Journal of the cardiometabolic syndrome最新文献

{"title":"Challenges to the Diagnosis, Evaluation, Treatment, and Management of Clustered Cardiometabolic Risk Factors","authors":"Peter W.F. Wilson MD, Henry R. Black MD, Anthony N. Fabricatore PhD, Ira J. Goldberg MD","doi":"10.1111/j.1559-4572.2008.00005.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00005.x","url":null,"abstract":"A panel was convened on February 18, 2008, to discuss the challenges to the diagnosis, evaluation, treatment, and management of clustered cardiometabolic risk factors. Peter W.F. Wilson, MD of Emory University School of Medicine, Atlanta, GA, moderated the panel. Henry R. Black, MD, New York University School of Medicine, New York, NY, Anthony N. Fabricatore, PhD, University of Pennsylvania, Philadelphia, PA, and Ira J. Goldberg, MD, Columbia University, New York, NY, participated in the discussion. This expert panel discussion was supported by and each author received an honorarium from Pfizer Inc for time and effort spent participating in the discussion and reviewing the transcript for important intellectual content before publication. The authors maintained full control of the discussion and the resulting content of this article.","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"177-182"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00005.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72327254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pancreatic Renin-Angiotensin-Aldosterone System in the Cardiometabolic Syndrome and Type 2 Diabetes Mellitus","authors":"Melvin R. Hayden MD, James R. Sowers MD","doi":"10.1111/j.1559-4572.2008.00006.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00006.x","url":null,"abstract":"Composite pancreatic function involves a complex interaction between the endocrine, exocrine, and gut neuroendocrine-incretin hormonal axis (insulino-acinar-ductal-incretin axis). This synchronous and dynamic interplay is required for assembly of nutritional intake into usable energy and proper gut uptake of nutrients. Cellular and extracellular matrix (ECM) remodeling may result in isletopathy and exocrinopathy, which contribute to the pathogenesis of the cardiometabolic syndrome (CMS) and type 2 diabetes mellitus (T2DM). These pancreatic end-organ remolding changes involve oxidative stress, islet amyloid deposition, endocrine and exocrine fibrosis, islet b-cell and exocrine acinar apoptosis, exocrine adipose replacement, and exocrine atrophy and may share dynamic interacting roles in the CMS and T2DM. The endocrine islet, exocrine acinar, and ductal system of the pancreas are intermingled to act as one organ dedicated to the goal of synchronizing oral nutritional intake to digestion, absorption, and energy metabolism. Their harmonious action is coordinated via an interdependent array of neural and endocrine, autocrine, and paracrine hormonal factors in conjunction with an intact neurovascular supply. In addition, there are contributing neuroendocrine cells in the gut, which make for a coordinated and synchronous endocrine-exocrine-gut incretin hormone axis. To date, no specific role for a pancreatic renin-angiotensin-aldosterone system (RAAS) in these complex mechanisms has been established. Its presence in both the endocrine and exocrine pancreas, however, may allow the RAAS to be involved in fine-tuning some of the above nutritional responses or coordinating some of its actions. There is emerging evidence, however, that an overactive tissue RAAS is involved in both islet and exocrine pancreatic cellular ECM remodeling and disease. A local tissue RAAS has now been identified in various organ systems such as the adrenal, pituitary, heart, vasculature, kidney, adipose, retina, nervous, reproductive, digestive, and recently the pancreas systems, including both the endocrine and exocrine pancreas. This local RAAS has many important functions including cell growth, differentiation, proliferation and apoptosis, reactive oxygen species generation via angiotensin II (Ang II) activation of its angiotensin type 1 receptor and activation of vascular nonphagocytic nicotine adenine dinucleotide phosphate (reduced) oxidase enzyme, inflammation, hormonal secretion, and importantly ECM remodeling fibrosis. The endocrine and exocrine pancreas are influenced by both circulating and locally generated Ang II. The endocrine pancreas is quite vascular and its blood supply is approximately 10 times greater than that of the exocrine pancreas. Ang II infusion dose-dependently reduces pancreatic blood flow, and this is especially detrimental in the highly vascularized endocrine islets. Further, RAAS blockade has been shown to enhance islet blood flow, oxygen tension, a","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"129-131"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00006.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72327252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Cardiac Rehabilitation on Coronary Risk Factors, Inflammation, and the Metabolic Syndrome in Obese Coronary Patients","authors":"Carl J. Lavie MD,&nbsp;Ali Morshedi-Meibodi MD,&nbsp;Richard V. Milani MD","doi":"10.1111/j.1559-4572.2008.00002.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00002.x","url":null,"abstract":"<p> <i>Obesity is a coronary heart disease (CHD) risk factor and is prevalent in patients with CHD. The authors reviewed data in 235 consecutive patients before and after formal cardiac rehabilitation and exercise training (CRET) programs and analyzed data in 72 lean patients (body mass index [BMI] &lt;25 kg/m</i>\u0000 ^{\u0000 <i>2</i>\u0000}\u0000 <i>) vs 73 obese patients (BMI≥30 kg/m</i>\u0000 ^{\u0000 <i>2</i>\u0000}\u0000 <i>). At baseline, obese patients were significantly younger (</i>P<i>&lt;.0001); had higher percentage of body fat (</i>P<i>&lt;.0001) and more dyslipidemia, including higher triglycerides (TG;</i> P<i>&lt;.01), lower high-density lipoprotein (HDL) cholesterol (</i>P<i>&lt;.0001), and higher TG/HDL ratio (</i>P<i>&lt;.0001); and had higher prevalence of metabolic syndrome (61% vs 26%;</i> P<i>&lt;.01) compared with lean patients. Following CRET, obese patients had small, but statistically significant, improvements in obesity indices, including weight (</i>P<i>&lt;.01), BMI (</i>P<i>&lt;.01), and percentage of fat (</i>P<i>=.03), and had more significant improvements in peak exercise capacity (</i>P<i>&lt;.001), HDL cholesterol (</i>P<i>&lt;.001), C-reactive protein (</i>P<i>&lt;.01), behavioral characteristics, and quality of life (</i>P<i>&lt;.0001). The prevalence of metabolic syndrome fell (62% to 51%;</i> P<i>=.1). These results support the benefits of CRET to reduce overall risk in obese patients with CHD.</i></p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"136-140"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00002.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin Resistance and Endothelin: Another Pathway for Renal Injury in Patients With the Cardiometabolic Syndrome?","authors":"Pantelis A. Sarafidis MD, MSc, PhD,&nbsp;Anastasios N. Lasaridis MD, PhD","doi":"10.1111/j.1559-4572.2008.00009.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00009.x","url":null,"abstract":"<p> <i>Recent population studies suggest that insulin resistance and hyperinsulinemia, as well as the presence of the cardiometabolic syndrome, are associated with increased risk of chronic kidney disease. A considerable number of background studies support this association, proposing several mechanisms through which insulin resistance and hyperinsulinemia can harm the normal kidney. Current knowledge suggests that activation of the endothelin system can be an important factor contributing to the development of renal injury. Moreover, data from in vitro and in vivo studies have clearly shown that hyperinsulinemia stimulates the production and action of endothelin-1, an effect that is sustained in insulin-resistant states. Thus, insulin-mediated activation of the endothelin system can be another important pathway linking insulin resistance with kidney injury. This article discusses the existing data on the interactions between insulin resistance, hyperinsulinemia, and endothelin and how these can lead to renal damage in patients with the cardiometabolic syndrome.</i> </p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"183-187"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00009.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Costs of and Reasons for Obesity","authors":"Maciej Witkos MSc,&nbsp;Michelle Uttaburanont MS,&nbsp;Christopher D. Lang BS,&nbsp;Rohit Arora MD","doi":"10.1111/j.1559-4572.2008.00012.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00012.x","url":null,"abstract":"<p> <i>The purpose of this literature review was to identify and describe the cost of obesity, the contributing factors, and the use of taxation as a possible method of control of this epidemic in a Canadian setting. A review of the current literature found on the PubMed/MEDLINE services of the National Institutes of Health as well as an analysis of Web content was conducted. The PubMed/MEDLINE search identified 677 articles pertaining to Canada and obesity, 323 articles relating to price policy, 26 articles concerning obesity and taxes, and 29 articles about obesity, Canada, and cost (1964–March 2007). The cost of obesity in Canada has been estimated at $4.3 billion per year, although no yearly figures are available. The contributing factors of obesity in Canada are multivariate, ranging from dietary patterns and physical inactivity to the availability of high-calorie foods at a low cost and greater accessibility. No Canadian studies have been conducted on the use of taxes to curb obesity or evaluating food price elasticity. The available literature suggests that the use of taxes is a viable option to address the issue of obesity in Canada.</i> </p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"173-176"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00012.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Controversy Regarding Contrast Echocardiography and How It Affects Patients With the Cardiometabolic Syndrome","authors":"Daniel L. Wagner MD,&nbsp;Julio E. Pérez MD,&nbsp;Linda R. Peterson MD,&nbsp;Ravi Rasalingam MBChB","doi":"10.1111/j.1559-4572.2008.00010.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00010.x","url":null,"abstract":"T T is a 59-year-old man with ischemic cardiomyopathy who was admitted with sudden onset of left arm and leg weakness as well as facial numbness. His symptoms were transient, resolving within a few hours. The patient had a history of cardiometabolic syndrome (hypertension, impaired fasting glucose, and abdominal adiposity with a body mass index of 31) and coronary artery disease requiring coronary artery bypass surgery. Head computed tomography and brain magnetic resonance imaging did not show evidence of acute stroke. Transthoracic echocardiography was performed for assessment of a cardiac source of embolism. Initial to intra-ventricular but images demonstrated apical mural The and later with a left ventricle free of thrombi stability. The microbubbles produced are approximately the size of red blood cells (6–8 µm in diameter) and can pass through the pulmonary capillary bed to the left heart. Ultrasonographic waves interact with these microbubbles, causing them to vibrate and generate sound waves at multiple frequencies that are detected by the ultrasound machine, and they are represented as an echogenic area on the generated echocardiographic image.","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"188-191"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00010.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity, Hypertension, and the Heart","authors":"David Good MD,&nbsp;Stephen A. Morse DO,&nbsp;Hector O. Ventura MD,&nbsp;Efrain Reisin MD","doi":"10.1111/j.1559-4572.2008.00011.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00011.x","url":null,"abstract":"<p> <i>Controversy exists regarding the amount of risk caused by obesity, but there is general consensus that it is associated with many serious disorders, mostly cardiovascular and neoplastic. Obesity is clearly associated with hypertension, ventricular remodeling with subsequent congestive heart failure, sleep-disordered breathing, and sudden death. The physiologic alterations associated with establishing and perpetuating the obese state are complex but are becoming clear. In discussing the cardiovascular consequences of obesity, the implications and mechanism of the associated hypertension need to be understood. There is growing recognition that adipose tissue is a very active in the neurohormonal axis and is not simply a passive storage depot. Among other things, adipocyte-related hormonal activity and resistance to feedback mechanisms are associated with increased plasma volume and increased sympathetic tone.</i> </p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"168-172"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00011.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72327251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity and Dysrhythmias","authors":"Rishi G. Anand MD,&nbsp;Robert W. Peters MD,&nbsp;Timothy P. Donahue MD","doi":"10.1111/j.1559-4572.2008.00003.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00003.x","url":null,"abstract":"<p> <i>In the United States, obesity has reached epidemic proportions. Results from the 2003–2004 National Health and Nutrition Examination Survey estimated that 66% of US adults are either overweight (body mass index [BMI] 25–30 kg/m</i>\u0000 ^{\u0000 <i>2</i>\u0000}\u0000 <i>) or obese (BMI&gt;30 kg/m</i>\u0000 ^{\u0000 <i>2</i>\u0000}\u0000 <i>) as defined by the BMI cutoffs established by the World Health Organization. In the 1970s, only 15% of the US population between the ages of 20 and 74 years was categorized as obese. In 2003, approximately 32% of the adult population was obese. Obesity plays an important role in the evolution of cardiovascular disease. This article reviews the histopathophysiologic changes that occur in cardiac structure and function in response to obesity, explores the relationship between obesity and arrhythmias such as atrial fibrillation and sudden cardiac death, and analyzes electrocardiographic changes in an obese patient.</i> </p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"149-154"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00003.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72327250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A 5-Year Follow-Up Study of 3 Polymorphisms in the Human Glucocorticoid Receptor Gene in Relation to Obesity, Hypertension, and Diabetes","authors":"Roland Rosmond MD, PhD,&nbsp;Göran Holm MD, PhD","doi":"10.1111/j.1559-4572.2008.00008.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00008.x","url":null,"abstract":"<p> <i>Glucocorticoid receptors (GRs) are cytoplasmatic</i>\u0000 <i>receptors regulating the expression of cortisol and bind to specific sites on chromatin. The glucocorticoid receptor gene (</i>GRL<i>) is located on chromosome 5q31 and encodes for either a 777-amino acid (GRα) or a 742-amino acid (GRβ) polypeptide. The objective of the current study was to examine the prospective association of 3 polymorphisms—a Tth111I restriction fragment in the promoter region, a BclI polymorphism in intron 2, and an A/G polymorphism in exon 2—of the</i> GRL <i>gene on estimates of obesity, hypertension, and diabetes in 163 unrelated Swedish men born in 1944. These data showed a significant increase in body weight, body mass index, abdominal obesity, fasting glucose, insulin, and homeostasis model assessment over the 5-year follow-up among homozygotes for the rare BclI allele. In contrast, no significant associations with the Tth111I or A/G polymorphism were detected. It is concluded that the genetic information about</i> GRL <i>would be useful for further genetic study of obesity, diabetes, and related metabolic diseases.</i></p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"132-135"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00008.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Obesity on the Pathogenesis and Prognosis of Coronary Heart Disease","authors":"M. Todd Miller MD,&nbsp;Carl J. Lavie MD,&nbsp;Christopher J. White MD","doi":"10.1111/j.1559-4572.2008.00004.x","DOIUrl":"https://doi.org/10.1111/j.1559-4572.2008.00004.x","url":null,"abstract":"<p> <i>Obesity has a significant adverse effect on coronary heart disease (CHD) risk factors, including hypertension, dyslipidemia, and the metabolic syndrome/diabetes. Obesity is an independent risk factor for CHD events; however, obese patients with CHD generally have a more favorable prognosis, with the worst prognosis associated with either underweight or morbidly obese patients. In this manuscript, the authors review the impact of obesity on overall CHD risk as well as the prognosis of obese patients with established CHD.</i> </p>","PeriodicalId":87477,"journal":{"name":"Journal of the cardiometabolic syndrome","volume":"3 3","pages":"162-167"},"PeriodicalIF":0.0,"publicationDate":"2008-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1559-4572.2008.00004.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72326787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}