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• W2904005451 abstract "HomeCirculation: Cardiovascular ImagingVol. 11, No. 5Chinese Ethnicity and Cardiac Remodeling in Obesity and Dysglycemia Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessEditorialPDF/EPUBChinese Ethnicity and Cardiac Remodeling in Obesity and DysglycemiaThe Importance of Understanding Differences to Find Commonalities Géraldine Ong, and MD Kim A. ConnellyMBBS, PhD Géraldine Ong,Géraldine Ong, Search for more papers by this author and Kim A. ConnellyKim A. Connelly Search for more papers by this author Originally published18 Jun 2018https://doi.org/10.1161/CIRCIMAGING.118.007829Circulation: Cardiovascular Imaging. 2018;11:e007829See Article by Lin et alType 2 diabetes mellitus (T2DM) and obesity-induced cardiac remodeling occur independently of the presence of coronary disease, hypertension, or valvular disease.1 Importantly, both conditions are associated with an increased risk for developing heart failure and other adverse clinical outcomes,2,3 leading to substantial morbidity, mortality, and costs to the healthcare system.4 Furthermore, epidemiological studies have shown that individuals with an hemoglobin A1c in the range of 6.0% to 6.4% have a high risk for the future development of T2DM, supporting the use of this range to define pre–diabetes mellitus.5Multiple pathophysiological processes contribute to the myocardial impairment seen in diabetes mellitus and pre–diabetes mellitus, including, but not limited to, hyperglycemia and hyperinsulinemia states, the increased uptake of free fatty acids into cardiomyocytes along with impaired glucose metabolism, myocardial triglyceride accumulation, and oxidative stress.1,2,4 These multifactorial metabolic, proinflammatory, and neurohormonal alterations collectively induce the process of pathological cardiac remodeling, which may manifest as different cardiac phenotypes.1 In patients with T2DM, cardiac remodeling such as the hypertrophic response may occur as a result of, but also independent of, the degree of left ventricular (LV) afterload. Potential pathogenesis include excess epicardial fat, along with the dysregulation of myocardial substrate oxidation leading to a reliance on free fatty acid oxidation.1 Mechanisms of remodeling in T2DM also occur in response to hyperinsulinemia and insulin resistance (eg, growth factor upregulation, such as Akt), along with altered calcium handling and myocardial apoptosis, which remain one of several mechanisms that may ultimately lead to diffuse and focal fibrosis.6 Importantly, even in the absence of overt diabetes mellitus, remodeling may occur. In a large, multiethnic, multiracial sample of American adults without cardiovascular disease, visceral adiposity was associated with concentric LV remodeling, independent of age, race, and sex.7 As a consequence of the remodeling process, changes in myocardial systolic and diastolic functions may occur.4,6 The combined influence of cardiac remodeling with impaired systolic and diastolic functions provides a substrate for the development of heart failure.In this issue of Circulation: Cardiovascular Imaging, Lin et al8 provide important insights into the relationship between different dysglycemic states (diabetes mellitus and pre–diabetes mellitus) or obesity with cardiac structural and functional remodeling in a Chinese population. The primary finding of this study was that Chinese patients with T2DM or pre–diabetes mellitus, irrespective of whether they were obese or not, have altered cardiac structure and function compared with patients who demonstrate normoglycemia. In this retrospective analysis of 3950 patients, prediabetic and diabetic patients had increasing LV wall thickness, LV diameter, and LV volumes, greater LV mass, and increased LV mass-to-volume ratio (all P<0.001). Along with these structural changes, functional changes such as altered diastolic function was demonstrated by prolonged deceleration time, and isovolumic relaxation time, lower mitral inflow E/A ratio, lower mitral annular systolic tissue velocity s′, lower mitral annular relaxation velocity e′, higher E/e′, and larger left atrial volumes (all P<0.001) were seen in these patients compared with patients with normal glucose levels. Furthermore, changes in cardiac mechanics correlated with glycemic status, where prediabetic and diabetic states were associated with impaired global longitudinal strain and enhanced torsion (all P<0.05) but similar global circumferential strain. In addition, lean individuals were younger, more likely to be women, showed smaller waist-hip ratio, lower blood pressure or prevalent hypertension, and better renal function, as well as lower LV wall thickness, smaller LV volumes, lesser degree LV remodeling, better diastolic parameters, and overall better global longitudinal strain and global circumferential strain (all P<0.05) compared with nonlean prediabetic and diabetic individuals. In both lean and nonlean individuals, prediabetic and diabetic conditions were associated with older age, larger body size, higher blood pressure, and trends toward increased LV wall thickness, greater degree of concentric remodeling, higher LV mass, more impaired diastolic indices (deceleration time, isovolumic relaxation time, and E/e′), and more impaired global longitudinal strain (all trend P<0.05).This study highlights the impact of pre–diabetes mellitus/diabetes mellitus and obesity on cardiac remodeling, specifically in Chinese patients, where it has been shown that diabetes mellitus frequently occurs at younger ages and at lower body mass index (BMI) when compared with white individuals.7 One potential issue in the interpretation of such data remains the use of BMI. Although BMI remains the most commonly recommended and used anthropometric measure to classify general obesity in clinical and epidemiological studies,5,9 it is not without limitations as it can be influenced by factors, such as age, sex, ethnicity, and muscle mass. Other measures, such as waist circumference or the waist-to-hip ratio, have been recommended as they do not experience the same limitations as BMI in predicting intra-abdominal fat accumulation, a marker for future cardiovascular events.10 Other proposed indices include body roundness index that has been suggested as a single more suitable anthropometric measure compared with BMI or waist-to-hip ratio measurement, especially in Chinese women.11 Future studies, however, are required to determine the ethnic-specific normal/abnormal ranges and to identify which measurement remain the most powerful predictor(s) for future events.In keeping with the existing literature, the study by Lin et al8 demonstrated an association between cardiac dysfunction and T2DM. Myocardial dysfunction in T2DM often evolves silently for several years, and studies have shown that the presence of subclinical LV dysfunction, as well as diastolic dysfunction, in T2DM is associated with increased mortality and risk for developing heart failure.12–14 These findings increase with diabetes mellitus duration.15 Strain imaging, as measured by echocardiography, is an emerging parameter to evaluate LV dysfunction.12 Importantly, the presence of subclinical LV dysfunction detected by echocardiography has been shown to have prognostic significance in patients with metabolic disease.1,16 Given the increasing recognition of the syndrome of heart failure with preserved ejection fraction, defined as LV ejection fraction >45% along with cardiac structural remodeling/diastolic dysfunction or elevated natriuretic peptides, the demonstration of precise cardiac remodeling responses across a range of ethnics groups and diabetic/nondiabetic states is required to understand and guide therapies, which is of particular importance given the well-described heterogeneity of heart failure with preserved ejection fraction.Despite a detailed analysis of cardiac structure and function, some key elements in the remodeling response were not assessed in the current study. Altered myocardial composition and the accumulation of pathological extracellular matrix have been reported in the myocardium of patients with diabetes mellitus, which correlates with impaired systolic and diastolic functions.1 The presence of focal or diffuse fibrosis was not assessed in the current study, and further detailed tissue characterization using integrated back scatter with ultrasound, or advanced tissue characterization techniques with cardiac magnetic resonance imaging, may provide further insights into structure and function that may assist in the development of therapeutic strategies. Second, how derangements in metabolism drive the development of and progression of cardiac remodeling was not studied, nor was microvascular function. Such assessments may give further insight into pathophysiology, as well as novel therapeutics. Finally, the present study did not evaluate the effect of weight loss, glycemic control, or pharmacological interventions on cardiac morphological and functional characteristics. As a result, future studies are required to demonstrate whether reversal of such abnormalities will improve outcomes and the remodeling response/function in patients with obesity, diabetes mellitus, and pre–diabetes mellitus.Lin et al8 deserve congratulations for highlighting the importance of cardiac remodeling and cardiac functional evaluation of patients with metabolic diseases in the ethnic-specific group of Chinese patients. Echocardiography, a safe, noninvasive, and widely available tool, will continue to play a central role in monitoring pathophysiological alterations related to T2DM and obesity. Continued refinements to the echocardiographic assessment of cardiac function will enhance our ability to care for patients with metabolic diseases through improved diagnostics, as well as guiding therapeutic decision making.Sources of FundingDr Connelly is supported by a New Investigator award from the Canadian Institute of Health Research and an Early Researcher award from the Ministry of Ontario.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.http://circimaging.ahajournals.orgKim A. Connelly, MBBS, PhD, Keenan Research Centre for Biomedical Science, St Michael’s Hospital, 30 Bond St, Toronto, Ontario, Canada. E-mail [email protected]References1. Kosmala W, Sanders P, Marwick TH. Subclinical myocardial impairment in metabolic diseases.JACC Cardiovasc Imaging. 2017; 10:692–703. doi: 10.1016/j.jcmg.2017.04.001.CrossrefMedlineGoogle Scholar2. 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Update on prevention of cardiovascular disease in adults with type 2 diabetes mellitus in light of recent evidence: a scientific statement from the American Heart Association and the American Diabetes Association.Circulation. 2015; 132:691–718. doi: 10.1161/CIR.0000000000000230.LinkGoogle Scholar5. Heianza Y, Hara S, Arase Y, Saito K, Fujiwara K, Tsuji H, Kodama S, Hsieh SD, Mori Y, Shimano H, Yamada N, Kosaka K, Sone H. HbA1c 5·7-6·4% and impaired fasting plasma glucose for diagnosis of prediabetes and risk of progression to diabetes in Japan (TOPICS 3): a longitudinal cohort study.Lancet. 2011; 378:147–155. doi: 10.1016/S0140-6736(11)60472-8.CrossrefMedlineGoogle Scholar6. Fang ZY, Prins JB, Marwick TH. Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications.Endocr Rev. 2004; 25:543–567. doi: 10.1210/er.2003-0012.CrossrefMedlineGoogle Scholar7. Bertoni AG, Goff DC, D’Agostino RB, Liu K, Hundley WG, Lima JA, Polak JF, Saad MF, Szklo M, Tracy RP, Siscovick DS. Diabetic cardiomyopathy and subclinical cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis (MESA).Diabetes Care. 2006; 29:588–594.CrossrefMedlineGoogle Scholar8. Lin JL, Sung KT, Su CH, Chou TH, Lo CI, Tsai JP, Chang SC, Lai YH, Hu KC, Liu CY, Yun CH, Hung CL, Yeh HI, Lam CSP. Cardiac structural remodeling, longitudinal systolic strain and torsional mechanics in lean and non-lean dysglycemic Chineses adults.Circ Cardiovasc Imaging. 2018; 11:e007047. doi: 10.1161/CIRCIMAGING.117.007047.LinkGoogle Scholar9. Gjesdal O, Bluemke DA, Lima JA. Cardiac remodeling at the population level–risk factors, screening, and outcomes.Nat Rev Cardiol. 2011; 8:673–685. doi: 10.1038/nrcardio.2011.154.CrossrefMedlineGoogle Scholar10. Abbasi SA, Hundley WG, Bluemke DA, Jerosch-Herold M, Blankstein R, Petersen SE, Rider OJ, Lima JA, Allison MA, Murthy VL, Shah RV. Visceral adiposity and left ventricular remodeling: the Multi-Ethnic Study of Atherosclerosis.Nutr Metab Cardiovasc Dis. 2015; 25:667–676. doi: 10.1016/j.numecd.2015.03.016.CrossrefMedlineGoogle Scholar11. Tian S, Zhang X, Xu Y, Dong H. Feasibility of body roundness index for identifying a clustering of cardiometabolic abnormalities compared to BMI, waist circumference and other anthropometric indices: the China Health and Nutrition Survey, 2008 to 2009.Medicine (Baltimore). 2016; 95:e4642. doi: 10.1097/MD.0000000000004642.CrossrefMedlineGoogle Scholar12. Holland DJ, Marwick TH, Haluska BA, Leano R, Hordern MD, Hare JL, Fang ZY, Prins JB, Stanton T. Subclinical LV dysfunction and 10-year outcomes in type 2 diabetes mellitus.Heart. 2015; 101:1061–1066. doi: 10.1136/heartjnl-2014-307391.CrossrefMedlineGoogle Scholar13. Kozakova M, Morizzo C, Fraser AG, Palombo C. Impact of glycemic control on aortic stiffness, left ventricular mass and diastolic longitudinal function in type 2 diabetes mellitus.Cardiovasc Diabetol. 2017; 16:78. doi: 10.1186/s12933-017-0557-z.CrossrefMedlineGoogle Scholar14. Ernande L, Bergerot C, Girerd N, Thibault H, Davidsen ES, Gautier Pignon-Blanc P, Amaz C, Croisille P, De Buyzere ML, Rietzschel ER, Gillebert TC, Moulin P, Altman M, Derumeaux G. Longitudinal myocardial strain alteration is associated with left ventricular remodeling in asymptomatic patients with type 2 diabetes mellitus.J Am Soc Echocardiogr. 2014; 27:479–488. doi: 10.1016/j.echo.2014.01.001.CrossrefMedlineGoogle Scholar15. Jørgensen PG, Jensen MT, Mogelvang R, Fritz-Hansen T, Galatius S, Biering-Sørensen T, Storgaard H, Vilsbøll T, Rossing P, Jensen JS. Impact of type 2 diabetes and duration of type 2 diabetes on cardiac structure and function.Int J Cardiol. 2016; 221:114–121. doi: 10.1016/j.ijcard.2016.07.083.CrossrefMedlineGoogle Scholar16. Liu JH, Chen Y, Yuen M, Zhen Z, Chan CW, Lam KS, Tse HF, Yiu KH. Incremental prognostic value of global longitudinal strain in patients with type 2 diabetes mellitus.Cardiovasc Diabetol. 2016; 15:22. doi: 10.1186/s12933-016-0333-5.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails May 2018Vol 11, Issue 5Article InformationMetrics Download: 125 © 2018 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.118.007829PMID: 29752395 Originally publishedJune 18, 2018 KeywordsEditorialsinsulin resistanceprediabetic statediabetes mellitus, type 2obesityPDF download SubjectsEchocardiography" @default.
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• W2904005451 title "Chinese Ethnicity and Cardiac Remodeling in Obesity and Dysglycemia" @default.
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