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Tesi sul tema "Cardiovascular diseases"
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1
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/.
Testo completo
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Grytsiuk, M. І. "Life and cardiovascular diseases". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18306.
Testo completo
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Agyemang, Edmund Adjei, Priscilla Okoh e 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.
Testo completoAbstract (sommario):
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, e 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.
Testo completoAbstract (sommario):
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
5
Yiu, Kai-hang, e 姚啟恆. "Cardiovascular manifestations in systemic inflammatory diseases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48541011.
Testo completoAbstract (sommario):
Systemic inflammatory diseases, including those of rheumatology and dermatology, are associated with increased cardiovascular events. Evidence demonstrates that the chronic systemic inflammation associated with these diseases plays a pivotal role in all stages of atherosclerotic plaque formation, from initiation of the fatty streak to plaque rupture and consequent acute coronary syndrome. Although a number of studies have evaluated the cardiovascular manifestations in systemic inflammatory disease, this thesis offers additional observations, including the vascular atherosclerotic pattern, the pathogenesis of premature atherosclerosis and the use of coronary calcification as a predictor of adverse cardiovascular outcome.
The work is divided into four sections. Section I provides an overview of the cardiovascular manifestation of systemic inflammatory diseases and the patients and methods of the current thesis. The objective of Section II is to evaluate the pattern of cardiovascular manifestation, in particular systemic vascular calcification and cardiac valve calcification in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and psoriasis, using multi-detector computed tomography (MDCT) and carotid intima-media thickness (c-IMT). It was found that both patients with RA, SLE and psoriasis had a greater prevalence and extent of vascular calcification compared with age and gender matched controls. Moreover, both aortic valve calcification (AVC), mitral valve calcification (MVC) was found to be more prevalent in patients with RA and SLE than controls. Interestingly, the presence of MVC, but not AVC, independently predicted the occurrence of premature atherosclerosis with arterial calcification in these patients.
Section III evaluates the potential underlying mechanisms that lead to cardiovascular manifestations in patients with systemic inflammatory disease. Bone marrow-derived endothelial progenitor cells (EPCs) play an important role in the maintenance of endothelial integrity and hemostasis. The relationship between the circulating EPCs and subclinical coronary atherosclerosis as determined by coronary calcification in RA patients nonetheless remains unclear. The study results demonstrated that RA patients with coronary atherosclerosis have significantly lower levels of CD133/KDR+ and CD133+ EPCs than those without. In addition to older age, lower levels of circulating CD133/KDR+ EPCs also predicted occurrence of coronary atherosclerosis. As with RA and SLE, psoriasis is associated with premature atherosclerosis, although the underlying mechanism remains unclear. The aim of the study was therefore to investigate the relationship of disease activity and systemic inflammation with macrovascular and microvascular function in patients with psoriasis. The results demonstrated that patients with psoriasis have increased arterial stiffness, but not microvascular dysfunction compared with healthy controls. More importantly, high-sensitivity C reactive protein positively correlated with, and independently predicted, arterial stiffness.
Section IV explores the prognostic value of a surrogate marker of atherosclerosis, coronary calcium score (CCS), in patients with RA and SLE. A total of 152 patients with RA (n=85) and SLE (n=69), and 106 healthy controls underwent MDCT to measure CCS. All patients were prospectively followed up for major cardiovascular events for a mean period of 4.3 years. The result demonstrated that presence of CCS >100 predicted the occurrence of a major cardiovascular event independent of other risk factors in RA and SLE patients.published_or_final_version
Medicine
Master
Doctor of Medicine
6
Li, Wai-sum Rachel, e 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.
Testo completo
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Wang, Qianyi. "Fatty Acids, Cardiovascular Diseases, and Diabetes Mellitus". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14117764.
Testo completoAbstract (sommario):
Cardiovascular disease (CVD) is the number one cause for mortality and morbidity around the world. Meanwhile, diabetes mellitus (DM) has become an emerging epidemic, causing 1.5 million deaths in 2012, with 80% occurring in low- and middle-income countries. Substantial evidence has linked both lifestyle and metabolic risk factors to increased risk of CVD and death, with suboptimal diet being the single leading modifiable cause of poor health (Lim. SS, et al, Lancet 2012). Of 20 top individual causes of disease burden worldwide, 8 are related to poor nutrition, including suboptimal intakes of various dietary fatty acids. Although previous studies have found divergent health effects of different dietary fatty acids on health, gaps still exist in terms of the scientific knowledge (e.g. how individual circulating vs. dietary trans fatty acid subtypes affect health) and related disease burdens (e.g. national CHD mortality burdens attributable to suboptimal intakes of fatty acids). These gaps have motivated my dissertation researches.
In chapter one and two, I investigated the prospective associations of five subtypes of plasma phospholipid trans fatty acid (TFA) levels with the risk of various disease endpoints, including total, CVD and non-CVD mortality, incident coronary heart disease (CHD) and DM. In chapter two, I also examined the prospective associations of total and subclasses dietary TFA with risk of DM. The analyses were conducted using the Cardiovascular Health Study, a community-based multicenter prospective cohort consisted of older Americans. The risks were estimated using the Cox proportional hazard model.
The study in chapter three was a collaborative effort of the Nutrition and Chronic Diseases Expert Group as part of the 2010 Global Burden of Diseases, Injuries, and Risk Factors study. Using the comparative risk assessment framework, I comprehensively quantified the CHD mortality attributable to suboptimal intakes of saturated fat, omega-6 polyunsaturated fat, and TFA in 186 countries in 1990 and 2010, by age and sex groups. I also estimated the regional and country level trends of these attributable CHD burdens from 1990 to 2010. The findings of this study are relevant for informing regional and country level public health policy priorities.
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BIFFI, ANNALISA. "Antidepressants and the risk of cardiovascular diseases". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199081.
Testo completoAbstract (sommario):
La sindrome depressiva è considerata una importante questione nel campo della sanità pubblica. Oggigiorno, circa 300 milioni di persone sono colpiti da disturbi depressivi e un quarto di questi solo in Europa. La terapia con antidepressivi AD come i farmaci triciclici TCA, inibitori selettivi della ricaptazione della serotonina SSRI e nuovi AD atipici, sembra essere il trattamento più appropriato per la cura dei sintomi depressivi. Diversi studi sono realizzati per valutare l’associazione tra trattamento con farmaci AD e insorgenza di patologie cardiovascolari CV.
Nel primo studio, è stata eseguita una sintesi della letteratura scientifica riguardante la possibile associazione tra l’utilizzo di AD e patologie CV. È stata eseguita una ricerca di studi osservazionali utilizzando termini collegati alle patologie CV e al trattamento con AD. In più, è stata valutata la qualità degli studi inclusi, l’eterogeneità tra questi e la presenza di publication bias.
La seconda parte della tesi riguarda studi condotti entro il progetto AIFA Agenzia Italiana del Farmaco, dove sono stati utilizzati dati da diversi database sanitari regionali partecipanti a I-GrADE Gruppo Italiano per l’Appropriata Prescrizione Farmacologica nei soggetti Anziani. Il progetto si focalizza sull’inappropriatezza delle prescrizioni in una popolazione anziana con diagnosi CV. Nel secondo studio, disegni caso-controllo innestati sono stati applicati per valutare la terapia AD rispetto all’insorgenza di patologie CV. Analisi di sensibilità sono state effettuate come una Monte Carlo Sensitivity Analysis, che ha valutato il potenziale bias introdotto dal confondente fumo e modificando l’ampiezza della finestra di esposizione.
Nel terzo studio, l’effetto acuto del trattamento con AD è stato valutato rispetto all’insorgenza di aritmia. La selezione della coorte è stata ristretta ai nuovi utilizzatori di AD senza precedente aritmia. Disegni caso-controllo innestato e case-crossover sono stati applicati e le stime sono state aggiustate per le prescrizioni di farmaci e i ricoveri. Analisi di sensibilità sono state effettuate utilizzando diversi criteri per definire l’outcome e modificando la finestra di esposizione.
Nel quarto studio, è stato valutato il link tra aderenza al trattamento con AD rispetto alla mortalità. La selezione è stata ristretta agli utilizzatori di AD trattati dal reclutamento in coorte. Un modello di Cox è stato applicato ed è stata valutata la combinazione tra diversi livelli di aderenza ad AD a co-trattamenti durante il periodo di osservazione. Le stime sono state aggiustate per diverse variabili, come la politerapia. Infine, analisi di sensibilità sono state effettuate applicando una diversa definizione per la copertura con AD.
I risultati della meta-analisi hanno mostrato un incremento di rischio di patologie cerebrovascolari e di cardiopatie acute rispettivamente per utilizzatori di SSRI e TCA. Questi risultati sono confermati dagli studi osservazionali effettuati nell'ambito del Progetto AIFA. Una relazione positiva è stata trovata tra esposizione con AD e malattie CV, in particolare un effetto proaritmico dell'esposizione AD è stato rivelato in una coorte di pazienti anziani già affetti da una malattia CV. Infine, l'aderenza al trattamento AD è stata associata ad un ridotto rischio di morte, considerando diversi livelli di aderenza di co-trattamenti assunti durante il periodo di osservazione. In conclusione, gli studi condotti hanno mostrato che l’uso di AD sembra incrementare il rischio di patologie CV, perciò i medici devono attentamente monitorare il trattamento con AD per assicurarne la corretta assunzione e provare a prevenire l’insorgenza di patologie CV. Poiché il potenziale aumento del rischio può comportare un impatto considerevole, le stime fornite da questi studi possono supportare sia le pratiche cliniche che normative.Depression is considered an important public health issue. Nowadays, about 300 million people are affected by depressive disorders and a quarter of them just in Europe. Antidepressant (AD) treatment like tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs) or newer atypical antidepressants (NAAs) seems to be the most appropriate therapy in order to treat depressive symptoms. In the first study, a synthesis of the available scientific literature was performed on the possible association between use of AD and cardiovascular diseases (CVD). A search of published observational studies was carried out using terms directly related with cardiovascular and antidepressive field. In addition, the quality of the included studies, the heterogeneity among them as well as the presence of publication bias was evaluated. The second part of the thesis regards the studies conducted within the Italian Medicines Agency (Agenzia Italiana del Farmaco, AIFA) project, where data from different regional healthcare utilization databases involved in the Italian Group for Appropriate Drug Prescription in the Elderly (I-GrADE) was used. The project is focused on the evaluation of inappropriate prescribing in a population of elderly hospitalized with a diagnosis of CVD. In the second study, nested-case control studies were applied for the evaluation of the role of AD respect to the occurrence of CVD, among the elderly population. Sensitivity analyses were performed, like a Monte Carlo Sensitivity Analysis (MCSA), which quantified the potential bias introduced by a particular confounder (smoking factor) and by changing the length of AD exposure’s window. In the third study, the acute effect of AD treatment was evaluated respect to the onset of arrhythmia. The cohort selection was restricted to the new AD users who did not developed a previous event of arrhythmia. Nested case-control and case-crossover studies were applied and estimates were adjusted for drug prescriptions and hospitalizations. Sensitivity analyses were performed by using different criteria to define the outcome of interest or by changing length of AD exposure’s window. In the fourth study, we focused on the role of AD medication respect to mortality. The possible link between adherence to AD and increased or decreased risk of mortality was tested among the elderly cohort. The selection was restricted to elderly who were all AD users and started AD therapy since cohort recruitment. A Cox model was applied and the combined levels of adherence to AD and co-treatments were evaluated during observation time. Estimates were adjusted for several variables such as the polypharmacy. Then, sensitivity analyses were performed on the basis of AD coverage’s definition. The results of the meta-analysis showed a significant increased risk of cerebrovascular disease and acute heart failure respectively for SSRIs and TCA users. Then, these results were confirmed by the observational studies performed within the AIFA Project. A positive relation was found between AD exposure and CVD in a cohort of elderly patients already affected by a CVD, in particular a proarrhythmic effect of AD exposure was revealed by our estimates. Finally, adherence to AD treatment was associated with a decreased risk of death by considering different levels of adherence to co-treatments assumed during the observation time. In conclusion, these studies showed that the use of AD could increase the risk of several CV disease, therefore, physicians need to carefully monitor their patients to ensure a correct assumption of the drugs and concurrently try to prevent the onset of CV outcomes. Since any potential increased risk may result in a considerable impact, the risk effect estimates provided by these studies may support both clinical practices and regulatory activities.
9
Rosenlund, Mats. "Environmental factors in cardiovascular disease /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-292-6/.
Testo completo
10
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.
Testo completo
11
Shanbhag, Preeti Pandurang. "Role of Mechanical Versus Humoral Effects of Angiotensin II on Vascular Remodeling". Thesis, Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/10446.
Testo completoAbstract (sommario):
In this study, we investigated the role of Ang II in pathological vascular remodeling. We sought to determine whether the humoral or the mechanical effects of Ang II are the dominant factor driving the remodeling process.
The following experimental groups were used: control group (untreated mice), mice treated with an angiotensin receptor blocker (Candesartan, 0.5 mg/kg/day,SQ), an ACE inhibitor (Captopril, 6 mg/kg/day), and a calcium-channel blocker (Amlodipine, 7.5 mg/kg/day). All mice (n=6 per experimental group) were from the C57Bl/6 background. The carotid ligation model was implemented to study the differences in vascular remodeling. Additionally, multiple time points (7-, 14-, and 21-days post-surgery) were used to track the progression of remodeling. In Day-7 analysis, all three treatment groups yielded similar remodeling patterns as evidenced by a significant reduction in neointimal area, medial thickening and hypertrophy compared with the control group. Histomorphometric analysis of carotid sections collected 1mm below the ligation demonstrated that the Amlodipine group had 26% reduction in total vessel area, Candesartan a 36% reduction, and Captopril a 28% reduction (p less than 0.05 in all groups compared with Control), as well as a parallel 38-40% drop in medial thickness. In Day-14 analysis, no significant differences between the Controls and treatment groups were observed, although differences were emerging between the treatment groups. Candesartan was found to reduce the extent of negative remodeling observed between the 7- and 14-day Control data, whereas the Captopril group did not exhibit this trend. All treatment groups exhibited less neointimal formation than Controls, similar to Day-7. By the 21-day time point, the Captopril group underwent positive remodeling, resembling the Candesartan and Amlodipine groups. Although total vessel area was analogous among all groups, neointimal areas were significantly decreased in the treatment groups.
Blood pressure plays a pivotal role in the modulation of vascular remodeling in response to mechanical injury. Although intermediate timepoint analysis suggests that humoral aspects of ACE inhibition or angiotensin-receptor blockade yielded unique effects on the overall vessel caliber, upon reaching the late, 21-day time point, the mechanical factors became predominant. These data support the importance of blood pressure control in the attenuation of pathological vascular remodeling.
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Alamin, Ali E., Arsham Alamian, Hadii M. Mamudu, Timir K. Paul, Liang Wang, Pooja Subedi e Matthew Budoff. "Associations Between Multiple Cardiovascular Disease Risk Factors and Diabetes Among Asymptomatic Individuals in a Hard To-Reach Population". Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/1386.
Testo completoAbstract (sommario):
Background: Diabetes is the sixth leading cause of death in the United States (U.S), and a major risk factor for cardiovascular disease (CVD). The prevalence of diabetes in central Appalachian region is higher than the rest of the nation (14.4% versus 9.0%, respectively). Objectives: Examine the association between multiple risk factors for CVD and diabetes in asymptomatic adults in central Appalachia. Methods: Between January 2012 and July 2016, 3,000 community-dwelling asymptomatic individuals from central Appalachia participated in screening for sub-clinical atherosclerosis. Participants were asked to report their diabetes status (yes/no). In addition, data on coronary artery calcium (CAC), a marker for sub-clinical coronary atherosclerosis, in quartiles (0, 1-99, 100-399, ≥400), obesity (body mass index ≥30 kg/m2), hypercholesterolemia (yes/no), hypertension (yes/no), current smoking (yes/no), sedentary lifestyle (yes/no), and family history of coronary artery disease (CAD) (yes/no), were collected. Multivariable logistic regression analyses were conducted to assess association between CVD risk factors and diabetes. Results: Of the 3,000 participants, 2,509 subjects (mean age: 58.3 years; SD = 9.8 years) had complete data on variables of interest. Approximately, 14% of the study population reported having type 2 diabetes. Among subjects with diabetes, 58% had a CAC score ≥1, 22% were obese, 17% had hypercholesterolemia, 20% had hypertension, 16% were current smokers, 17% had a sedentary lifestyle, and 15% had a family history of CAD. After adjusting for sex and age, having a CAC score of 1-99, 100-399, and ≥400 increased the odds of having diabetes (Odds ratio (OR): 1.4, 95% Confidence interval (CI) = 1.02-1.9; OR: 2.0, 95% CI = 1.4-2.8; OR: 3.1, 95% CI = 2.1-4.7, respectively) in a linear fashion. Being obese (OR: 3.2; 95% CI = 2.5-4.0), having hypercholesterolemia (OR: 1.8; 95% CI=1.4-2.4), being hypertensive (OR: 3.0; 95% CI= 2.3-3.8), being a smoker (OR: 1.5; 95% CI = 1.1-2.1), and being sedentary (OR: 1.6; 95% CI = 1.3-2.0) were significantly associated with diabetes. Having three (OR: 3.0; 95% CI=1.3-6.6), four (OR: 4.4; 95% CI=2.0-9.7), five (OR: 7.0; 95% CI=3.1-16.1) or six (OR: 9.9; 95% CI= 3.5-27.7) CVD risk factors significantly increased the odds of diabetes. Subjects with any of the seven risk factors under study were 1.7 times (95% CI= 1.5-1.9) more likely to have diabetes. Conclusion. Odds of type 2 diabetes increase with higher number of risk factors for CVD. Results support the use of multifaceted CVD and diabetes prevention programs to lower the incidence of type 2 diabetes.
13
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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Nasser, Zeina. "Outdoor air pollutants and cardiovascular diseases in Lebanon". Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/221755.
Testo completoAbstract (sommario):
Outdoor air pollution is increasingly considered as a serious risk factor for cardiovascular diseases (CVD). High levels of airborne particulate matter (PM) constitute the greatest international air pollution threat. The purpose of this thesis is to broaden our knowledge regarding the relationship between outdoor air pollution and cardiovascular diseases in the Middle Eastern countries, specifically in Lebanon. Moreover, we aimed to develop a scale as CVD screening tool among the Lebanese population. To achieve these goals, we conducted three studies. The first was a systematic review of the literature aiming to assess levels and sources of PM across the Middle East area and to search for an evidence of relationship between PM exposure and CVD (Paper I).The second manuscript was a multicenter case-control study investigating the association between outdoor pollutants and cardiovascular diseases among Lebanese adults (Paper II) while the third study was conducted to develop a score that can be used as a screening tool in clinical and epidemiological settings among the Lebanese adults (Paper III).The annual average values of PM pollutants in the Middle East region are considered to be much higher than the WHO 2006 tolerated levels (PM2.5 = 10 µg/m3, PM10 = 20 µg/m3). We uncovered evidence of an association between PM and CVD in 4 Middle East countries: Iran, Kingdom of Saudi Arabia, Qatar and the United Arab Emirates. Ambient PM pollution is considered a potential risk factor for platelet activation and atherosclerosis. Moreover, it was associated with CVD and found to be linked with an increased risk for mortality and hospital admissions (Paper I). Increased risk of CVD with an odds ratio OR of 5.04, 95% CI (4.44-12.85) for living near busy highway and 4.76, 95% CI (2.07-10.91) for living close to local diesel generator was noticed among population exposed to outdoor air pollution (Paper II). In addition, our results highlight the importance of scale generation, which includes air pollution as predictive factor, as screening tool for patients at risk of CVD. This scale can foresee the cardiovascular disease outcomes better than the established score which use the traditional CVD risk factors (Paper III).In conclusion this study brings new evidence regarding the effects of particulate matter on cardiac diseases, points out the harmful role of diesel exhaust on health and suggest a an important role of traffic exhaust particles in exacerbating heart diseases in the Middle East Region. The developed scale could detect persons at high risk for CVD in the clinical and epidemiological settings. In addition, it serves as an essential public health screening tool for the primary prevention of CVD.Doctorat en Santé Publique
info:eu-repo/semantics/nonPublished
15
Butterfield, M. C. "Cardiovascular receptor changes induced by drugs and diseases". Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316867.
Testo completo
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Mazlan-Kepli, Wardati. "Antiplatelet therapy and clinical outcomes in cardiovascular diseases". Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7831/.
Testo completoAbstract (sommario):
Cardiovascular diseases (CVD) is a leading cause of death in the world. Despite effective treatment regimens for ischaemic heart disease (IHD) and ischaemic stroke, mortality and recurrence rates remain high. Antiplatelet therapy is on effective treatment and reduces the risk of recurrent heart attack and stroke. Nevertheless, there are patients who stopped or interrupted their antiplatelet therapy for certain reasons or some patients may be resistant or poor responders to antiplatelet therapy. Furthermore, there is evidence of rebound effect in platelet activity after antiplatelet cessation and this may associate with increased risk of cardiovascular event. This thesis is divided into five main chapters (chapters 3 to 7) which attempt to provide data to help resolve the uncertainty. Chapter 1 highlights the background of cardiovascular diseases and the global burden of cardiovascular and cerebrovascular diseases. The metabolism of platelets, antiplatelet therapy and current antiplatelet therapy guidelines are described, followed by discussion of the risk of cardiovascular event and changes in antiplatelet therapy. Chapter 2 describes the data source from Virtual International Stroke Trial Archive (VISTA) and National Health Service Greater Glasgow and Clyde (NHSGGC) Safe Haven, followed by definition of outcome measures. In chapter 3, Virtual International Stroke Trial Archive (VISTA) data was examined to test whether continue with the same antiplatelet therapy or changing to a new antiplatelet regimen reduces the risk of subsequent events in patients who experience a stroke whilst taking antiplatelet therapy. The findings indicate that subjects who switch to a new antiplatelet regimen after stroke did not have a lower early recurrence rate than subjects who continued with the same antiplatelet therapy. Observations on bleeding complications were similar in both groups. However, changing antiplatelet regimen after stroke was associated with more favourable functional outcome across a full scale modified Rankin Scale (mRS) at 90 days. In chapter 4, association between early or later initiation of antiplatelet with a recurrent ischaemic stroke and bleeding complications was assessed using VISTA data. The findings indicate that there was no association between a recurrent ischaemic stroke and timing of initiation of antiplatelet drug after stroke. However, early initiation was associated with increased risk of bleeding. In terms of functional outcomes, this study demonstrated that the mid-time and late initiation of antiplatelet therapy after acute stroke are associated with better functional outcomes compared with early initiation. In chapter 5, a nested case-control study was performed to explore the rate of antiplatelet cessation and interruption in a sample of patients with recent ischaemic stroke and to assess the risk of cardiovascular events associated with cessation and interruption of antiplatelet. It was found that there was no increased risk of cardiovascular event among patients who had early cessation or interrupted/stopped antiplatelet therapy within 90 days following acute ischaemic stroke. In chapter 6, the incidence and predictors of cardiovascular events after DAPT cessation were evaluated. The incidence of cardiovascular event while taking DAPT and following discontinuation of DAPT was 15.7% and 16.7% respectively. This study found that increasing age was associated with an increased risk of cardiovascular event, whereas, revascularization-treated patients and longer duration of DAPT, were each associated with a decreased risk. The duration of DAPT six months and less was associated a significantly higher risk for cardiovascular event. In chapter 7, an untargeted metabolomics analysis was performed while on DAPT (aspirin plus ticagrelor) and once they stopped ticagrelor to identify metabolite changes associated with cardiovascular events after stopping DAPT. Ten ACS patients were recruited in this study and data were analysed for seven patients. Three hundred eleven putative metabolites were identified. This study found 16 putative metabolites significantly altered following ticagrelor cessation. Of these, seven metabolites were from lipid pathway and down-regulated some up to 3-fold. On the other hand, adenosine, from nucleotide metabolism was upregulated up to 2.6-fold. It concluded that there are changes in numerous pathways following DAPT discontinuation and whether these changes differ in patients who have cardiovascular event after stopping DAPT warrant further investigation. In chapter 8, a summary of the findings of this thesis are presented as well as the future directions of research in this area.
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Foin, Nicolas. "Hemodynamics and endothelial cell biology in cardiovascular diseases". Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6392.
Testo completoAbstract (sommario):
Atherosclerotic plaques develop preferentially in curved and branching arteries in-vivo. Lipids and inflammatory cells accumulation in the intimal layer of the arterial wall is considered as the main driving mechanism in the disease progression. Evidences suggest that this focal distribution of plaques may result from the combination of systemic risk factors including high plasma cholesterol, smoking, diabetis, hypertension or genetic pre-disposition and local hemodynamic risk factors such as low and oscillatory flows. The exact mechanism of the biological and biomechanical interactions between the endothelium, blood flow and the growing lesion underneath still remains unclear. This thesis is a study on the relationship between biomechanical factors found in proatherogenic flow and endothelial inflammation. The thesis focuses in particular on the effect of secondary flows on wall shear stress and mass transport distribution. To that end, we have combined different techniques from flow imaging, 3D flow reconstruction, vascular biology and mathematical simulation of biological network. In particular, shear stress is involved in the regulation of the pro-inflammatory transcription factor nuclear factor -kB (NF-kB) and the vasoregulator Nitric Oxide. The role of endothelial Nitric Oxide and wall shear stress on NF-kB activation is still controversial. We investigated here the hypothesis that NO negatively regulates NF- kB activation in flow chamber with sheared endothelial cells and using a mathematical model of the NF-kB-NO pathway. Understanding the underlying relationship between hemodynamic factors and inflammatory cells transport to the wall may contribute to the development of better therapies or interventional practices to treat patients with atherosclerotic diseases.
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Neubeck, Alicia Helen. "Increasing access to secondary prevention of cardiovascular disease". Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/27329.
Testo completoAbstract (sommario):
Background: Access to secondary prevention remains disconcertingly low despite proven
benefits. The objectives of this thesis were: to evaluate telehealth models of secondary
prevention; to determine barriers to participation in secondary prevention; to evaluate the
long-term outcomes of a previously proven telehealth model, CHOICE (Choice of Health
Options In prevention of Cardiovascular Events); to determine the replicability and
generalisability of CHOICE; and to determine future directions for delivery of secondary
prevention.
Methods: Mixed methods were utilised to achieve the objectives of this thesis. To
evaluate telehealth models, a systematic review and meta-analysis process was followed.
To determine the barriers to participation in secondary prevention, a systematic review and
meta-synthesis process was followed; to evaluate the long-term outcomes of CHOICE,
patients who had participated in the original single centre trial had a repeat assessment at
four-years after their baseline assessment; to determine the replicability and generalisability
of CHOICE, a multi-centre replication trial involving 270 participants was conducted; and
to determine future directions for delivery of SP, both quantitative and qualitative methods,
including survey and focus groups, were undertaken.
Results: Telehealth based models of secondary prevention can improve access, reduce risk
factors and improve quality of life in patients who do not participate in facility-based
secondary prevention programs. While there are a number of barriers to participation in
facility-based secondary prevention, some of which are potentially modifiable, it was clear
from our review that a one-size fits all approach will not be suitable and telehealth models
can provide additional options for access to secondary prevention. Results of the long-term
follow-up of the single centre trial demonstrated that at four years participants in CHOICE had maintained the significant improvements that they had made at one year. In the current
replication study results showed that participants were at lower baseline risk than in the
previous single-centre study, but still made improvements in multiple cardiovascular risk
factors. Finally, we determined that an Internet-based model of secondary prevention
would suit some, but not all, patients with cardiovascular disease and may provide an
additional option for patients not accessing facility-based programs
Conclusion: There are multiple barriers to the uptake of secondary prevention and
telehealth models can offer an evidence-based alternative to patients who do not access
facility-based programs. The CHOICE program is a flexible telehealth model that provides
long-term behaviour change and is readily translated into multiple clinical settings. Future
work could focus on utilising new technology to increase uptake to proven secondary
prevention models such as CHOICE.
19
Slusher, Aaron L. "COUNTERREGULATORY EFFECTS OF PTX3 ON INFLAMMATION AND CELLULAR AGING". VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5287.
Testo completoAbstract (sommario):
Pentraxin 3 (PTX3) is a vital regulator of innate immune function that has been shown to counterregulate pro-inflammatory signaling and protect against the development of cardiovascular disease (CVD). Less is known about how PTX3 may mitigate against CVD risk by regulating the pro-inflammatory response at the cellular level. Therefore, this dissertation details four manuscripts which aimed to examine the capacity of PTX3 to regulate the innate immune response of peripheral blood mononuclear cells (PBMCs) isolated from healthy adults. Manuscript 1 examined the capacity of PTX3 to alter the inflammatory milieu following in vitro stimulation of isolated PBMCs with the pro-inflammatory lipid palmitate. In addition, Manuscript 2 sought to examine how participation in acute exercise, a powerful anti-inflammatory behavior that reduces CVD risk, alters the inflammatory phenotype and response of mononuclear cells following ex vivo stimulation with lipopolysaccharide (LPS). Manuscript 3 aimed to further elucidate the potential impact of cardiorespiratory fitness on the capacity of PTX3 to stimulate an innate immune response prior to and immediately following acute exercise in aerobically trained and untrained individuals. Finally, Manuscript 4 investigated the impact of healthy aging on plasma PTX3 concentrations and its relationship with telomere length in middle-aged compared to young adults. The capacity of isolated PBMCs to express a key cellular mechanism involved in maintaining longer telomere lengths, human telomerase reverse transcriptase (hTERT), following cellular stimulation with LPS, PTX3, and PTX3+LPS was also examined to address a mechanism that might explain how persistent exposure of circulating immune cells to the age-related pro-inflammatory milieu contributes to the shortening of telomere lengths.
20
Mascall, Keith S. "Sphingolipids and angiogenesis : role in cardiovascular disease". Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=189442.
Testo completoAbstract (sommario):
Following myocardial infarction, as a result of thrombus formation, angiogenesis occurs and permits reperfusion of damaged myocardium. Sphingolipids, sphingosine 1-phosphate (S1P) and sphingosylphosphorylcholine (SPC) are naturally occurring lipid mediators released from platelets and found in high concentrations at sites of thrombosis. S1P and SPC may therefore be involved in regulating angiogenesis following myocardial infarction and may influence reperfusion. The aims of this study were to determine the effects of S1P and SPC in human coronary arterial cell angiogenesis and delineate the subsequent mechanisms. An in vitro model of angiogenesis was developed using a co-culture of human coronary artery endothelial cells, human coronary smooth muscle cells and human fibroblasts. In this model S1P and SPC inhibited angiogenesis and this was dependent on the presence of smooth muscle cells. The mechanism of the inhibitory effect was via S1P-/SPC-induced release of a soluble mediator from smooth muscle cells. This mediator was identified as tissue inhibitor of metalloproteinase-2 (TIMP- 2). TIMP-2 release was dependent on sphingolipid-induced activation of S1P2 receptor and Rho-kinase signalling and directly contributed to incomplete formation of endothelial cell adherens junctions. This was observed as a diffuse localization of VE-cadherin leading to decreased tubulogenesis. This effect may occur via both matrix metalloproteinase-dependent and/or matrix metalloproteinase-independent pathways. A similar inhibitory response to S1P was demonstrated in ex vivo human and mouse arterial models of angiogenesis. In summary, S1P- and SPC-induced inhibition of angiogenesis in human artery endothelial cells mediated by TIMP-2 from vascular smooth muscle cells. This reduces the integrity of intercellular junctions between nascent endothelial cells. S1P and SPC may therefore inhibit the angiogenic response following myocardial infarction.
21
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.
Testo completo
22
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.
Testo completoAbstract (sommario):
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.
23
Leung, Yiu-por, e 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.
Testo completo
24
Pitzer, Ashley. "Contribution of ASC-Inflammasome to Vascular Endothelial Dysfunction: Role of RNA Receptor RIG-I". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/5050.
Testo completoAbstract (sommario):
Retinoic acid-inducible gene-I (RIG-I) is a putative RNA helicase and recently identified as a cytosolic RNA receptor in mammalian cells. The role of RIG-I in the regulation of vascular function under physiological and pathological conditions is unknown. Recent studies have shown that the inflammasome serves as a crucial initiator of cytokine-mediated inflammation mediating the pathogenesis of cardiovascular disease. The present study tested whether RIG-I activation triggers inflammasome formation and subsequent cytokine-mediated inflammation in the endothelium of mice coronary arteries. Using both genetic and pharmacological interventions of the RIG-I inflammasome, we first characterized whether specific activation of RIG-I via 3pRNA transfection induced the formation of an ASC-containing inflammasome in mouse vascular endothelial cells (MVECs). We confirmed that 3pRNA dose-dependently increased RIG-I protein levels and release of of type I IFNβ and IL-1b (a prototype cytokine from inflammasome activation), confirming RIG-I activation. We found that MVECs transfected with 3pRNA exhibited increased colocalization of RIG-I with apoptosis-associated speck-like protein (ASC) or caspase-1 and elevated active caspase-1 and IL-1β levels, indicating the formation and activation of the RIG-I inflammasome. This RIG-I inflammasome activation was accompanied by endothelial barrier dysfunction. In the presence of 3pRNA, ZO-1 and ZO-1 and VE-Cadherin expression diminished, and inhibiting caspase-1 and silencing inflammasome components attenuated this effect. To test the functional role of RIG-I and its affect on the permeability of mouse ECs, we performed a transwell permeability assay. Results confirmed that 3pRNA induced increased permeabilization of these mouse ECs, which was attenuated when inhibiting and silencing inflammasome components. These data indicate that increased expression and activity of RIG-I activate IL-1b producing inflammasomes in ECs, which may represent an early molecular mechanism mediating vascular inflammation and endothelial dysfunction independent of Nlrp3. Furthermore, we investigated the role of anti-aging gene Klotho in the regulation of RIG-I inflammasome activation. The Klotho protein has been shown to directly interact with RIG-I in senescent cells to block RIG-I multimerization and downstream production of pro-inflammatory cytokines. Administration of D-saccharic acid 1,4-lactone (saccharolactone) in vitro, a pharmacological inhibitor of Klotho activity, substantially increased inflammasome activation. In addition, mice injected with saccharolactone exhibited increased RIG-I inflammasome formation and activation within the coronary artery endothelium. These results suggest that decreased Klotho activity may activate RIG-I and thereby increase inflammasome activity. Therefore, the present study defines a novel role for RIG-I inflammasome activation in vascular dysfunction.
25
劉巨基 e Kui-kai Gary Lau. "Surrogate markers of atherosclerosis and cardiovascular disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40733749.
Testo completo
26
Svenungsson, Elisabet. "Cardiovascular disease in systemic lupus erythematosus /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-501-8.
Testo completo
27
Gil, Ana Cecilia Montes. "Avaliação farmacologica do aspirinato de atenolol como droga antiplaquetaria e anti-hipertensiva". [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309492.
Testo completoAbstract (sommario):
Orientador: Gilberto de NucciTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-11T00:01:00Z (GMT). No. of bitstreams: 1 Gil_AnaCeciliaMontes_D.pdf: 1050627 bytes, checksum: 72f41a4bdcddba6633b8b082cc0ee0a0 (MD5) Previous issue date: 2007
Resumo: No presente trabalho, foram avaliados os efeitos farmacológicos do Aspirinato de atenolol (AA T) uma potencial pró-droga mútua resultado da combinação química entre ácido acetilsalicílico (AAS) e atenolo!. As propriedades do AA T como droga antitrombótica foram avaliadas na inibição da agregação plaquetária estimulada in vitro e na inibição da produção de tromboxano estimulada ex-vivo em sangue de animais tratados. Por outro lado, o AA T foi avaliado como droga anti-hipertensiva no modelo de hipertensão induzida pela inibição crônica da síntese de NO em ratos, e seus efeitos como antagonista dos adrenoceptores 13 foram avaliados na resposta cronotrópica ao isoproterenol em átrios isolados. Foi determinada a estabilidade metabólica em diferentes frações subcelulares hepáticas, plasma e soluções tampão de diferente pH, assim como seu perfil farmacocinético após administração endovenosa. Também foram avaliadas as propriedades ulcerogênicas gástricas e o potencial mutag'ênico através do Teste de Ames. Os resultados mostraram na avaliação do efeito antiplaquetário, que o AA T não inibiu a agregação plaquetária induzida pelo ácido araquidônico em nenhuma das concentrações testadas e apesar d~ ini~ir significativamente a produção de tromboxano estimulada ex-vivo em rat6s e na maior dose testada em camundongos, este efeito inibitório foi menor quando comparado com o AAS. O acoplamento com AAS, na molécula de AAT, suprimiu os efeitos do atenolol como antagonista dos adrenoceptores 13. Igualmente, o AA T não reduziu a freqüência cardíaca e pressão arterial após tratamento oral crônico de ratos hipertensos, estes resultados indicaram que não houve liberação de atenolol desde a molécula de AA T. Na avaliação da estabilidade metabólica e farmacocinética, observamos que o AA T seguiu uma rápida e completa hidrólise no grupo orto-acetila, gerando salicilato de atenolol (SA T), este produto foi formado quando o AA T foi submetido à hidrólise plasmática (T% 7,6 min) e aquosa (T% 56,5; 24,9 e 6,4 nos pH 2,5; 7,4 e 9.4 respectivamente) metabolização hepática e também após administração endovenosa em cães. o salicilato de atenolol formado a partir do AA T nas frações subcelulares hepáticas foi metabolizado apenas na fração microssomal gerando dois metabólitos hidroxilados em posições diferentes na molécula, a formação destes metabólitos foi dependente do tempo e paralela à cinética de desaparecimento do SAT. Após administração endovenosa, concentrações de AA T não foram detectadas em plasma. Atenolol e ácido salicílico (AS), foram liberados a partir da molécula de SAT (após clivagem da ligação éster benzoato) em concentrações significativamente menores às concentrações obtidas nos grupos tratados com AAS ou atenoloL A ASC0-24h calculada para o AS no grupo tratado com AA T correspondeu ao 0,71% da área calculada para o grupo que recebeu AAS. Similarmente, a ASC0-24h do atenolol no grupo tratado com AA T correspondeu a 1,44% da área calculada para ~ grupo tratado com atenolol. O AA T e seu principal metabólito SA T, não apresentaram propriedades mutagênicas, obtendo-se resultados negativos no Teste de Ames. O AA T produziu lesões na mucosa gástrica significativamente menores às observadas com o AAS após administração oral aguda e crônica durante 4 semanas. Devido às relevantes diferenças obtidas entre o AA T, AAS ou atenolol na caracterização farmacológica e farmacocinética, concluímos que o AA T não atua como pró-droga mútua de AAS e atenolol, e modificações futuras na molécula devem ser consideradas com a finalidade de desenvolver aspirinatos cardioativos com potencial efeito farmacológico
: In this study, we evaluated the pharmacologica/ effects of Atenolol Aspirinate (A TA) a potential mutual prodrug that resulted of the chemical combination between Acetyl Salicylic Acid (ASA) and atenolo!. The properties of ATA as anthithrombotic drug were evaluated on the inhibition of in vitro stimulated platelet aggregation and on the inhibiton of ex-vivo stimulated thromboxane production in blood from treated animais. Additionally, A TA was evaluated as an antihypertensive drug on the hypertension induced by chronic inhibition of NO in rats, its effects as antagonist of f3 adrenoceptors were evaluated in the chronotropic response to isoproterenol in isolated atria. The metabolic stability was determined in different hepatic subcellular fractions, plasma and buffer solutions as well as its pharmacokinetic profile after intravenous administration. The gastric ulcerogenic properties and mutagenic potencial, using the Ames test, were toa evaluated. In the evaluation of the antiplatelet effect, our results showed that ATA had no effect on arachidonic acid induced platelet aggregation. Although it inhibited significantly the ex-vivo stimulated thromboxane production in rats and in the highest tested dose in mice, ATA showed lower inhibitory effect than ASA. The coupling with ASA, in the ATA mOlecule, abolished the atenolol effects as antagonist of f3 adrenoceptors. In the sa~e"way, ATA had no effect reducing the heart rate and blood pressure after chropic oral treatment of hypertensive rats, these results showed that atenolol was not liberated from ATA molecule. In the evaluation of the metabolic stability and pharmacokinetics, we observed that ATA followed a rapid and complete hydrolysis at the o-acetyl group, generating atenolol salicylate (A T8), this product was formed when ATA was submitted to plasma hydro/ysis (T% 7;6 min) and aqueous hydrolysis (T% 56,5; 24,9 and 6,4 at pH 2,5; 7,4 and 9.4 respectively), hepatic metabolization and after intravenous administration to dogs. ATA was biotransformed to A TS in ali hepatic subcellular fractions, then A TS was metabolized only in the microsomal fraction generating two hydroxylated metabolites, whose formation was time dependent and parallel to the kinetics of A TS consumption. After intravenous administration, concentrations of A TS instead ATA were found in plasma dog samples, SA and atenolol were originated from cleavage of A TS molecule at the benzoate ester linkage, generating concentration levels to a lesser extent than levels found after treatment with an equimolar dose of the drugs ',nóiviõua
Doutorado
Doutor em Farmacologia
28
Yan, Y. (Ying). "The antichlamydial effects of drugs used in cardiovascular diseases". Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514293153.
Testo completoAbstract (sommario):
Abstract
Chronic Chlamydia pneumoniae infections have been associated with cardiovascular diseases (CVD), but the treatment is difficult. Some drugs used for CVD have been found to have an inhibitory effect on the C. trachomatis infection, which is not considered to be associated with CVD. The purpose of this study was to investigate the effects of heparan sulfate-like glycosaminoglycans, COX inhibitors and rapamycin on the C. pneumoniae infection with cell culture methods.
Almost any conceivable factors may affect the results of cell cultures. This study showed the complex interaction between temperature, time and medium during the pre-treatment before inoculation. The influences of these factors on the results overlapped and interlaced. The simple washing procedure could enhance the infectivity of C. pneumoniae although it is generally considered to cause the loss of chlamydial EBs and sequentially decrease the chlamydial infectivity.
Although the detailed mechanisms were not studied, the results of this study showed that selective COX inhibitors and rapamycin can inhibit the infectivity of C. pneumoniae by inhibiting the growth and maturation, whereas heparan sulfate-like glycosaminoglycans perhaps inhibit the attachment of C. pneumoniae EBs onto the host cells. Recovery and repassage results showed that the growth can be only delayed by selective COX inhibitors, and it can recover to normal level once the drugs were removed. However, rapamycin inhibited the maturation of chlamydial EBs and therefore the infectivity fell down further even when the rapamycin was removed. This study also presented the variations of pathogenicity between different C. pneumoniae strains in vitro. This study is based on in vitro experiments with an acute infection model. Thus, any definite conclusions on the possible antichlamydial effects of the drugs tested in the treatment of cardiovascular diseases which are associated with chronic C. pneumoniae infections cannot be drawn on the basis of this study.
29
Qiu, Hong. "Leukotrienes and leukotriene receptors : potential roles in cardiovascular diseases /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-056-5/.
Testo completo
30
Hergens, Maria-Pia. "Swedish moist snuff and the risk of cardiovascular diseases /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-372-6/.
Testo completo
31
Wong, Chun-kit Arthur, e 黃俊傑. "Serum uric acid and its relationship with cardiovascular diseases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208600.
Testo completoAbstract (sommario):
Serum uric acid (SUA) is in many ways related to cardiovascular morbidity and mortality. In this thesis, the objectives were to (1) to review the role of SUA in cardiovascular diseases; (2) to study the effects of elevated SUA on vascular function in subjects with high cardiovascular risk; (3) to evaluate the prognostic significance of SUA and vascular function; (4) to study the effect of pharmacological reduction of SUA on vascular function.
A literature review was performed at the beginning to summarise the key findings from epidemiological, cross-sectional, and interventional studies that examined the relationship of SUA with cardiovascular diseases, vascular dysfunction, and its associated pathophysiological mechanisms in vascular dysfunction. The results from available studies that evaluated the association of elevated SUA with vascular dysfunction are inconsistent. Therefore the role that elevated SUA plays in the pathogenesis of vascular dysfunction and cardiovascular diseases remains controversial. With this background information in mind, we performed a series of studies to give more evidence to the controversial areas.
A cross-sectional study on subjects with high cardiovascular risk was first performed. The markers of vascular function assessed were brachial arterial flow-mediated dilation (ba-FMD), and nitroglycerin-mediated dilation (ba-NMD). It showed that elevation of SUA was independently associated with impairment of ba-NMD, but not with impairment of ba-FMD. This suggested that ba-NMD impairment may be part of the underlying mechanism in the vasculature by which elevated SUA increases the risk of adverse cardiovascular outcomes.
To test the above hypothesis, the prognostic significance of SUA and ba-NMD was evaluated by conducting an analysis on the risk of developing major adverse cardiovascular events (MACE) in the above cohort. The outcome variables of MACE (acute coronary syndrome, myocardial infarction, congestive heart failure, stroke etc.) within the follow-up period were collected. The time-to-event analysis demonstrated that both SUA and ba-NMD independently predicted the development of MACE. The causal mediation analysis confirmed that ba-NMD was the mediator between elevated SUA and MACE.
Finally, a randomised placebo-controlled trial was performed to assess the effect of pharmacological reduction of SUA on vascular function. A novel herbal agent “UricsilTM” was used as the active treatment. The SUA-lowering effect of UricsilTM was insignificant compared with placebo at 12 weeks. No significant change in vascular function (ba-FMD and ba-NMD) was observed following treatment.
The key research finding in this thesis, which demonstrated that ba-NMD is a potential mediator between elevated SUA and MACE, is a novel one. Future clinical and experimental studies could be performed to further enhance our understanding of this potential mechanism.published_or_final_version
Medicine
Master
Master of Philosophy
32
Bobak, Martin. "Determinants of the epidemic of cardiovascular diseases in Czechoslovakia". Thesis, London School of Hygiene and Tropical Medicine (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362820.
Testo completo
33
Biduchak, A. S. "The problem of cardiovascular diseases among children and adolescents". Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18858.
Testo completo
34
Обухова, Ольга Анатоліївна, Ольга Анатольевна Обухова e Olha Anatoliivna Obukhova. "The association between the VDR polymorphisms and cardiovascular diseases". Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27494.
Testo completoAbstract (sommario):
The vitamin D receptor (VDR), through the binding of 1,25 vitamin D and subsequently modulating the transcription of target genes, mediates the vitamin D endocrine system.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/27494
35
Fernández, Valverde Diana Elizabeth. "Estimación del riesgo cardiovascular en población española adulta y control de los factores de riesgo en pacientes con enfermedad cardiovascular establecida". Doctoral thesis, Universitat Rovira i Virgili, 2021. http://hdl.handle.net/10803/673091.
Testo completoAbstract (sommario):
Introducció:
La malaltia cardiovascular (MCV) és la principal causa de morbimortalitat a nivell mundial.
Objectius
-Desenvolupar una funció predictiva del risc cardiovascular (RCV) de per vida.
-Avaluar les conseqüències clíniques d'utilitzar les taules SCORE/SCORE OP a Espanya.
-Avaluar el control dels factors de RCV en pacients amb ECV establerta.
Metodologia
Estudi1. Estudi de cohorts. Van participar treballadors (18-65 anys) visitats entre 2004-2007. El 70% de la cohort es va utilitzar per a desenvolupar l'equació, el 30% restant per a validar-la.
Estudi2: Estudi transversal. Van participar subjectes sense antecedents de ECV entre 65-85 anys, amb registres vàlids de pressió arterial sistòlica (PAS) i colesterol total (CT).
Estudi3: Estudi transversal, europeu. Es van seleccionar subjectes de 18-85 anys d'edat amb MCV establerta entre els 6 mesos i els 3 anys després del diagnòstic.
Resultats
Estudi1: van participar 762.054 subjectes, edat mitjana: 35,48 anys, 71,14% homes. Intervenen en el model: ocupació, tabaquisme, diabetis mellitus, tractament antihipertensiu i hipolipemiant, PAS, CT; en homes, a més: consum d'alcohol, índex de massa corporal, antecedents familiars de malaltia coronària precoç , malaltia renal i pressió arterial diastòlica.
Estudi2: Es van incloure 3.425 pacients. Un 25,46% tenien risc alt segons SCORE i 22,90% segons SCORE OP. Utilitzant el SCORE tractaríem amb hipolipemiantes un 16,43% dels individus , mentre que i amb SCORE OP només 13,45%.
Estudi3: Van participar 973 pacients, 32,4% dones, 14% fumadors, 32% inactius físicament, 30% amb hàbits alimentaris poc saludables. 75% va aconseguir un bon control de la pressió arterial (<140/80mmHg), només un 23% controlaven el c-LDL (<70 mg/dl). Les dones estaven infratractades.
Conclusions
El model per a calcular el RCV per a tota la vida va mostrar una discriminació i calibratge satisfactoris. Les taules SCORE OP identifiquen menys pacients d'alt risc el que implica tractar menys. Un alt percentatge de pacients amb ECV establerta no modifiquen el seu estil de vida, ni aconsegueixen els objectius terapèutics.Introducción La enfermedad cardiovascular (ECV) es la principal causa de morbimortalidad a nivel mundial. Objetivos -Desarrollar una función predictiva del riesgo cardiovascular (RCV) de por vida. -Evaluar las consecuencias clínicas de utilizar las tablas SCORE/SCORE OP en España. -Evaluar el control de los factores de RCV en pacientes con ECV establecida. Metodología Estudio1. Estudio de cohortes. Participaron trabajadores (18-65 años) visitados entre 2004-2007. El 70% de la cohorte se utilizó para desarrollar la ecuación, el 30% restante para validarla. Estudio2: Estudio transversal. Participaron sujetos sin antecedentes de ECV entre 65-85 años, con registros válidos de presión arterial sistólica (PAS) y colesterol total (CT). Estudio3: Estudio transversal, europeo. Se seleccionaron sujetos de 18-85 años de edad con ECV establecida entre los 6 meses y los 3 años después del diagnóstico. Resultados Estudio1: participaron 762.054 sujetos, edad media: 35,48 años, 71,14% varones. Intervienen en el modelo: ocupación, tabaquismo, diabetes mellitus, tratamiento antihipertensivo e hipolipemiante, PAS, CT; en varones, además: consumo de alcohol, índice de masa corporal, antecedentes familiares de enfermedad coronaria precoz, enfermedad renal y presión arterial diastólica. Estudio2: Se incluyeron 3.425 pacientes. Un 25,46% tenían riesgo alto según SCORE y un 22,90% según SCORE OP. Utilizando el SCORE trataríamos con hipolipemiantes un 16,43% de los individuos, mientras que con SCORE OP sólo un 13,45%. Estudio3: Participaron 973 pacientes, 32,4% mujeres, 14% fumadores, 32% inactivos físicamente, 30% con hábitos alimenticios poco saludables. 75% alcanzó un buen control de la presión arterial (<140/80mmHg), sólo un 23% controlaban el c-LDL (<70 mg/dl). Conclusiones El modelo para calcular el RCV de por vida mostró una discriminación y calibración satisfactoria. Las tablas SCORE OP identifican menos pacientes de alto riesgo lo que implica tratar menos. Un alto porcentaje de pacientes con ECV establecida no modifican su estilo de vida, ni alcanzan los objetivos terapéuticos.
Introduction Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide. Objectives -To develop a predictive function of lifetime cardiovascular risk (CVR). -To assess the impact of using SCORE / SCORE OP tools in Spain. -To assess the control of CVR factors in patients with established CVD. Methods Study1: Cohort study. Workers (18-65 years old) visited between 2004-2007 participated. 70% of the cohort was used to develop the equation, the remaining 30% was used as the validation cohort. Study2: Cross-sectional study. Subjects without history of CVD between 65-85 years of age participated, with valid records of systolic blood pressure (SBP) and total cholesterol (TC). Study3: European cross-sectional study. Subjects aged 18-85 years with established CVD between 6 months and 3 years after diagnosis were selected. Results Study1: 762,054 subjects were included, mean age: 35.48 years, 71.14% male. The final model included: occupation, smoking, diabetes mellitus, antihypertensive and lipid-lowering treatment, SBP, TC; in men, in addition it was included: alcohol consumption, body mass index, family history of early coronary disease, renal failure and diastolic blood pressure. Study2: 3,425 patients were included. 25.46% were at high risk using SCORE and 22.90% using SCORE OP. Using the SCORE we would treat with lipid-lowering drugs 16.43% of the individuals, while using with the SCORE OP only 13.45%. Study3: 973 patients participated, 32.4% women, 14% smokers, 32% physically inactive, 30% with unhealthy eating habits. 75% and 23% achieved good blood pressure control (<140/80mmHg), and good LDL-c control (<70mg/dl), respectively. Women were under-treated. Conclusions The model to calculate the lifetime CVR showed satisfactory discrimination and calibration. SCORE OP tables identify fewer high-risk patients, which means treating less older patients, thus avoiding overtreatment. A high percentage of patients with established CVD do not modify their lifestyle and do not reach the therapeutic goals.
36
Cho, Jinsoo. "Velocity-based cardiac segmentation and motion-tracking". Diss., Available online, Georgia Institute of Technology, 2004:, 2003. http://etd.gatech.edu/theses/available/etd-04082004-180106/unrestricted/cho%5Fjinsoo%5F200312%5Fphd.pdf.
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37
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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38
Pandey, Raghav. "MicroRNA Mediated Proliferation of Adult Cardiomyocytes to Regenerate Ischemic Myocardium". University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1505124343198575.
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39
Eccles, Bree A. "Effect of Cannabinoids on Osteogenic Differentiation of Cultured Vascular Smooth Muscle Cells". Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/honors/392.
Testo completoAbstract (sommario):
Vascular calcification is strongly correlated with the clinical manifestations of atherosclerosis, heart attacks and strokes. The calcification process resembles bone formation and involves the osteogenic trans-differentiation of smooth muscles cells within the arterial wall. Cannabinoid receptors are known to modulate bone formation and are present in atherosclerotic vessels, suggesting they may also play a role in modulating calcification. Therefore, we evaluated the effects of cannabinoids on the expression of osteogenic proteins by vascular smooth muscle cells undergoing calcification.
40
Mamadu, Hadii M., Timir Paul, Liang Wang, Sreenivas P. Veeranki, Hemang B. Panchal, Arsham Alamian, Pooja Subedi e Mattew Budoff. "Association Between Multiple Modifiable Risk Factors of Cardiovascular Disease and Hypertension in Rural Appalachia. Arteriosclerosis, Thrombosis and Vascular Biology (ATVB)/Peripheral Vascular Disease (PVD) 2016 Scientific Sessions". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/1394.
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41
Appannah, Geeta. "Dietary patterns, obesity and cardiovascular risk factors in young people". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648138.
Testo completo
42
Ajwani, Shilpi. "Periodontal disease in an aged population, and its role in cardiovascular mortality". Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/hamma/vk/ajwani/.
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43
Barker, Ann Elizabeth. "Wild Blueberry Consumption and Risks for Cardiovascular Disease". Fogler Library, University of Maine, 2006. http://www.library.umaine.edu/theses/pdf/BarkerAE2006.pdf.
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44
Loke, Wai Mun. "Cardiovascular protective effects of dietary polyphenols". University of Western Australia. School of Biomedical and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0051.
Testo completoAbstract (sommario):
Polyphenols are naturally-occurring phytochemicals, which form an integral part of the human diet. Results from epidemiological studies have associated polyphenol intake with reduced risk of cardiovascular diseases. Previous human intervention studies suggested that dietary polyphenols exert their cardioprotective effects through their antioxidant and anti-inflammatory effects. While most in vitro experiments have not accounted for the bioavailability and metabolism of these polyphenols, our work has provided direct evidence, using quercetin, that metabolic transformation, together with bioavailability, exert profound effects on bioactivity. We examined the effect of quercetin and its major metabolites on the production of pro-inflammatory eicosanoids by human leukocytes. Studies comparing free radical scavenging, antioxidant activity and eicosanoid production demonstrate that there are different structural requirements for antioxidant and anti-inflammatory activity. We also investigated the effect of metabolic transformation on flavonoid bioactivity by comparing the activity of quercetin and its major metabolites to inhibit inflammatory eicosanoid production from human leukocytes. Quercetin was a potent inhibitor of leukotriene B4 formation in leukocytes (IC50 ~ 2µM), and its activity was dependent on specific structural features, particularly the 2,3 double bond of the C ring. Functionalisation of the 3'-OH group with either methyl or sulfate reduced inhibitory activity up to 50% while a glucuronide substituent at the 3-OH effectively removed the leukotriene B4 inhibitory activity. The major quercetin metabolite quercetin-3'-O-sulfate retained considerable lipoxygenase inhibitory activity (IC50 ~ 7 µM) while quercetin-3-O-glucuronide maintained antioxidant activity but had no lipoxygenase inhibitory activity at physiologically relevant concentrations. We conclude that structural modification of quercetin due to metabolic transformation had a profound effect on bioactivity, and that the structural features required for antioxidant activity of 8 quercetin and related flavonoids were unrelated to those required for inhibition of inflammatory eicosanoids.
45
CORREA, VALERIA R. "Avaliacao e epidemiologia da cardiopatia chagasica em pacientes atendidos em Araguaina - Tocantins". reponame:Repositório Institucional do IPEN, 2010. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9588.
Testo completoAbstract (sommario):
Made available in DSpace on 2014-10-09T12:28:21Z (GMT). No. of bitstreams: 0Made available in DSpace on 2014-10-09T13:56:30Z (GMT). No. of bitstreams: 0
Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP
46
Sigvant, Birgitta. "Epidemiological aspects of peripheral arterial disease". Stockholm : Department of Molecular Medicine and Surgery, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-670-5/.
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47
Chan, Hiu-ting, e 陳曉庭. "The effect of diet intake on vascular function and therapeutic effect of cardiovascular medicine in patients with cardiovascular disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50434342.
Testo completoAbstract (sommario):
Cardiovascular diseases (CVDs) remain to be the leading causes of morbidity and mortality in Hong Kong and worldwide. Among different modifiable risk factors, dietary pattern is on the major determinant for CVD and overall mortality. Other than pharmacological therapies for cardiovascular risk factors, such as hypertension, hyperlipidemia and diabetes, maintaining a healthy diet is a more sustainable method in general population to prevent CVDs. Current lifestyle intervention in the West countries focus on high intake of fruit and vegetables with more than 400g per day and limited saturated fats with less than 10% of energy, there is very limited data on impact of dietary pattern on CVDs in Chinese. Prior studies among Chinese in Hong Kong have shown that only half of the local population fell within these recommended ranges for fat, saturated fatty acid and cholesterol intakes.
Several different dietary patterns have been recommended for CVDs prevention based on: i) food groups, such as Mediterranean diet, the Dietary Approaches to Stop Hypertension (DASH) diet; ii) macronutrients: the low-carbohydrate diet, low glycemic index diet, very-low- fat diet and iii) nutrition or vitamin supplement. However, the effect of different dietary patterns based on modulations of food group, macronutrients and particular micronutrients on vascular structure and function in Chinese subjects is unclear. In the first part of this thesis, the relationships between different dietary pattern and surrogate markers of subclinical atherosclerosis and vascular function in different high risk populations for CVDs were investigated.
In Chapter 3, we compared the assessment of dietary pattern in Chinese using different tool, including Food Frequency Questionnaire (FFQ); Dietary Record; and Dietitian assessment. In this study, we demonstrated that suitable dietary assessments tools should be chosen for the assessment of different dietary pattern, according to characteristics of assessments.
In Chapter 4, the relationship between the fruit intake and subclinical atherosclerosis as measured by carotid intimal thickness (IMT) was investigated in patient with type II diabetes mellitus (DM). Our results showed that high fruit intake was associated with lower burden of carotid atherosclerosis, independent of level of vitamin intake in patients with type II DM.
In Chapter 5, we compared the impact of high carbohydrate diet on arterial stiffness between control subjects without CVDs and patients with high risk for CVDs. Our findings showed that high carbohydrate diet mainly affected patients with established CVDs, and their increased arterial stiffness was associated with an elevation of blood pressure.
In Chapter 6, we determined the effect of dietary vitamin intake on oxidative stress in patients with high risk of CVDs. In those high risk patients for CVDs, we demonstrated that increased dietary intake of vitamin A, beta-carotene and alpha tocopherol were associated with decreased oxidative stress, but these relationships were not observed in those control subjects without CVDs. It is likely attributed to the higher systemic oxidative stress levels in patients with high risk of CVDs.
On the other hand, food intake may also affect the clinical efficacy of cardiovascular therapies. In particularly, it has been well established that herbal intake which is commonly used by Chinese can affect the anticoagulant effect of warfarin on patients with non-valvular atrial fibrillation (AF). Thus, in this second part of the thesis, we investigated the effect of concomitant herbal intake on anticoagulation control in patients with non-valvular AF treated with warfarin. Our results showed that patients with AF treated with warfarin had limited knowledge on potential interaction between herbal substances in foods and warfarin, in which increased herbal substances intake significantly reduced the percentage time of anticoagulant effect within the therapeutic range. Moreover, a single section of education on knowledge of herbal ingredients did not improve their percentage time of therapeutic range for these patients.
In conclusion, these findings suggest that dietary pattern in Chinese might have significant impact of vascular function in patients with type II DM and high risk for CVDs. Moreover, the herbal substances in the diet among Chinese could have significant impact of the therapeutic effects in some of the cardiovascular medications, such as warfarin. Future clinical studies will be needed to confirm these potential beneficial effects of particular diet intake on vascular function in patients with high risks of CVDs as well as potential interaction between herbal substances in Chinese diet and cardiovascular medications.published_or_final_version
Medicine
Doctoral
Doctor of Philosophy
48
Hurtig, Wennlöf Anita. "Cardiovascular risk factors in children /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-179-2/.
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Buhlin, Kåre. "The role of periodontitis in cardiovascular disease /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-766-5.
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50
Kim, Jin Hee. "Functional genomics of cardiovascular disease risk". Thesis, Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/51769.
Testo completoAbstract (sommario):
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.