Relevant bibliographies by topics / Cardiovascular disease

Academic literature on the topic 'Cardiovascular disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 June 2024

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Journal articles on the topic "Cardiovascular disease"

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Silva Junior, Delcio G. "Cardiovascular Disorders in Autoimmune Disease." Clinical Cardiology and Cardiovascular Interventions 2, no. 2 (November 12, 2019): 01–04. http://dx.doi.org/10.31579/2641-0419/015.

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The presence of Cardio Vascular Disease (CVD) impacts negatively on expectation and quality of life of the population, being one of the main causes of disability. Many of those who become cardiovascular patients throughout their life could have had different evolution if preventive attitudes were taken. Since 50’s decade, Framingham studies have shown the importance of predetermining factors for CVD occurrence. The classical CVD risk factors such as diabetes, metabolic syndrome, dyslipidemia, hypertension, smoking and family history are well established as predictors of cardiovascular events. The presence of Cardio Vascular Disease (CVD) impacts negatively on expectation and quality of life of the population, being one of the main causes of disability. Many of those who become cardiovascular patients throughout their life could have had different evolution if preventive attitudes were taken. Since 50’s decade, Framingham studies have shown the importance of predetermining factors for CVD occurrence. The classical CVD risk factors such as diabetes, metabolic syndrome, dyslipidemia, hypertension, smoking and family history are well established as predictors of cardiovascular events. However, in certain clinical conditions, traditional risk factors seem not to fully explain the incidence of CVD. Coronary artery disease and early atherosclerosis in young women with Systemic Lupus Erythematosus (SLE) are one of the best examples of how chronic inflammatory diseases can affect individuals who are normally poorly exposed to traditional risk factors. Even with the plurality of extra-articular manifestations of rheumatologic diseases, such as pulmonary hypertension and SLE encephalopathy, uveitis in spondyloarthritis, or as Achalasia in scleroderma, attention is being paid to the frequent cardiovascular system involvement in these patients, especially in the vascular territory
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Almutairi, Emad Ayidh, Naif Mufleh Alshahrani, Monahi Nasser Alyami, Manal Fnaitel Alanazi, Salwa Fnaitel Alanazi, Mohammad Saeed Abdulrahman Alamri, Abdulmohsen Obaysan Alotaibi, Ohoud Abdulrahman Al-Luhaidan, and Asama Mathkar Alqahtani. "Prevalence of Cardiovascular Disease Risk." International Journal Of Pharmaceutical And Bio-Medical Science 02, no. 12 (December 9, 2022): 592–96. http://dx.doi.org/10.47191/ijpbms/v2-i12-03.

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At the worldwide level, heart disease is the leading cause of death. The primary goals of this study were to look into cardiac risk variables in datasets available on Kaggle. The data included 303 people, 138 of whom had cardiac disease and 165 of whom did not. Age, gender, chest pain, resting blood pressure, cholesterol level, fast blood sugar, electrocardiogram at rest, maximum heart rate during the stress test, angina during exercise, old peak, slope of the ST segment, result of the blood flow observed with radioactive dye, and number of main blood vessels colored by the radioactive dye were all included in the dataset. Descriptive analysis includes means and standard deviations for non-classified variables, as well as frequencies and percentages for categorized variables. The independent T test was used to assess the associations between variables. If 0.05, significance was considered. Except for cholesterol and rapid blood sugar, all of the variables listed above were found to be strongly linked with heart disease. When rapid blood sugar and cholesterol readings are combined, they should be evaluated with caution due to their participation as risk factors for cardiovascular disease.
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Banerjee, Monoswini. "Omega-3 Fatty Acid and Cardiovascular Disease." International Journal of Science and Research (IJSR) 12, no. 6 (June 5, 2023): 2132–40. http://dx.doi.org/10.21275/mr23622135209.

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Nasonov, E. L., T. V. Popkova, and D. S. Novikova. "Cardiovascular disease in rheumatic diseases." Terapevticheskii arkhiv 88, no. 5 (2016): 4. http://dx.doi.org/10.17116/terarkh20168854-12.

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Nguyen, Thomas T., Kevin Y. Wu, Maude Leclerc, Hieu M. Pham, and Simon D. Tran. "Cardiovascular Diseases and Periodontal Disease." Current Oral Health Reports 5, no. 1 (January 17, 2018): 13–18. http://dx.doi.org/10.1007/s40496-018-0165-3.

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Salton, Yanka Dalmolin, João Augusto Possamai, Leonardo de Lucca Schiavon, and Janaina Luz Narciso-Schiavon. "CELIAC DISEASE AND CARDIOVASCULAR DISEASES." Revista Contemporânea 4, no. 4 (April 22, 2024): e4037. http://dx.doi.org/10.56083/rcv4n4-131.

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Background: Celiac disease, an immune-mediated enteropathy that occurs in susceptible individuals after gluten ingestion, has clinical manifestations that go beyond the classical malabsorption syndrome and can affect other systems. Objective: To review the current literature for cardiovascular changes described in patients with celiac disease. Method: We conducted a search in the PubMed database and selected articles based on their relevance to the objective. Results: Celiac patients have a 1.2 times higher risk of cardiovascular events compared to non-celiac patients. The most common cardiovascular manifestations include atherosclerosis, cardiac arrhythmias (especially atrial fibrillation), myocarditis, coronary artery disease, dilated cardiomyopathy, impaired aortic function, and cerebrovascular diseases. There are several possible explanations for this relationship, including: prothrombotic changes, accelerated atherosclerosis compared to patients without celiac disease, associated comorbidities, such as antiphospholipid syndrome and Type 1 Diabetes mellitus, subclinical chronic inflammation and genetic factors. Celiac disease patients have a 38% higher risk of developing atrial fibrillation and a 19% higher risk of coronary artery disease. Furthermore, celiac patients have a 22% higher risk of coronary artery disease-related death, regardless of small intestine histopathology. Patients with celiac disease also show an increased prevalence of dilated cardiomyopathy (5.7%) and a 73% higher risk of developing dilated cardiomyopathy, particularly within the first year of celiac disease diagnosis. Conclusion: Celiac disease may be associated with cardiovascular changes, especially in newly diagnosed patients who have not adhered to a gluten-free diet. Therefore, cardiovascular assessment should be considered as part of the initial assessment and follow-up of individuals with celiac disease.
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Kadirovna, Muratova Saodat, Shukurova Nodira Tillayevna, Baratov Bobur, and Teshayev Shoxjahon. "PREDICTIVE MODELING OF THE PROBABILITY OF DEVELOPING PERIODONTAL DISEASES IN PATIENTS WITH CARDIOVASCULAR DISEASE." European International Journal of Multidisciplinary Research and Management Studies 4, no. 4 (April 1, 2024): 65–70. http://dx.doi.org/10.55640/eijmrms-04-04-10.

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Currently, the forecast of the development of pathology is an important part of all branches of healthcare. [3,4,5]. However, despite the importance and scientific and practical significance of forecasting in dentistry, at present we have not found information about predictive models of individual risk of developing periodontitis in patients with hypertension.
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Mooney, Tracy. "Cardiovascular disease." Nursing Standard 26, no. 39 (May 30, 2012): 59–60. http://dx.doi.org/10.7748/ns.26.39.59.s54.

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Mooney, Tracy. "Cardiovascular disease." Nursing Standard 26, no. 39 (May 30, 2012): 59. http://dx.doi.org/10.7748/ns2012.05.26.39.59.c9135.

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Thiara, Balvinder. "Cardiovascular disease." Nursing Standard 29, no. 33 (April 15, 2015): 60. http://dx.doi.org/10.7748/ns.29.33.60.s44.

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Dissertations / Theses on the topic "Cardiovascular disease"

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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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Books on the topic "Cardiovascular disease"

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Cardiovascular disease. Ibadan: Spectrum Books, 1987.

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Gallo, Linda L., ed. Cardiovascular Disease. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5296-9.

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Wang, Qing K., ed. Cardiovascular Disease. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-159-8.

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Lorimer, A. Ross, and W. Stewart Hillis. Cardiovascular Disease. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-3120-5.

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Akinkugbe, O. O. Cardiovascular disease. Oxford: Blackwell Scientific, 1987.

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Akinkugbe, O. O. Cardiovascular disease. Ibadan: Spectrum Books, 1987.

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1943-, Hillis W. Stewart, ed. Cardiovascular disease. Berlin: Springer-Verlag, 1985.

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Cardiovascular disease. New York, N.Y: Facts on File, 1987.

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Wood, David. Cardiovascular disease prevention. London: Mosby, 2004.

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Gallo, Linda L., ed. Cardiovascular Disease 2. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1959-1.

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Book chapters on the topic "Cardiovascular disease"

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Strandberg, Timo E., and Tuomo Nieminen. "Cardiovascular Disease." In Practical Issues in Geriatrics, 123–36. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61997-2_13.

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Findlay, Damian, Gregory S. Tentindo, and Robert Reti. "Cardiovascular Disease." In Oral Board Review for Oral and Maxillofacial Surgery, 355–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48880-2_13.

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Wenger, Nanette K. "Cardiovascular Disease." In Geriatric Medicine, 152–63. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4757-2093-8_14.

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Bellg, Albert J. "Cardiovascular Disease." In Comprehensive Handbook of Clinical Health Psychology, 125–52. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118269657.ch6.

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Wenger, Nanette Kass. "Cardiovascular Disease." In Geriatric Medicine, 357–74. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4757-2705-0_26.

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Ebell, Mark H. "Cardiovascular Disease." In Evidence-Based Diagnosis, 13–105. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4757-3514-7_2.

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Sorescu, Dan, and Nanette K. Wenger. "Cardiovascular Disease." In Encyclopedia of Women’s Health, 214–16. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48113-0_72.

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Severs, Nicholas J. "Cardiovascular Disease." In Novartis Foundation Symposium 219 - Gap Junction-Mediated Intercellular Signalling in Health and Disease, 188–211. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515587.ch12.

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Congdon, Jonathan M. "Cardiovascular Disease." In Canine and Feline Anesthesia and Co-Existing Disease, 1–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118834305.ch1.

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Sankaran, Sujatha. "Cardiovascular Disease." In Encyclopedia of Immigrant Health, 361–68. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5659-0_118.

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Conference papers on the topic "Cardiovascular disease"

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Jain, Daksh, Vardan Yadav, Manavi Kumari, Kundan Chandravansi, Gurakonda Reddy, and Jeba Cheltha. "Cardiovascular Disease Predictor." In Proceedings of The International Conference on Emerging Trends in Artificial Intelligence and Smart Systems, THEETAS 2022, 16-17 April 2022, Jabalpur, India. EAI, 2022. http://dx.doi.org/10.4108/eai.16-4-2022.2318172.

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Perva, Fejsal, Harun Tucakovic, Muhammed Musanovic, and Emine Yaman. "Prediction of cardiovascular disease." In 2022 XXVIII International Conference on Information, Communication and Automation Technologies (ICAT). IEEE, 2022. http://dx.doi.org/10.1109/icat54566.2022.9811108.

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Rindge, David. "Laser therapy in cardiovascular disease." In SPIE BiOS: Biomedical Optics, edited by Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory, et al. SPIE, 2009. http://dx.doi.org/10.1117/12.808050.

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Esina, Е. Y., A. A. Zuykova, N. V. Strachova, V. V. Lyutov, and V. N. Tsigan. "Unresolved Cardiovascular Disease Prevention Issues." In Proceedings of the International Conference on Health and Well-Being in Modern Society (ICHW 2019). Paris, France: Atlantis Press, 2019. http://dx.doi.org/10.2991/ichw-19.2019.24.

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Okada, Masayoshi. "Laser angioplasty for cardiovascular disease." In 2004 Shanghai international Conference on Laser Medicine and Surgery, edited by Jing Zhu. SPIE, 2005. http://dx.doi.org/10.1117/12.639345.

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Harris, William, and Irum Zahara. "Omega-3 and cardiovascular disease." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/rrxh5251.

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Despite the fact that the “omega-3 lowers risk for CVD” story is now 50 years old, controversies remain regarding the short and long-term utility of omega-3 supplementation to reduce risk for CVD. The earlier studies (published roughly before 2007) were generally favorable, however a spate of studies published since then were not nearly as clear. The one stand-out in the latter set was REDUCE-IT, which used 4 g/d of EPA ethyl esters (instead of EPA+DHA ethyl esters). In this study, the treated subjects experienced about 25% fewer CVD events than the placebo group. This resulted in FDA approval for this drug for reducing risk for CVD in specific patient populations. The next large study to report out – STRENGTH – was expected to be positive as well (3.1 g EPA+DHA as free fatty acids), but it was stopped early for “futility” (i.e., the event rates were not different between active and placebo groups). Many hypotheses have been raised to explain these wildly different outcomes, and this has engendered considerable confusion in the field. These hypotheses will be discussed in this presentation. On the other hand, observational prospective cohort studies based on measured blood omega-3 levels (not on fish intake questionnaires) have consistently shown that higher levels are associated with lower risk for CVD (and total mortality). These two different study designs (RCTs vs observational epidemiology) ask different questions. This talk will synthesize these two apparently divergent conclusions regarding the utility of omega-3 fatty acids for reducing risk for CVD.
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Abdul Hussein Mahmeed, Bayader, Hend Ahmed Abass, Wasan T. Al-Rubayee, and Rayah Sulaiman Baban. "The Effect of Serum Glypican-4 (GLY-4) in Patients with Cardiovascular Disease in Iraq." In IX. International Scientific Congress of Pure, Applied and Technological Sciences. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress9-31.

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Glypicans, a family of heparan sulfate proteoglycans that are attached to the cell membrane by a glycosyl-phosphatidylinositol anchor, and they include six members, GPC1-GPC6. Glypicans are emerging as an important family of compounds that may play a role in cardiovascular diseases. Therefore, this study aimed to investigate the levels of Glypican-4 (GLY-4) in Iraqi patients with cardiovascular disease. Methods the study included 80 subject divided into 40 patients with cardiovascular disease and 40 controls. Measured Serum GPC4 levels were determined using an enzyme-linked immunosorbent assay. Result Serum GPC4 was significantly associated with cardiovascular disease and negative correlation between gly-4 and Troponin (r= - 0.1511), while a positive correlation was found between gly-4 and CRP (r= 0.157). Conclusions the study indicates that elevated serum GLY-4 levels are significantly associated with an increased risk of cardiovascular disease
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Narasimhan, Lakshmi, Di Wu, and Narinder Gill. "Meta-Analysis of Clinical Cardiovascular Data towards Evidential Reasoning for Cardiovascular Life Cycle Management." In InSITE 2007: Informing Science + IT Education Conference. Informing Science Institute, 2007. http://dx.doi.org/10.28945/3147.

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The cardiovascular disease is one of the serious and life-threatening diseases in the developed world. One aspect of medical treatment is using drugs with blood pressure reducing or cholesterol lowering functions. Importantly, such treatment needs to be individually tailored and is significantly correlated to the particular conditions of individual patients. However, such pathologies and mechanisms are still only under investigation. Several novel and unique computational methods, called meta-analyses techniques, for formatting and analyzing a wide variety of cardiac datasets are discussed in this paper with the aim to building cardiovascular database and related patient life-cycle management services. In this paper we also present an overview of a second order inference engine underlying the meta-analyses, which yields evidenced-based reasoning that is more likely to better assist decision-making on the effectiveness of cardiovascular treatment than what is available currently. Furthermore, the software architecture and other details of such a medical informatics system tailored to cardiovascular disease are also described. Research and development work on this project yields itself to application to many other areas, such as disease control and prevention in Epidemiology, and dietics. The system can therefore make a profound impact to medical informatics.
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Khare, Sangita, and Deepa Gupta. "Association rule analysis in cardiovascular disease." In 2016 Second International Conference on Cognitive Computing and Information Processing (CCIP). IEEE, 2016. http://dx.doi.org/10.1109/ccip.2016.7802881.

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Silva, Cristiana, Joana Pereira, Luis Costa, Hugo Peixoto, Jose Machado, and Antonio Abelha. "Business Intelligence for Cardiovascular Disease Assessment." In 2017 IEEE 5th International Conference on Future Internet of Things and Cloud: Workshops (W-FiCloud). IEEE, 2017. http://dx.doi.org/10.1109/ficloudw.2017.90.

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Reports on the topic "Cardiovascular disease"

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Pohost, Gerald M., Barton L. Guthrie, and Charles Steiner. Surgical Robotics Research in Cardiovascular Disease. Office of Scientific and Technical Information (OSTI), February 2008. http://dx.doi.org/10.2172/924449.

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Cutler, David, Mary Beth Landrum, and Kate Stewart. Intensive Medical Care and Cardiovascular Disease Disability Reductions. Cambridge, MA: National Bureau of Economic Research, May 2006. http://dx.doi.org/10.3386/w12184.

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Heymsfield, Steven, Carol Boushey, Heather Leidy, Richard Mattes, Ronald Kleinman, Emily Callahan, Gisela Butera, Nancy Terry, and Julie Obbagy. Frequency of Eating and Cardiovascular Disease: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, July 2020. http://dx.doi.org/10.52570/nesr.dgac2020.sr0602.

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Jihwan Park, Jihwan Park. Are climate change and air pollution triggering cardiovascular disease? Experiment, September 2022. http://dx.doi.org/10.18258/29517.

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Zyriax, Birgit-Christiane, and Eberhard Windler. Lifestyle changes at midlife to prevent cardiovascular disease: a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0061.

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Review question / Objective: What kind of evidence-based diet and physical activity should or can be recommended to adults in order to reduce their cardiovascular risk. Condition being studied: Cardiovascular disease. Eligibility criteria: Publications will be extracted independently by two researchers according to defined search string and get color coded as agreed on: Yellow: studies and RCTs of the association of nutrients, physical activity and cardiovascular outcomes for discussion. Green: meta-analysis of studies and RCTs of the association of nutrients, physical activity and cardiovascular outcomes. Green subgroup AMSTAR-2: meta-analysis of studies and RCTs of the association of food-patterns and cardiovascular outcomes. The AMSTAR-2 checklist will be used for evaluating the methodological quality of these studies.
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Hua, Minglei, Ling Li, and Linlin Diao. Bronchial asthma and risk of cardiovascular disease and cardiovascular mortality: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0083.

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Cutler, David, Mark McClellan, and Joseph Newhouse. The Costs and Benefits of Intensive Treatment for Cardiovascular Disease. Cambridge, MA: National Bureau of Economic Research, April 1998. http://dx.doi.org/10.3386/w6514.

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Boushey, Carol, Jamy Ard, Lydia Bazzano, Steven Heymsfield, Elizabeth Mayer-Davis, Joan Sabaté, Linda Snetselaar, et al. Dietary Patterns and Risk of Cardiovascular Disease: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, July 2020. http://dx.doi.org/10.52570/nesr.dgac2020.sr0102.

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Snetselaar, Linda, Regan Bailey, Joan Sabaté, Linda Van Horn, Barbara Schneeman, Charlotte Bahnfleth, Julia Kim, et al. Types of Dietary Fat and Cardiovascular Disease: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, July 2020. http://dx.doi.org/10.52570/nesr.dgac2020.sr0501.

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Lampley, Katrice, and Nicole Therrien. "Geisinger Ambulatory Pharmacy Care Program Field Notes". National Center for Chronic Disease Prevention and Health Promotion (U.S.)., 2023. http://dx.doi.org/10.15620/cdc:126232.

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These Field Notes summarize the Geisinger Ambulatory Care Program’s care coordination work with pharmacists alongside other health care team members to manage chronic diseases including cardiovascular disease.
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