle advice intervention was able to increase physical activity in adults at increased CVD risk.
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Agyemang, Edmund Adjei, Priscilla Okoh, and K. O. Bobkovych. "Cardiovascular Diseases in Ghana." Thesis, «Інновації в медицині»: Тези доповідей 85-ої науково-практичної конференції студентів і молодих вчених із міжнародною участю (м. Івано-Франківськ, 24-25 березня 2016 р.). – м. Івано-Франківськ, 2016, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11247.
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Furthermore about 10% of the adult populations are tobacco smokers and 5-7% - obesity. All these data positively show why the occurrence of cerebrovascular diseases in Ghana is a rampant and should be of concern to all stakeholders.Кафедра пропедевтики внутрішніх хвороб
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Abdi, Faduma Najmo Abdulrahman, and K. O. Bobkovych. "Cardiovascular diseases in Somalia." Thesis, «Інновації в медицині»: Тези доповідей 85-ої науково-практичної конференції студентів і молодих вчених із міжнародною участю (м. Івано-Франківськ, 24-25 березня 2016 р.). – м. Івано-Франківськ, 2016, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11248.
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Although the incidence has declined there appeared some fears that the aging population is increasing number of cases. As with other cardiovascular disease heart failure occurs more commonly in eastern and northern Somalia than in the south and southwest Somalia. The number of sufferers is probably declining. In 2010 the special rights to compensation of heart failure medication about 43 000 Somalis were given.Кафедра пропедевтики внутрішніх хвороб
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Guo, Xiaohui. "Effects of Total Polyphenol Intakes on Cardiovascular Disease Risk Factors in an Elderly Population at High Cardiovascular Risk." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/399542.
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There is a consensus that CVD has been the leading cause of death worldwide in recent decades, and it is predicted that will raise from 17.5 million in 2012 to 22.2 million in 2030. Besides, CVD is a heavy economic burden on the health care system at both global and national scales. For the primary prevention, prediction models based on established risk factors are useful tools in the prevention of CVD. In this study, the cardiovascular risk factors among the elderly population have been assessed, which used to set up associations between total polyphenol intakes from a Mediterranean diet and prevention of CVD.
The Mediterranean diet is a nutritional recommendation that has recently shown beneficial effects on human health. Numerous studies have demonstrated there is a negative association between consumption of the Mediterranean diet and the prevalence of CVD. The evidence concerning the potential mechanisms of action which underlie the cardio-protective effects may be attributed to a high amount of dietary fiber, vitamins, folic acid, natural antioxidants, monounsaturated fat; moderate amounts of animal protein, moderate amount of alcohol mainly in the form of wine; and low amount of saturated and trans fat. However, only limited studies have focused on the observed protection from the most abundant antioxidants in nature, polyphenol. Therefore, in this study, we hypothesized that a high dietary polyphenol intakes, recorded by urinary polyphenol excretion, could be associated with low CVD risk parameters, diabetes, and obesity in an elderly population with high cardiovascular risk.
Traditional methods of obtaining information on polyphenol intakes, such as from dietary recalls, FFQs, and databases on the polyphenol content of foods, are not accurate enough to reflect polyphenol concentration after metabolism. To solve this problem, we used excretion of urine as a reliable and effective biomarker to track polyphenol after digestion.
High glucose levels, TG concentration, DBP are classic cardiovascular risk factors for developing of CVD. In this thesis, we found significant inverse correlations between changes in TPE and plasma TG concentration, glucose concentration, and DBP after adjustment for potential confounders after a 5-year of intervention.
Overweight and obesity are also important risk factors for developing of CVD. Inverse correlations were observed between TPE at 5 years of follow-up and BW, BMI, WC and WHtR after adjustment for potential confounders, indicating higher polyphenol intakes improve body weight managements.
Prevalence of T2D is positively associated with incidence of CVD. We found a high intake of total polyphenols, calculated by FFQs and the Phenol-Explorer database, was associated with a reduced risk of diabetes in elderly people at high risk of CVD.
To conclude, we suggest that a high consumption of polyphenol-rich foods in the frame of a Mediterranean diet could potentially help to reduce multiple risk factors of CVD.Las enfermedades cardiovasculares (CVD) representan la principal causa de mortalidad en el mundo. Numerosos estudios han demostrado una asociación negativa entre el consumo de la dieta mediterránea y la prevalencia de las CVD. Sin embargo, sólo algunos estudios se han centrado en evaluar la protección que pueden ejercer los polifenoles. En este trabajo se propuso la siguiente hipótesis de que una ingesta elevada de polifenoles a través de la dieta, podría estar asociada a una disminución de parámetros de bajo riesgo de CVD, diabetes y obesidad en una población de edad avanzada con alto riesgo de enfermedades cardiovasculares. Se observó que una alta ingesta de polifenoles totales, calculado por las encuestas de frecuencia de consumo (FFQ) y la base de datos de Phenol-Explorer, se asoció con un menor riesgo de diabetes en personas de edad avanzada con alto riesgo de CVD. Los métodos tradicionales para obtener las informaciones de la ingesta de polifenoles, como los recordatorios de la dieta, las encuestas de frecuencia de consumo y bases de datos, no son suficientemente precisos. Para resolver este problema, se utilizó la además la excreción de los polifenoles en la orina (TPE) como un biomarcador fiable, robusto y eficaz para realizar un seguimiento del consumo de polifenoles. Hemos observado correlaciones inversas significativas entre los cambios en la concentración plasmática de TPE a los 5 años de seguimiento y triglicéridos plasmáticos, la concentración de glucosa y la presión sanguínea diastólica después de ajustar por posibles factores de confusión. El sobrepeso y la obesidad también son importantes factores de riesgo cardiovascular. Se observaron correlaciones inversas entre TPE a los 5 años de seguimiento y peso corporal (BW), índice de masa corporal (BMI), circunferencia de la cintura (WC) y cintura a la altura (WHtR) después del ajuste por posibles factores de confusión. Para concluir, se sugiere que un alto consumo de alimentos con alto contenido en polifenoles en el marco de una dieta mediterránea podría reducir múltiples factores de riesgo de CVD.
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Colom, Sanmartí Glòria. "A Multiplexed diagnostic approach for cardiovascular disease biomarkers." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/396304.
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In the course of this thesis, the optimal epitopes for the subsequent polyclonal rabbit antibody production for cTnI and NT-proBNP have been studied and chosen. cTnI and NT-proBNP are the most relevant cardio-specific biomarkers for the diagnosis of cardiovascular diseases. With these antibodies, a sandwich ELISA for the detection of cTnI has been developed together with a competitive ELISA for the detection of NT-proBNP, both in a microplate format.
It has been observed that cTnI has an extraordinary tendency to non-specifically adsorb itself onto surfaces and other biomolecules. This, with the inability to achieve the required detectability for this biomarker, have been the main problems to face with. Regarding the non-specific adsorption, different additives in the analyte or sample buffer have been evaluated. Thus, 0.15% casein in PBST combined with the use of low adsorption microplates (ImmulonTM 2HB) helps considerably to solve this problem. However, the sensitivity obtained for this assay in aqueous buffer is much lower than that required corresponding to the basal levels of cTnI in the blood.
For the NT-proBNP ELISA development, the required limit of detection was achieved after studying various parameters related to heterology and other physicochemical parameters. Moreover, a good accuracy with NT-proBNP fortified plasma samples was obtained.
It has been possible to develop a multiplexed microarray for the simultaneous detection of 5 biomarkers (cTnI, NT-proBNP, very important in the process of developing cardiovascular diseases, CRP, Cys C and H-FABP). Once the microarray is biofunctionalized using a spatial encoding with the corresponding bioconjugates or capture antibodies, immunoreagents and other biomarkers can be used in a cocktail. Neither cooperativity phenomena (union of immunoreagents that are in solution in sites where there are other biomarkers immobilized) nor cross-reactivity (recognition of different biomarkers from those for which immunoreagents have been developed) have been observed in any case. Only Lp(a) immunoreagents produced such interferences and therefore they were discarded.
It has been highlighted the fact that the biomarkers present in different concentration ranges remains one of the main challenges for the multiplexed diagnosis when simultaneous measurements are desired. In this research, it was impossible to quantify the CRP and Cys C in the same microarray than H-FABP, cTnI and NT-proBNP employing direct samples. Fortunately, the fact of using glass surfaces in which 24 microarrays can be printed, has allowed making these measurements in a simultaneous and parallel way.
With the multiplexed microarray, it has been possible to measure samples from patients with different pathologies. The results show that the efficiency of this microarray is much higher than that of analyzers currently used in clinical laboratories, regarding the ability to measure multiple biomarkers in a large number of samples in a short time and the coherence of the results. Thus, the microarray developed in this PhD thesis has been able to measure all the biomarkers from all patient samples, while analyzers only analyzed some of them,
depending on the pathology, due to the cost (financial and time). The microarray was then able to detect high levels of CRP from patient samples that were not analyzed in clinical laboratory. Additionally, the microarray results are coherent with those obtained with analyzers for those cases in which measures had been made, and the disease had been diagnosed. The results have been satisfactory even in the case of NT-proBNP, which had not reached the detectability baseline even though it was very close. Unfortunately, it was not possible to measure cTnI levels with the microarray as it was expected according to previous studies done with the same immunoreagents. Thus, we can consider this multiplexed microarray as a semi-quantitative method useful for improving the diagnosis of cardiovascular disease for patients who are at different stages of the disease.
Finally, preliminary studies have been realized to implement the multiplexed immunochemical system in a fluorescent optical sensor based on the evanescent wave. This was done with the aim to achieve a POC (point-of-care) device suitable to be used outside hospital premises, adapted to non-specialist users, and facilitate the diagnosis of cardiovascular diseases. Unfortunately, the results obtained point to the need to make greater efforts to increase the detectability of the system, since the LOD values obtained are worse than those achieved with the ELISA or the microarray, far from the basal levels in the case of NT-proBNP.
The main problem in this thesis has been to reach the detection limits required by some biomarkers. Although in the literature and in the market there are assays that have achieved it, this fact mainly lies in the signal acquisition method as well as in the intrinsic sensitivity of the instrument addressed to do so.En el transcurs d'aquesta tesi s'han escollit els epítops òptims per a la conseqüent producció d'anticossos policlonals de conill per a cTnl i NT-proBNP, dos dels biomarcadors més cardio-específics i rellevants pel diagnòstic de malalties cardiovasculars. Amb aquests anticossos s'ha desenvolupat un ELISA sandvitx per a la detecció de cTnl i un ELISA competitiu per a la detecció de NT-proBNP, tots dos en format de microplaca. S'ha observat que la cTnl te una extraordinària tendència a adsorbir-se de forma inespecífica a superfícies i també a altres biomolècules. Pel que fa a l'adsorció inespecífica s'han avaluat diferents additius en el tampó de la mostra o analit veient-se que la caseïna al 0,15% en PBST combinat amb l'ús de microplaques de baixa adsorció (ImmulonTM 2HB) ajuda considerablement a solucionar aquest problema. Tot i això, la sensibilitat obtinguda per aquest assaig en tampó aquós és molt inferior a la requerida corresponent als nivells basals d'aquest analit a la sang. En el desenvolupament de l'ELISA per NT-proBNP, després d'estudiar diferents paràmetres relacionats amb l'heterologia i altres paràmetres físico-químics, s'ha aconseguit assolir el límit de detecció necessari obtenint una bona exactitud amb mostres de plasma fortificades amb l'analit en qüestió. Ha estat possible desenvolupar un microarray multiplexat per a la detecció de 5 biomarcardors (cTnl, NT-proBNP, CRP, Cys C i H-FABP). Un cop biofuncionalitzat el microarray amb els corresponents bioconjugats o anticossos de captura, la resta d'immunoreactius i biomarcadors poden ser utilitzats en forma de còctel sense que en cap cas s'hagin observat fenòmens de cooperativitat ni de reactivitat creuada. Tant sols els immunoreactius de Lp(a) van produir aquestes interferències i per aquest motiu es van descartar. En aquest treball de recerca va ser impossible quantificar la CRP i Cys C en el mateix microarray que la H-FABP, cTnl i NT-proBNP de mostres directes. Afortunadament, el fet d'utilitzar superfícies de vidre en les quals es podien imprimir fins a 24 microarrays ha permès poder fer aquestes mesures de forma simultània i paral•ela. Amb el microarray multiplexat ha estat possible mesurar mostres de pacients amb diferents patologies. Malauradament, no va ser possible mesurar els nivells de cTnl amb aquest microarray, tal com era de preveure d'acord amb els estudis previs fets amb els immunoreactius utilitzats. Així doncs, podem considerar aquest microarray com un mètode semi-quantitatiu multiplexat útil per a la millora del diagnòstic de malalties cardiovasculars. Finalment, s'han realitzat estudis preliminars per implementar el sistema immunoquímic multiplexat en un sensor òptic fluorescent d'ona evanescent amb l'objectiu d'aconseguir un dispositiu POC (point-of-care). Malauradament, els resultats obtingut apunten a que és necessari fer un major esforç per a incrementar la detectabilitat d'aquest sistema, donat que els valors de LOD assolits són pitjors que els aconseguits amb l'ELISA o el microarray i, per casos com l'NT-proBNP, es troben molt allunyats dels valors basals.
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Valls, Zamora Rosa Maria. "Dietary effects on cardiovascular disease risk biomarkers." Doctoral thesis, Universitat Rovira i Virgili, 2009. http://hdl.handle.net/10803/8873.
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La tesis consta de 4 proyectos: dos estudios de intervención, aleatorizados, paralelos y controlados, uno sobre los efectos de productos del cacao y otro sobre los de fibra soluble, Plantago ovata husk (Po-husk), sobre biomarcadores de enfermedad cardiovascular (ECV) en sujetos hipercolesterolémicos. El tercero es la identificación de compuestos fenólicos del aceite de oliva virgen (AOV) en plasma humano (en ayunas y en fase postprandial) y el cuarto, el desarrollo de una aplicación informática para implementar los criterios CONSORT.Los productos del cacao y Po-husk reducen las concentraciones plasmáticas de c-LDL y ejercen efectos beneficiosos sobre otros biomarcadores de ECV.
Además se han detectado hasta 10 compuestos fenólicos del AOV, incluido el 3,4-DHPEA-EDA, en plasma humano postprandrial.
Finalmente, la incorporación de productos del cacao o Po-husk o el AOV o su combinación a una dieta cardiosaludable se adecuará al perfil de biomarcadores de riesgo de ECV de cada paciente.
The thesis is based on 4 projects: 2 randomised, controlled, interventional studies, one of the cocoa cream products and the other of the soluble fibre (Plantago ovata husk (Po-husk) on biomarkers of CVD. Third, the virgin olive oil (VOO) phenolic compounds identification in fasting and postprandial human plasma, and fourth, designed a technology application to facilitate the implementation of criteria CONSORT statement.
The cocoa cream products and Po-husk reduced in plasma LDL-c and also, had beneficial effects on other CVD biomarkers and risk factors.
Also, had been detected until 10 phenolic compounds from VOO, including 3,4-DHPEA-EDA, in human postprandial plasma.
Finally, applying cocoa products or Po-husk or VOO or in combination in a cardio-protective diet warrants consideration as individualised therapeutic measures based on the individual's CVD risk factor profile.
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Wiklund, Peder. "Adipose tissue, the skeleton and cardiovascular disease." Doctoral thesis, Umeå universitet, Geriatrik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42083.
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Cardiovascular disease (CVD) is the leading cause of death in the Western World, although the incidence of myocardial infarction (MI) has declined over the last decades. However, obesity, which is one of the most important risk factors for CVD, is increasingly common. Osteoporosis is also on the rise because of an aging population. Based on considerable overlap in the prevalence of CVD and osteoporosis, a shared etiology has been proposed. Furthermore, the possibility of interplay between the skeleton and adipose tissue has received increasing attention the last few years with the discovery that leptin can influence bone metabolism and that osteocalcin can influence adipose tissue. A main aim of this thesis was to investigate the effects of fat mass distribution and bone mineral density on the risk of MI. Using dual-energy x-ray absorptiometry (DEXA) we measured 592 men and women for regional fat mass in study I. In study II this was expanded to include 3258 men and women. In study III 6872 men and women had their bone mineral density measured in the total hip and femoral neck using DEXA. We found that a fat mass distribution with a higher proportion of abdominal fat mass was associated with both an adverse risk factor profile and an increased risk of MI. In contrast, a higher gynoid fat mass distribution was associated with a more favorable risk factor profile and a decreased risk of MI, highlighting the different properties of abdominal and gynoid fat depots (study I-II). In study III, we investigated the association of bone mineral density and risk factors shared between CVD and osteoporosis, and risk of MI. We found that lower bone mineral density was associated with hypertension, and also tended to be associated to other CVD risk factors. Low bone mineral density was associated with an increased risk of MI in both men and women, apparently independently of the risk factors studied (study III). In study IV, we investigated 50 healthy, young men to determine if a high-impact loading intervention in the form of a series of jumps would lead to changes in glucose and lipid metabolism. We found that the intervention group had significantly lowered serum glucose levels compared to the control group. Changes in all metabolic parameters favored the intervention group with an increase in lipolysis from baseline and a decrease in cholesterol. In summary, the proportion of abdominal and gynoid fat mass displayed contrasting associations to both CVD risk factors and MI risk. Abdominal fat mass was associated with a higher risk while a high proportion of gynoid fat mass was associated with a lower risk. Bone mineral density displayed an inverse association with MI risk, seemingly independently of CVD risk factors, suggesting other explanations to a shared pathogenesis. Finally, high impact loading on the skeleton in young, healthy men decreased serum glucose levels and tended to improve other metabolic parameters, suggesting that the skeleton can affect energy metabolism.