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Journal articles on the topic 'Cardiovascular and metabolic disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Hummel, M., E. Standl, and O. Schnell. "Chromium in Metabolic and Cardiovascular Disease." Hormone and Metabolic Research 39, no. 10 (October 2007): 743–51. http://dx.doi.org/10.1055/s-2007-985847.

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12

Aggoun, Yacine. "Obesity, Metabolic Syndrome, and Cardiovascular Disease." Pediatric Research 61, no. 6 (June 2007): 653–59. http://dx.doi.org/10.1203/pdr.0b013e31805d8a8c.

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13

Bonora, Enzo. "The metabolic syndrome and cardiovascular disease." Annals of Medicine 38, no. 1 (January 2006): 64–80. http://dx.doi.org/10.1080/07853890500401234.

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14

Jensen, Majken K., Monica L. Bertoia, Leah E. Cahill, Isha Agarwal, Eric B. Rimm, and Kenneth J. Mukamal. "Novel metabolic biomarkers of cardiovascular disease." Nature Reviews Endocrinology 10, no. 11 (September 2, 2014): 659–72. http://dx.doi.org/10.1038/nrendo.2014.155.

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15

Grundy, Scott M. "Obesity, Metabolic Syndrome, and Cardiovascular Disease." Journal of Clinical Endocrinology & Metabolism 89, no. 6 (June 2004): 2595–600. http://dx.doi.org/10.1210/jc.2004-0372.

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16

Bisaccia, Giandomenico, Fabrizio Ricci, Cesare Mantini, Claudio Tana, Gian Luca Romani, Cosima Schiavone, and Sabina Gallina. "Nonalcoholic fatty liver disease and cardiovascular disease phenotypes." SAGE Open Medicine 8 (January 2020): 205031212093380. http://dx.doi.org/10.1177/2050312120933804.

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Nonalcoholic fatty liver disease is increasingly recognized as a major global health problem. Intertwined with diabetes, metabolic syndrome, and obesity, nonalcoholic fatty liver disease embraces a spectrum of liver conditions spanning from steatosis to inflammation, fibrosis, and liver failure. Compared with the general population, the prevalence of cardiovascular disease is higher among nonalcoholic fatty liver disease patients, in whom comprehensive cardiovascular risk assessment is highly desirable. Preclinical effects of nonalcoholic fatty liver disease on the heart include both metabolic and structural changes eventually preceding overt myocardial dysfunction. Particularly, nonalcoholic fatty liver disease is associated with enhanced atherosclerosis, heart muscle disease, valvular heart disease, and arrhythmias, with endothelial dysfunction, inflammation, metabolic dysregulation, and oxidative stress playing in the background. In this topical review, we aimed to summarize current evidence on the epidemiology of nonalcoholic fatty liver disease, discuss the pathophysiological links between nonalcoholic fatty liver disease and cardiovascular disease, illustrate nonalcoholic fatty liver disease–related cardiovascular phenotypes, and finally provide a glimpse on the relationship between nonalcoholic fatty liver disease and cardiac steatosis, mitochondrial (dys)function, and cardiovascular autonomic dysfunction.
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17

Sonnweber, Thomas, Alex Pizzini, Manfred Nairz, Günter Weiss, and Ivan Tancevski. "Arachidonic Acid Metabolites in Cardiovascular and Metabolic Diseases." International Journal of Molecular Sciences 19, no. 11 (October 23, 2018): 3285. http://dx.doi.org/10.3390/ijms19113285.

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Lipid and immune pathways are crucial in the pathophysiology of metabolic and cardiovascular disease. Arachidonic acid (AA) and its derivatives link nutrient metabolism to immunity and inflammation, thus holding a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease. We herein present a synopsis of AA metabolism in human health, tissue homeostasis, and immunity, and explore the role of the AA metabolome in diverse pathophysiological conditions and diseases.
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18

Zhou, Ji-Yin, Lawrence Chan, and Shi-Wen Zhou. "Omentin: Linking Metabolic Syndrome and Cardiovascular Disease." Current Vascular Pharmacology 12, no. 1 (March 31, 2014): 136–43. http://dx.doi.org/10.2174/1570161112999140217095038.

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19

Fotherby, K. "Metabolic Interrelationships, Cardiovascular Disease, and Sex Steroids." Contraception 57, no. 3 (March 1998): 183–87. http://dx.doi.org/10.1016/s0010-7824(98)00017-1.

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20

Blackburn, H. "Nutritional and metabolic bases of cardiovascular disease." Nutrition, Metabolism and Cardiovascular Diseases 22, no. 2 (February 2012): 160. http://dx.doi.org/10.1016/j.numecd.2011.09.003.

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21

Glass, C. K. "Going nuclear in metabolic and cardiovascular disease." Journal of Clinical Investigation 116, no. 3 (March 1, 2006): 556–60. http://dx.doi.org/10.1172/jci27913.

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22

Vega, Gloria Lena. "Obesity, the metabolic syndrome, and cardiovascular disease." American Heart Journal 142, no. 6 (December 2001): 1108–16. http://dx.doi.org/10.1067/mhj.2001.119790.

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23

Müller, Alexander, and John P. Mulhall. "Cardiovascular disease, metabolic syndrome and erectile dysfunction." Current Opinion in Urology 16, no. 6 (November 2006): 435–43. http://dx.doi.org/10.1097/01.mou.0000250284.83108.a6.

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24

van Loon, Nienke M., Patrick C. N. Rensen, and Noam Zelcer. "IDOL in metabolic, neurodegenerative and cardiovascular disease." Aging 10, no. 11 (October 14, 2018): 3042–43. http://dx.doi.org/10.18632/aging.101597.

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25

Carulli, N. "Metabolic syndrome - cardiovascular disease risk and more." Alimentary Pharmacology and Therapeutics 22, s2 (November 2005): 1–2. http://dx.doi.org/10.1111/j.1365-2036.2005.02586.x.

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26

Kastelein, John. "Metabolic and cardiovascular disease: complications and consequences." Atherosclerosis Supplements 6, no. 2 (May 2005): 1–2. http://dx.doi.org/10.1016/j.atherosclerosissup.2005.02.001.

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27

Corona, Giovanni, Giulia Rastrelli, Linda Vignozzi, Edoardo Mannucci, and Mario Maggi. "Testosterone, cardiovascular disease and the metabolic syndrome." Best Practice & Research Clinical Endocrinology & Metabolism 25, no. 2 (April 2011): 337–53. http://dx.doi.org/10.1016/j.beem.2010.07.002.

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28

Cai, Jingjing, Meng Xu, Xiaojing Zhang, and Hongliang Li. "Innate Immune Signaling in Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (January 24, 2019): 153–84. http://dx.doi.org/10.1146/annurev-pathmechdis-012418-013003.

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The physiological significance of innate immune signaling lies primarily in its role in host defense against invading pathogens. It is becoming increasingly clear that innate immune signaling also modulates the development of metabolic diseases, especially nonalcoholic fatty liver disease and cardiovascular diseases, which are characterized by chronic, low-grade inflammation due to a disarrangement of innate immune signaling. Notably, recent studies indicate that in addition to regulating canonical innate immune-mediated inflammatory responses (or immune-dependent signaling-induced responses), molecules of the innate immune system regulate pathophysiological responses in multiple organs during metabolic disturbances (termed immune-independent signaling-induced responses), including the disruption of metabolic homeostasis, tissue repair, and cell survival. In addition, emerging evidence from the study of immunometabolism indicates that the systemic metabolic status may have profound effects on cellular immune function and phenotypes through the alteration of cell-intrinsic metabolism. We summarize how the innate immune system interacts with metabolic disturbances to trigger immune-dependent and immune-independent pathogenesis in the context of nonalcoholic fatty liver disease, as representative of metabolic diseases, and cardiovascular diseases.
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29

Walker, Brian R. "Glucocorticoids and Cardiovascular Disease." European Journal of Endocrinology 157, no. 5 (November 2007): 545–59. http://dx.doi.org/10.1530/eje-07-0455.

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AbstractChronic excessive activation of glucocorticoid receptors induces obesity, insulin resistance, glucose intolerance, dyslipidaemia and hypertension. Subtle abnormalities of the hypothalamic–pituitary–adrenal axis and/or of tissue sensitivity to glucocorticoids are also associated with these cardiovascular risk factors in patients with the metabolic syndrome. Furthermore, glucocorticoids have direct effects on the heart and blood vessels, mediated by both glucocorticoid and mineralocorticoid receptors and modified by local metabolism of glucocorticoids by the 11β-hydroxysteroid dehydrogenase enzymes. These effects influence vascular function, atherogenesis and vascular remodelling following intra-vascular injury or ischaemia. This article reviews the systemic and cardiovascular effects of glucocorticoids, and the evidence that glucocorticoids not only promote the incidence and progression of atherogenesis but also modify the recovery from occlusive vascular events and intravascular injury. The conclusion is that manipulation of glucocorticoid action within metabolic and cardiovascular tissues may provide novel therapeutic avenues to combat cardiovascular disease.
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30

BEJAN, Gabriel Cristian, Dumitru MATEI, and Adela IANCU. "Prevalence of metabolic syndrome within hypertensive population and the risk of developing atherosclerotic cardiovascular diseases." Romanian Journal of Medical Practice 10, no. 2 (June 30, 2015): 187–94. http://dx.doi.org/10.37897/rjmp.2015.2.17.

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Metabolic syndrome, also called insulin resistance syndrome or excess of catecholamines, is represented by several cardiometabolic factors that result in increased incidence of cardiovascular disease and type 2 diabetes. Due to sedentary lifestyle and hypercaloric food, with a high percent of saturated fats and carbohydrates, that characterize modern lifestyle of the population, especially in urban areas, the prevalence of metabolic syndrome recorded an ascending slope that makes it a very topical issue for the medical world. During the years 2013-2014 we conducted an observational study on a sample of 111 hypertensive patients without major cardiovascular events such as myocardial infarction or stroke, with age between 48 and 83 years, in whom we determined the prevalence of metabolic syndrome and cardiovascular disease. The survey results showed an increased prevalence of metabolic syndrome, considering that we related to a hypertensive population, and an increased risk of non-fatal atherosclerotic cardiovascular diseases in men and fatal cardiovascular events in next 10 years especially for women.
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31

Cerf, Marlon. "High Fat Programming and Cardiovascular Disease." Medicina 54, no. 5 (November 13, 2018): 86. http://dx.doi.org/10.3390/medicina54050086.

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Programming is triggered through events during critical developmental phases that alter offspring health outcomes. High fat programming is defined as the maintenance on a high fat diet during fetal and/or early postnatal life that induces metabolic and physiological alterations that compromise health. The maternal nutritional status, including the dietary fatty acid composition, during gestation and/or lactation, are key determinants of fetal and postnatal development. A maternal high fat diet and obesity during gestation compromises the maternal metabolic state and, through high fat programming, presents an unfavorable intrauterine milieu for fetal growth and development thereby conferring adverse cardiac outcomes to offspring. Stressors on the heart, such as a maternal high fat diet and obesity, alter the expression of cardiac-specific factors that alter cardiac structure and function. The proper nutritional balance, including the fatty acid balance, particularly during developmental windows, are critical for maintaining cardiac structure, preserving cardiac function and enhancing the cardiac response to metabolic challenges.
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32

Batyn, S. Z., A. V. Chernyak, G. V. Neklyudova, Zh K. Naumenko, E. A. Ermakova, V. A. Shtabnitskiy, Z. R. Aysanov, and A. G. Chuchalin. "Mobile cardiorespiratory and metabolic laboratory: diagnosis of chronic obstructive pulmonary disease, cardiovascular and metabolic diseases." Russian Pulmonology 26, no. 2 (January 1, 2016): 215–21. http://dx.doi.org/10.18093/0869-0189-2016-26-2-215-221.

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33

Zamarrón, Carlos, Luis Valdés Cuadrado, and Rodolfo Álvarez-Sala. "Pathophysiologic Mechanisms of Cardiovascular Disease in Obstructive Sleep Apnea Syndrome." Pulmonary Medicine 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/521087.

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Obstructive sleep apnea syndrome (OSAS) is a highly prevalent sleep disorder, characterized by repeated disruptions of breathing during sleep. This disease has many potential consequences including excessive daytime sleepiness, neurocognitive deterioration, endocrinologic and metabolic effects, and decreased quality of life. Patients with OSAS experience repetitive episodes of hypoxia and reoxygenation during transient cessation of breathing that provoke systemic effects. Furthermore, there may be increased levels of biomarkers linked to endocrine-metabolic and cardiovascular alterations. Epidemiological studies have identified OSAS as an independent comorbid factor in cardiovascular and cerebrovascular diseases, and physiopathological links may exist with onset and progression of heart failure. In addition, OSAS is associated with other disorders and comorbidities which worsen cardiovascular consequences, such as obesity, diabetes, and metabolic syndrome. Metabolic syndrome is an emerging public health problem that represents a constellation of cardiovascular risk factors. Both OSAS and metabolic syndrome may exert negative synergistic effects on the cardiovascular system through multiple mechanisms (e.g., hypoxemia, sleep disruption, activation of the sympathetic nervous system, and inflammatory activation). It has been found that CPAP therapy for OSAS provides an objective improvement in symptoms and cardiac function, decreases cardiovascular risk, improves insulin sensitivity, and normalises biomarkers. OSAS contributes to the pathogenesis of cardiovascular disease independently and by interaction with comorbidities. The present review focuses on indirect and direct evidence regarding mechanisms implicated in cardiovascular disease among OSAS patients.
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34

Ha, Mina, and Jungsun Park. "Shiftwork and Metabolic Risk Factors of Cardiovascular Disease." Journal of Occupational Health 47, no. 2 (March 2005): 89–95. http://dx.doi.org/10.1539/joh.47.89.

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35

Abramowitz, Matthew K. "Metabolic Acidosis and Cardiovascular Disease Risk in CKD." Clinical Journal of the American Society of Nephrology 13, no. 10 (September 20, 2018): 1451–52. http://dx.doi.org/10.2215/cjn.10120818.

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36

Martinez-Hervás, Sergio, José T. Real, Antonia Priego, Javier Sanz, Jose M. Martín, Rafael Carmena, and Juan F. Ascaso. "Familial Combined Hyperlipidemia, Metabolic Syndrome and Cardiovascular Disease." Revista Española de Cardiología (English Edition) 59, no. 11 (January 2006): 1195–98. http://dx.doi.org/10.1016/s1885-5857(07)60069-3.

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37

Chen, Yabing, Xinyang Zhao, and Hui Wu. "Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (October 2019): 1911–24. http://dx.doi.org/10.1161/atvbaha.119.312192.

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Mammalian cells metabolize glucose primarily for energy production, biomass synthesis, and posttranslational glycosylation; and maintaining glucose metabolic homeostasis is essential for normal physiology of cells. Impaired glucose homeostasis leads to hyperglycemia, a hallmark of diabetes mellitus. Chronically increased glucose in diabetes mellitus promotes pathological changes accompanied by impaired cellular function and tissue damage, which facilitates the development of cardiovascular complications, the major cause of morbidity and mortality of patients with diabetes mellitus. Emerging roles of glucose metabolism via the hexosamine biosynthesis pathway (HBP) and increased protein modification via O -linked β- N -acetylglucosamine ( O -GlcNAcylation) have been demonstrated in diabetes mellitus and implicated in the development of diabetic cardiovascular complications. This review will discuss the biological outcomes of the glucose metabolism via the hexosamine biogenesis pathway and protein O -GlcNAcylation in regulating cellular homeostasis, and highlight the regulations and contributions of elevated O -GlcNAcylation to the pathogenesis of diabetic cardiovascular disease.
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38

Wilcken, D. E. L. "Overview of inherited metabolic disorders causing cardiovascular disease." Journal of Inherited Metabolic Disease 26, no. 2-3 (March 2003): 245–57. http://dx.doi.org/10.1023/a:1024445402983.

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39

Lee, Sewon, and Hyo-Bum Kwak. "Role of adiponectin in metabolic and cardiovascular disease." Journal of Exercise Rehabilitation 10, no. 2 (April 30, 2014): 54–59. http://dx.doi.org/10.12965/jer.140100.

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40

Salerno, M. P., P. Piselli, E. Rossi, E. Favi, A. Gargiulo, G. Spagnoletti, A. Agresta, and F. Citterio. "Metabolic Syndrome and Cardiovascular Disease in Kidney Transplantation." Transplantation Proceedings 43, no. 4 (May 2011): 1067–68. http://dx.doi.org/10.1016/j.transproceed.2011.03.019.

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41

Cooper-DeHoff,, Rhonda M., and Carl J. Pepine,. "Metabolic Syndrome and Cardiovascular Disease: Challenges and Opportunities." Clinical Cardiology 30, no. 12 (2007): 593–97. http://dx.doi.org/10.1002/clc.7.

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42

Jiamsripong, Panupong, Martina Mookadam, Mohsen S. Alharthi, Bijoy K. Khandheria, and Farouk Mookadam. "The Metabolic Syndrome and Cardiovascular Disease: Part 2." Preventive Cardiology 11, no. 4 (September 2008): 223–29. http://dx.doi.org/10.1111/j.1751-7141.2008.00002.x.

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43

Jiamsripong, Panupong, Martina Mookadam, Tadaaki Honda, Bijoy K. Khandheria, and Farouk Mookadam. "The Metabolic Syndrome and Cardiovascular Disease: Part I." Preventive Cardiology 11, no. 3 (October 20, 2008): 155–61. http://dx.doi.org/10.1111/j.1751-7141.2008.07809.x.

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44

Martins, David, Chizobam Ani, Deyu Pan, Omolola Ogunyemi, and Keith Norris. "Renal Dysfunction, Metabolic Syndrome and Cardiovascular Disease Mortality." Journal of Nutrition and Metabolism 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/167162.

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Background. Renal disease is commonly described as a complication of metabolic syndrome (MetS) but some recent studies suggest that Chronic Kidney disease (CKD) may actually antecede MetS. Few studies have explored the predictive utility of co-clustering CKD with MetS for cardiovascular disease (CVD) mortality.Methods. Data from a nationally representative sample of United States adults (NHANES) was utilized. A sample of 13115 non-pregnant individuals aged years, with available follow-up mortality assessment was selected. Multivariable Cox Proportional hazard regression analysis techniques explored the relationship between co-clustered CKD, MetS and CVD mortality. Bayesian analysis techniques tested the predictive accuracy for CVD Mortality of two models using co-clustered MetS and CKD and MetS alone.Results. Co-clustering early and late CKD respectively resulted in statistically significant higher hazard for CVD mortality (HR = 1.80, CI = 1.45–2.23, and HR = 3.23, CI = 2.56–3.70) when compared with individuals with no MetS and no CKD. A model with early CKD and MetS has a higher predictive accuracy (72.0% versus 67.6%), area under the ROC (0.74 versus 0.66), and Cohen's kappa (0.38 versus 0.21) than that with MetS alone.Conclusion. The study findings suggest that the co-clustering of early CKD with MetS increases the accuracy of risk prediction for CVD mortality.
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45

Vlasuk, George P., and Robert M. Scarborough. "Cardiovascular and metabolic disease: new opportunities for therapy." Current Opinion in Pharmacology 5, no. 2 (April 2005): 119–21. http://dx.doi.org/10.1016/j.coph.2005.02.002.

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46

Chan, Wai Ping Alicia, Aaron Leonid Sverdlov, and John David Horowitz. "Management of the metabolic syndrome in cardiovascular disease." Current Treatment Options in Cardiovascular Medicine 10, no. 1 (January 30, 2008): 27–38. http://dx.doi.org/10.1007/s11936-008-0004-2.

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47

Guize, Louis, Bruno Pannier, Frédérique Thomas, Kathy Bean, Bertrand Jégo, and Athanase Benetos. "Recent advances in metabolic syndrome and cardiovascular disease." Archives of Cardiovascular Diseases 101, no. 9 (September 2008): 577–83. http://dx.doi.org/10.1016/j.acvd.2008.06.011.

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48

Meshkani, Reza, and Khosrow Adeli. "Hepatic insulin resistance, metabolic syndrome and cardiovascular disease." Clinical Biochemistry 42, no. 13-14 (September 2009): 1331–46. http://dx.doi.org/10.1016/j.clinbiochem.2009.05.018.

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49

Geyeregger, R., M. Zeyda, and T. M. Stulnig. "Liver X receptors in cardiovascular and metabolic disease." Cellular and Molecular Life Sciences 63, no. 5 (February 2, 2006): 524–39. http://dx.doi.org/10.1007/s00018-005-5398-3.

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50

Comley, Robert A., and David Kallend. "Imaging in the cardiovascular and metabolic disease area." Drug Discovery Today 18, no. 3-4 (February 2013): 185–92. http://dx.doi.org/10.1016/j.drudis.2012.09.008.

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