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Relevant bibliographies by topics / Cardiovascular and metabolic disease

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Academic literature on the topic 'Cardiovascular and metabolic disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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Journal articles on the topic "Cardiovascular and metabolic disease"

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Cha, Bong Soo, and Hae Jin Kim. "Metabolic Syndrome and Cardiovascular Disease." Korean Circulation Journal 33, no. 8 (2003): 645. http://dx.doi.org/10.4070/kcj.2003.33.8.645.

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Krentz, Andrew J., Nathan D. Wong, Andrew J. Krent, and Nathan D. Wong. "METABOLIC SYNDROME AND CARDIOVASCULAR DISEASE." Shock 27, no. 5 (May 2007): 591. http://dx.doi.org/10.1097/01.shk.0000258381.48362.80.

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Citrome, Leslie. "Metabolic Syndrome and Cardiovascular Disease." Journal of Psychopharmacology 19, no. 6_suppl (November 2005): 84–93. http://dx.doi.org/10.1177/0269881105058375.

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Metabolic syndrome is a constellation of clinical findings that identify individuals at higher than normal risk of developing diabetes mellitus or cardiovascular disease. There are two principal definitions, one emerging from the American National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, and the other from the World Health Organization. Both definitions share the common elements of abdominal obesity, hypertriglyceridaemia, low HDL-cholesterol, hypertension and abnormal glucose regulation. The syndrome is relatively common across continents, and also among those without marked obesity. It is even more common among patients with major mental health disorders such as schizophrenia. Metabolic syndrome can be used to assess risk for cardiovascular disorder and death, and is an alternative to Framingham Risk Calculations. C-reactive protein may play an additional role in risk prediction. Ongoing monitoring for all components of the metabolic syndrome is necessary. Individuals at high risk require multimodal interventions, including lifestyle interventions and targeted medications as appropriate.

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Sorrentino, Matthew J. "Metabolic Syndrome and Cardiovascular Disease." Medicine & Science in Sports & Exercise 39, no. 6 (June 2007): 1027. http://dx.doi.org/10.1249/mss.0b013e318074e839.

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Qiao, Qing, Weiguo Gao, Lei Zhang, Regzedmaa Nyamdorj, and Jaakko Tuomilehto. "Metabolic syndrome and cardiovascular disease." Annals of Clinical Biochemistry 44, no. 3 (May 1, 2007): 232–63. http://dx.doi.org/10.1258/000456307780480963.

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Aryal, Binod, Nathan L. Price, Yajaira Suarez, and Carlos Fernández-Hernando. "ANGPTL4 in Metabolic and Cardiovascular Disease." Trends in Molecular Medicine 25, no. 8 (August 2019): 723–34. http://dx.doi.org/10.1016/j.molmed.2019.05.010.

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Huang, Paul L. "eNOS, metabolic syndrome and cardiovascular disease." Trends in Endocrinology & Metabolism 20, no. 6 (August 2009): 295–302. http://dx.doi.org/10.1016/j.tem.2009.03.005.

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Shimamoto, Kazuaki. "2. Metabolic Syndrome and Cardiovascular Disease." Nihon Naika Gakkai Zasshi 97, no. 3 (2008): 591–97. http://dx.doi.org/10.2169/naika.97.591.

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Mazur, Marta Izabela, Grzegorz Zieliński, Joanna Witek, Katarzyna Szamotulska, and Przemysław Witek. "Cushing’s disease – cardiovascular and metabolic complications." Pediatria i Medycyna Rodzinna 15, no. 3 (November 29, 2019): 266–70. http://dx.doi.org/10.15557/pimr.2019.0044.

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Altinbas, Kursat, Filiz Alkan, Serhat Tuni, and Sema Yesilyurt. "Metabolic syndrome related cardiovascular disease risk." International Clinical Psychopharmacology 26 (September 2011): e40-e41. http://dx.doi.org/10.1097/01.yic.0000405699.60866.b7.

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Dissertations / Theses on the topic "Cardiovascular and metabolic disease"

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Gobin, Reeta Rukmini Devi. "Metabolic syndrome and cardiovascular disease." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610102.

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Rodie, Vanessa Angela. "Metabolic complications of pregnancy and cardiovascular disease risk." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421118.

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Vorkas, Panagiotis. "Metabolic profiling and pathway mapping of cardiovascular disease." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/38633.

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In this thesis, metabolic profiling (MP) platforms were utilised to interrogate the manifestation of cardiovascular disease and provide candidate biomarkers. A number of LC-MS and NMR methodologies were employed. Data processing was followed by assessment using multivariate (MVDA) and univariate (UV) statistics. MP is applied under three cardiovascular disease themes: 1) plaque rupture, 2) plaque formation, and 3) arterial ectopic calcification. Statistically significant features were structurally assigned. Identified metabolites were mapped to their corresponding biochemical pathways. For MP of ruptured plaque, tissue from symptomatic and asymptomatic patients for stroke was used. After detection of statistically significant features and structural assignment, two biochemical pathways showed dysregulations: the arachidonic acid pathway, indicating increased levels of inflammation, and the β-oxidation pathway with increased levels of three acyl-carnitines. Tissue extracts were used to investigate plaque formation. Arterial intima tissue, incorporating plaque lesions (carotid and femoral), was compared to intimal thickening tissue. Intima thickening demonstrated distinct MP compared to plaques. Plaques from different anatomical locations also demonstrated altered MP. After metabolite assignment, pathway mapping revealed dysregulations common to both anatomical locations. These were cholesterol, ceramide, purine, pyrimidine and β-oxidation pathways. These pathways are related to inflammation and apoptosis. A metabolite previously unassociated to atherogenesis was detected with strong statistical significance (t-test; p≥9.8x10-12), namely phosphatidylethanolamine-ceramide. It also demonstrated high correlations to cholesterol, a well-established risk-factor of atherosclerosis. The third theme of the project explores ectopic cardiovascular calcification. Experiments were conducted on blood serum. Patients with coronary artery and aortic valve calcification were compared with non-calcified controls. Phosphatidylcholine moieties and sphingomyelins were the major discriminating metabolites between cases and controls. These are involved in inflammation and apoptosis. The two diseases manifested different profiles with only three commonly dysregulated metabolites. A number of experiments using additional samples and bottom-up approaches will follow to provide validation of results.

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Zullo, Melissa D. "Cardiovascular Disease Management and Functional Capacity in Patients With Metabolic Syndrome." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1232721609.

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Alamin, Ali E., Arsham Alamian, Hadii M. Mamudu, Timir K. Paul, Liang Wang, Pooja Subedi, and 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.

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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.

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McClendon, Deborah. "Perceived Susceptibility of Cardiovascular Disease as a Moderator of Relationships between Perceived Severity and Cardiovascular Health Promoting Behaviors among Female Registered Nurses." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/nursing_diss/22.

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Significance: Morbidity and mortality related to CVD among women in the U.S. and most developed countries surpasses that of all cancers combined (AHA, 2008). Yet, CVD in women remains understudied, yielding low awareness among women and healthcare providers. The purpose of this study was to examine whether the relationship between health beliefs related to perceived cardiovascular disease (CVD) severity and health promoting behaviors were different in women with high self perception of CVD susceptibility versus women with low self perception of CVD susceptibility. Methods: This study used a descriptive, correlational design. A convenience sample (N = 220) included female registered nurses (RNs), 23-66 years old (M = 48; SD = 9.7), mostly white (N = 143; 65%), who had worked in nursing an average of 21 years (SD = 11.3) and reported their job as stressful/very stressful (N = 129; 59%). Nurses were recruited from five acute care hospital systems in a large southeastern city. Data were collected using standard questionnaires that measured perceived CVD severity and susceptibility, social support, depression, stress, exercise and nutrition. Participants completed data collection via an online survey method. Results: Data were analyzed using MANCOVA. For every standardized unit increase in perceived severity of CVD, participants had a 1.26 (95% CI: 0.02, 2.50) unit reduction in their healthy food choice score (lower scores = healthier food choices), and a 0.12 increase in their physical activity score (higher scores = more physical activity) (90% CI: 0.01, 0.23) unit. For every standardized unit increase in perceived CVD susceptibility there was an increase in the healthy food choice score by 2.37 (95% CI: 1.09, 3.65) units, and a reduction in the physical activity score by 0.27 (95% CI: 0.12, 0.41) unit. Greater age (p = 0.01) and greater depression (p = 0.001) were statistically significant predictors of lower physical activity. CVD susceptibility did not moderate the effect of CVD severity on nutrition or physical activity. Conclusions: Higher perceived CVD severity was associated with increased likelihood for healthy food choices and physical activity. In contrast, higher perceived CVD susceptibility was associated with decreased likelihood for healthy food choices and physical activity. More research is needed to understand how susceptibility beliefs around CVD are formed in women and how to better engage women in risk reduction behavior.

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Do, Ron. "Global Analysis of genetic variants associated with cardiovascular disease and related metabolic traits." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95134.

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Coronary heart disease (CHD) is the leading cause of morbidity and mortality in the western world. CHD is common throughout the world and is multifactorial, caused by the accumulation or interaction of quantitative changes in various intermediate traits (risk factors or metabolic phenotypes). Intermediate traits that are commonly studied include plasma levels of cholesterol (ie. low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and total cholesterol), body mass index (BMI) and blood pressure, which are all believed to be influenced by a combination of genetic and environmental factors (such as diet, alcohol, and exercise). In this thesis, the identification of novel genetic variants in candidate genes (a non-synonymous variant in farnesyl-diphosphate farnesyltransferase 1 (FDFT1) and a non-coding variant in insulin-induced gene 2 protein (INSIG2)) that are associated with total cholesterol and low density lipoprotein cholesterol is described. In addition, detailed investigation of common genetic variants in known genes identified from genome-wide association studies in the context of other genetic, phenotypic and environmental factors are reported. In particular, INSIG2 variants were observed to act in concert with a trans-acting variant in the sorbin and SH3 domain containing 1 gene (SORBS1) to influence LDL-C and apoB levels in Quebec, European and South Asian population samples. In addtition, fat mass and obesity associated gene (FTO) variants were observed to influence adiposity-related traits, resting metabolic rate and plasma leptin levels. I also report the role of dietary intake in modifying the effect of 9p21 variants on myocardial infarction and cardiovascular disease in the multi-ethnic INTERHEART study and in a Finnish sample, FINRISK. Finally, the utility of exome sequencing in identifying the genetic cause of a mendelian lipid disorder is demonstrated in a study that identifies compound heterozygo
La maladie coronarienne athéroscléreuse est l'une des causes principales de morbidité et de mortalité dans le monde occidental. Elle est commune à travers le monde et est multifactorielle, causée par une accumulation ou une interaction de changements quantitatifs de divers traits intermédiaires (facteurs de risque ou phénotypes métaboliques). Les traits intermédiaires souvent étudiés comprennent les taux plasmatiques de cholestérol (e.g. le cholestérol des lipoprotéines de faible densité (C-LDL), le cholestérol lié aux lipoprotéines de haute densité (C-HDL) et le cholestérol total), l'indice de masse corporelle (IMC) et la pression artérielle, qui sont tous présumés être influencés par une combinaison de facteurs génétiques et environnementaux (tels que l'alimentation, l'alcool, et l'exercice). Dans cette thèse, l'identification de nouveaux variants génétiques (un variant non-synonyme du gène farnesyl-diphosphate farnesyltransferase 1 (FDFT1) et un variant non-codant du gène insulin-induced gene 2 protein (INSIG2)) de gènes candidats associés au cholestérol total et au C-LDL est décrite. De plus, une investigation détaillée des variants génétiques communs dans des gènes connus identifiés à partir d'études d'associations pangénomiques dans le contexte d'autres facteurs génétiques, phénotypiques et environnementaux sont aussi présentés dans cette thèse. En particulier, il a été démontré que les variants du gène INSIG2 agissent de concert avec un variant 'trans-acting' du gène sorbin and SH3 domain containing 1 (SORBS1) pour influencer les niveaux de C-LDL et les niveaux d'apoB dans des populations du Québec, d'Europe et d'Asie du Sud. De même, les variants du gène de fat mass and obesity associated (FTO) ont été observés à influencer des traits liées à l'adiposité, au taux métabolique au repos et au niveaux de leptine plasmatique. Dans ma thèse, je décris également le rôle de l'apport aliment

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Fogli-Cawley, Jeanene. "2005 Dietary Guidelines for Americans and intermediate metabolic risk factors for cardiovascular disease /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2006.

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Suttie, Joseph. "Characterising metabolic mechanisms of disease in cardiomyopathies using multiparametric cardiovascular magnetic resonance imaging." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555329.

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In addition to pathological ventricular remodeling, the failing heart is characterised by impaired myocardial energetics and profound alterations in glucose and fatty acid metabolism. Understanding these complex metabolic pathways is crucial to improving clinical risk stratification and developing targeted therapeutic interventions. Cardiac magnetic resonance imaging (CMR) and magnetic resonance spectroscopy (MRS) are powerful tools in the interrogation of cardiac disease. Although technically challenging, the assessment of myocardial energetics by 3'p MRS has been possible for several decades. More recent techniques have allowed for the rapid assessment of cardiac steatosis using 'H MRS. The relationship between cardiac steatosis and other parameters of myocardial function such as myocardial energetics, contractility, fibrosis and perfusion have not been previously investigated. I assessed these parameters in patients with dystrophinopathy, a cause of inherited dilated cardiomyopathy in which disease pathways have not been well described. This study found myocardial contractility is strongly correlated with the myocardial PCr/ATP ratio, and that in those patients with impaired myocardial energetics there is significant cardiac steatosis. These changes were independent of body mass index and occurred in patients with normal glucose and lipid profiles. In order to further elucidate the phenotype, we investigated these markers of myocardial dysfunction in dystrophinopathic patients with and without prior exposure to Coxsackie B infection, an acquired cause of dystrophinopathy. Previous Coxsackie B exposure predicts worsening myocardial fibrosis, but was not associated with parameters of metabolic dysfunction. 17 - Suttie J.J. In order to further investigate the significance of cardiac steatosis in inborn errors of metabolism, I phenotyped a cohort of patients with mitochondrial myopathy. Mitochondrial myopathies are associated with profound cardiac steatosis, impaired myocardial energetics, inflammation and fibrosis. Furthermore, we report cardiac steatosis also occurs in patients with impaired myocardial energetics due to hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy and asymptomatic aortic stenosis. Finally, even higher spatial resolution imaging may be achieved be achieved at higher field strength, and I therefore undertook the first validation of CMR cardiac functional imaging at 7 T. This work significantly expands our understanding of cardiac steatosis in the energetically failing heart and supports its potential role as a novel biomarker in a range of cardiomyopathies.

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Klyza, James Philip. "Ancestor and Descendant Gender-Stratified Analysis Concerning the Heritability of Cardiovascular Disease Risk Factors." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1285688451.

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Books on the topic "Cardiovascular and metabolic disease"

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Peplow, Philip, James Adams, and Tim Young, eds. Cardiovascular and Metabolic Disease. Cambridge: Royal Society of Chemistry, 2015. http://dx.doi.org/10.1039/9781782622390.

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Metabolic syndrome and cardiovascular disease. Philadelphia, PA: Saunders/Elsevier, 2007.

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Levine, T. Barry. Metabolic syndrome and cardiovascular disease. Philadelphia, PA: Saunders, 2006.

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Association, American Heart, ed. Metabolic risk for cardiovascular disease. Dallas, TX: American Heart Association, 2010.

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Levine, T. Barry. Metabolic syndrome and cardiovascular disease. 2nd ed. Chichester, West Sussex: Wiley-Blackwell, 2013.

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Levine, T. Barry, and Arlene B. Levine. Metabolic Syndrome and Cardiovascular Disease. Oxford, UK: Blackwell Publishing Ltd., 2012. http://dx.doi.org/10.1002/9781118480045.

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Levine, T. Barry. Metabolic syndrome and cardiovascular disease. 2nd ed. Chichester, West Sussex: Wiley-Blackwell, 2013.

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Nutritional and metabolic bases of cardiovascular disease. Chichester, West Sussex: Wiley-Blackwell, 2011.

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Mancini, Mario, José M. Ordovas, Gabriele Riccardi, Paolo Rubba, and Pasquale Strazzullo, eds. Nutritional and Metabolic Bases of Cardiovascular Disease. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444318456.

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1933-, Simopoulos Artemis P., ed. Nutrition and fitness: Obesity, the metabolic syndrome, cardiovascular disease, and cancer. Basel: Karger, 2005.

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Book chapters on the topic "Cardiovascular and metabolic disease"

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Kraut, Jeffrey A., and Glenn T. Nagami. "Metabolic Acidosis and Cardiovascular Disease." In Metabolic Acidosis, 87–99. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_9.

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Rosengren, Annika. "Metabolic Syndrome and Diabetes." In Stress and Cardiovascular Disease, 285–95. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-419-5_16.

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Pistrosch, Frank, Frank Schaper, and Markolf Hanefeld. "The Metabolic Syndrome and Cardiovascular Disease." In The Metabolic Syndrome, 43–54. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1331-8_4.

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Pathak, Neha. "Cardiovascular Disease and Metabolic Syndrome." In Improving Women's Health Across the Lifespan, 425–40. New York: CRC Press, 2021. http://dx.doi.org/10.1201/9781003110682-24.

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Kreuder, Joachim, and Stephen G. Kahler. "Approach to the Patient with Cardiovascular Disease." In Inherited Metabolic Diseases, 69–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-74723-9_15.

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Kreuder, Joachim, and Stephen G. Kahler. "Approach to the Patient with Cardiovascular Disease." In Inherited Metabolic Diseases, 175–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49410-3_23.

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Creely, S. J., Aresh J. Anwar, and Sudhesh Kumar. "The Metabolic Syndrome and Vascular Disease." In Diabetes and Cardiovascular Disease, 281–306. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-908-7:281.

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Ceriello, Antonio. "Oxidative Stress, Insulin Resistance and Cardiovascular Disease." In The Metabolic Syndrome, 189–205. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470025131.ch7.

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Ziegler, Dan. "Inflammation, Cardiovascular Disease and the Metabolic Syndrome." In The Metabolic Syndrome, 207–38. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470025131.ch8.

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Ford, Earl S., and Simin Liu. "Insulin Resistance, Metabolic Syndrome, and Cardiovascular Disease." In The Metabolic Syndrome, 75–84. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-116-5_5.

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Conference papers on the topic "Cardiovascular and metabolic disease"

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Choy, E. "SP0125 Inflammation and cardiovascular disease – relevant metabolic biomarkers." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7237.

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Chan, C., and S. Baek. "Model Based Surface Design to Incorporate the Effect of Soluble Cues." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53439.

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Many disease states such as obesity and Type 2 diabetes are polygenic and involve multiple organs with inter-related metabolic and vascular abnormalities, and furthermore are risk factors for other diseases such as nonalcoholic steatohepatitis (NASH), cardiovascular or Alzheimer’s diseases. Tissue engineering is attempting to address these diseases from the perspective of developing “spare” or “replacement” parts. Cell and tissue engineering integrates cellular and molecular biology with the principles and methods of chemical and mechanical engineering to develop biological substitutes that can restore, maintain, or control tissue function.

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Muhammad, Noryanti, Mirza Rizwan Sajid, Roslinazairimah Zakaria, and Ahmad Shahbaz. "The mediating role of metabolic syndrome in cardiovascular diseases." In THE 4TH INNOVATION AND ANALYTICS CONFERENCE & EXHIBITION (IACE 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5121125.

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Kanıtez, Nilüfer Alpay, Sema Kaymaz Tahra, Ayten Yazici, Ayse Cefle, Mete Kara, Handan Yarkan-Tuğsal, Önay Gerçik, et al. "AB0575 THE EFFECT OF METABOLIC SYNDROME ON CARDIOVASCULAR DISEASE AND CUMULATIVE ORGAN DAMAGE IN TAKAYASU’S ARTERITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4055.

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Chirila, Cristina, Ovidiu Rusalim Petris, Milena Adina Man, Adina Magdalena Turcanu, Ioana Buculei, and Antigona Carmen Trofor. "Healthy smokers at risk for cardiovascular disease: the usefullness of left ventricular function and metabolic status evaluation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2984.

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Garcia-Larsen, Vanessa, James Potts, Patricia Bustos, Hugo Amigo, and Roberto Rona. "Ventilatory function as predictor of cardio-metabolic markers of cardiovascular disease: 10 year follow-up in young adults." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa618.

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Thiele, M., V. Rausch, B. Straub, M. Lupsor-Platon, V. Ledinghen, HK Seitz, S. Detlefsen, B. Madsen, A. Krag, and S. Mueller. "Controlled attenuation parameter predicts steatosis in alcoholic liver disease and correlates with poor metabolic phenotype and cardiovascular risk: A biopsy-controlled multicenter study." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605183.

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Khan, Faheem, Greg Myers, Abi Subramaniam, Ed Moloney, and S. Lane. "Higher Prevalence Of Hypertension, Other Cardiovascular And Metabolic Co-Morbidities Than Pulmonary Diseases In Patients Investigated For Sleep Apnea." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5041.

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Lantz, Jonas, Roland Gårdhagen, Joakim Wren, and Matts Karlsson. "Heating in a Stenosed Coronary Artery With Pulsating Flow and Non-Newtonian Viscosity." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192532.

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Abstract:

Cardiovascular disease is the most prevalent cause of death in the developed countries and most deaths are due to coronary atherosclerosis [1]. During the development of atherosclerosis, several stages can be distinguished including vulnerable plaque. This group of plaque has an inclination for erosion and rupture and is therefore of particular interest. Due to the inflammatory response of vulnerable plaque including an increased metabolism and thereby a locally increased temperature, it is possible to detect such warm cores by intracoronally temperature measurement under some prerequisitions. Temperature differences up to 2.2 K on the surface of carotid plaques have been measured [2], but the relation between plaque vulnerability, inflammatory response, temperature increase and possibility to detection by means of temperature measurement is far from fully perceived.

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Fiorello, Maria Luisa, Andrew T. Treweeke, David MacFarlane, and Ian L. Megson. "RW3 Hyperglycaemia induces reversible changes to metabolism and cell function in cultured endothelial cells: implications for the link between diabetes and cardiovascular disease." In The Scottish Cardiovascular Forum 2019, Saturday 2nd February 2019, The Centre for Health Science, Old Perth Road, Inverness, Scotland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-scf.8.

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Reports on the topic "Cardiovascular and metabolic disease"

1

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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Luke, Nancy, Kaivan Munshi, Anu Oommen, and Swapnil Singh. Economic Development, the Nutrition Trap and Metabolic Disease. Cambridge, MA: National Bureau of Economic Research, August 2021. http://dx.doi.org/10.3386/w29132.

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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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Balk, Ethan M., Gaelen P. Adam, Valerie Langberg, Christopher Halladay, Mei Chung, Lin Lin, Sarah Robertson, et al. Omega-3 Fatty Acids and Cardiovascular Disease: An Updated Systematic Review. Agency for Healthcare Research and Quality, August 2016. http://dx.doi.org/10.23970/ahrqepcerta223.

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Takeda, Mayumi. Comparison of Cardiovascular Disease Risk In Japanese Natives and Japanese Americans. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7244.

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Steckel, Richard, and Garrett Senney. Historical Origins of a Major Killer: Cardiovascular Disease in the American South. Cambridge, MA: National Bureau of Economic Research, December 2015. http://dx.doi.org/10.3386/w21809.

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Chris Stach, Chris Stach. In plain sight: Do bacterial toxins cause cardiovascular disease and type 2 diabetes? Experiment, September 2014. http://dx.doi.org/10.18258/3434.

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Legault, Jenna. Supplemental Project to Assess the Transparency of Reporting Requirements: Omega-3 Fatty Acids and Cardiovascular Disease. Agency for Healthcare Research and Quality (AHRQ), May 2017. http://dx.doi.org/10.23970/ahrqepcmeth3.

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Stoumpos, Sokratis, Patrick Mark, David Kingsmore, Giles Roditi, and Aleksandra Radjenovic. Use of Ferumoxytol enhanced Magnetic Resonance Angiography for cardiovascular assessment in late-stage chronic kidney disease. University of Glasgow, April 2020. http://dx.doi.org/10.36399/gla.pubs.215112.

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