South Asians and Cardiovascular Risk

Abstract

HomeCirculationVol. 113, No. 25South Asians and Cardiovascular Risk Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBSouth Asians and Cardiovascular RiskWhat Clinicians Should Know Milan Gupta, MD, Narendra Singh, MD and Subodh Verma, MD, PhD Milan GuptaMilan Gupta From the Division of Cardiology, William Osler Health Centre (M.G.), McMaster University, Hamilton, Canada; Division of Cardiology, Northside Hospital (N.S.), Emory University, Atlanta, Ga; and Division of Cardiac Surgery, St. Michael’s Hospital (S.V.), University of Toronto, Toronto, Canada. Search for more papers by this author , Narendra SinghNarendra Singh From the Division of Cardiology, William Osler Health Centre (M.G.), McMaster University, Hamilton, Canada; Division of Cardiology, Northside Hospital (N.S.), Emory University, Atlanta, Ga; and Division of Cardiac Surgery, St. Michael’s Hospital (S.V.), University of Toronto, Toronto, Canada. Search for more papers by this author and Subodh VermaSubodh Verma From the Division of Cardiology, William Osler Health Centre (M.G.), McMaster University, Hamilton, Canada; Division of Cardiology, Northside Hospital (N.S.), Emory University, Atlanta, Ga; and Division of Cardiac Surgery, St. Michael’s Hospital (S.V.), University of Toronto, Toronto, Canada. Search for more papers by this author Originally published27 Jun 2006https://doi.org/10.1161/CIRCULATIONAHA.105.583815Circulation. 2006;113:e924–e929Case presentation: A 36-year-old nonsmoking, normotensive South Asian man presented to the emergency department of a community hospital with retrosternal chest pain of &60 minutes’ duration. His 12-lead ECG demonstrated 10 mm of ST-segment elevation in leads V2 through V6, and he received fibrinolytic therapy within 90 minutes of symptom onset. His pain resolved, but his ST segments only partially normalized; he had a peak creatine kinase of 4564 IU/L, and he showed signs of early heart failure. LDL cholesterol was 135 mg/dL, HDL 32 mg/dL, triglycerides 20 mg/dL, and total cholesterol 206 mg/dL; his body mass index (BMI) was 24 kg/m2. Cardiac catheterization demonstrated severe and diffuse triple-vessel disease, including occlusion of the proximal left anterior descending artery, as well as moderate left ventricular dysfunction. While in the hospital, he was diagnosed with new-onset type 2 diabetes mellitus and subsequently underwent uncomplicated coronary bypass surgery.South Asians and Cardiovascular DiseaseSouth Asians are individuals whose ethnic roots originate from the Indian subcontinent, a large geographic area that includes India, Pakistan, Sri Lanka, Nepal, and Bangladesh. Collectively, South Asians represent one fifth of the global population. In North America, more than 2 million South Asians reside in the United States and almost 1 million in Canada. It is important to recognize that the term “South Asian” refers to a heterogeneous population, with important differences in diet, culture, and lifestyle among different South Asian populations and religions. Multiple studies of migrant South Asian populations have, however, confirmed a 3- to 5-fold increase in the risk for myocardial infarction and cardiovascular death as compared with other ethnic groups.1–3In an analysis of age-standardized coronary heart disease (CHD) mortality in Canada over a 15-year period, South Asians had the highest CHD mortality compared with individuals of Chinese and European descent.4 In addition, South Asians are prone to developing CHD at a younger age, often before the age of 40 years in men.5 Case-control studies have shown that compared with whites, South Asians in Canada present to the hospital later in the course of acute myocardial infarction and are more likely to have an anterior location of infarction.6 South Asians are younger at the time of cardiac catheterization than whites yet are more likely to have significant left main, multivessel, and distal coronary artery disease.7 In addition, South Asians are significantly younger at the time of first hospitalization for heart failure.8Traditional Cardiac Risk FactorsThe INTERHEART study demonstrated that traditional cardiovascular disease risk factors play an important role in the prediction of myocardial infarction in populations around the world, including South Asians.9 However, numerous case-control studies documenting premature CHD in South Asians demonstrate similar or lower prevalence of traditional risk factors than with other populations.10,11 A review of cross-sectional data from the United Kingdom, including the 1999 Health Survey of England, reveals that the prevalence of hypertension is similar in South Asians and the white population.12,13 Tobacco use is generally low among South Asian men and almost unheard of among South Asian women.14 Tobacco consumption is rapidly increasing in South Asian countries in conjunction with economic expansion.Although South Asians have levels of LDL cholesterol comparable to other populations, LDL particle size tends to be smaller.15 Small LDL particles, through increased susceptibility to oxidation, are more atherogenic than larger particles. HDL particle size, in addition to the actual level of HDL cholesterol, also appears to be an important predictor of CHD risk. South Asians not only have lower HDL levels but also have a higher concentration of small, less-protective HDL particles.16 Asian Indian males have a higher prevalence of low HDL2b than non-Asian Indians, which suggests impaired reverse cholesterol transport. This finding was also observed in Asian Indian men with apparently normal HDL values.17Unlike other traditional risk factors, the prevalence of diabetes mellitus is uniformly higher in South Asians than in many other populations. In fact, India alone is projected to experience the greatest global increase in type 2 diabetes mellitus by 2025.18 In rural settings within India, the prevalence of diabetes is quite low, at &2%. This prevalence, however, rises dramatically in urban communities throughout India, and even more so among South Asian immigrants to the Western world.19 In the United Kingdom, the prevalence of diabetes in South Asians approaches 15% to 20%.12 This large variation in diabetes prevalence among South Asians suggests an interaction between genetic predisposition and environmental influences, the so-called “thrifty gene” hypothesis. In a contemporary, community-based study of Asian Indian immigrants in the Atlanta, Ga, area, the prevalence of diabetes was 18.3%, a rate markedly higher than reported for other populations in the United States, including whites, blacks, and Hispanics.19An analysis of the California Mortality Database between 1990 and 2000 showed that Asian Indian men and women had the highest proportional mortality ratios for CHD compared with 6 other racial groups.20 Although CHD mortality declined in all groups between 1985 and 1990, Asian Indian women actually experienced a 5% increase in CHD mortality during this period. In the Study of Health Assessment and Risk in Ethnic groups (SHARE), individuals of South Asian, Chinese, and European origin were randomly selected from telephone directories in 3 Canadian cities to volunteer for laboratory and clinical testing. South Asians were found to have a higher prevalence of subclinical atherosclerosis, and South Asian ethnicity was an independent predictor of cardiovascular disease.14Abdominal Obesity and the Metabolic SyndromeThe metabolic syndrome identifies individuals at increased risk of developing both type 2 diabetes mellitus and CHD. Although the diagnostic criteria for this syndrome continue to evolve, integral components include abdominal obesity, glucose intolerance, hypertension, reduced HDL cholesterol, and increased triglycerides. There has been considerable debate as to whether the underlying cause of the metabolic syndrome is genetically or environmentally determined (innate insulin resistance versus consequences of obesity). Subjects with the metabolic syndrome face a 2-fold greater risk of all-cause mortality and a 2- to 3-fold increased risk of cardiovascular mortality compared with those without the syndrome.21Visceral or abdominal obesity has recently been recognized as an important player in the pathogenesis of both glucose intolerance and atherosclerosis. Historically, obesity has been characterized by calculation of BMI. However, large studies have suggested that waist circumference and/or waist-hip ratio may provide a better estimate of both the degree of abdominal obesity and the risk for cardiovascular disease.22 Compared with European populations, South Asians have increased abdominal visceral fat and greater insulin resistance at similar levels of BMI, which suggests that reliance on BMI alone may underestimate true risk in South Asians.23–25 In addition, insulin resistance is commonly noted in South Asians at BMI levels that are traditionally considered “ideal” (<25 kg/m2).26 This body type, often termed “thin-fat phenotype” (muscle thin but body fat) is associated with an increased risk of developing diabetes. A comparison of newborns in the United Kingdom and in Mysore, India revealed that the thin-fat phenotype was more common in Mysore newborns and persisted into childhood.27 The World Health Organization has recognized the need for definitions of obesity that are specific to individual populations.28 Consequently, it has revised the obesity cutoff in Asians from BMI >30 kg/m2 to BMI >25 kg/m2. A more appropriate estimate of visceral fat and insulin resistance in South Asians may be measurement of waist circumference, a concept furthered by population-specific cutoffs suggested by the International Diabetes Federation.29 Population-specific definitions for abdominal obesity have been incorporated into the diagnostic criteria for the metabolic syndrome by the National Cholesterol Education Program Adult Treatment Panel III Panel in the United States (Figure 1). Download figureDownload PowerPointFigure 1. International Diabetes Federation ethnicity-based definition of metabolic syndrome (adapted from Reference 29).In the SHARE study, one third of South Asian volunteers had either glucose intolerance or overt diabetes as diagnosed by fasting glucose and a 2-hour glucose tolerance test, a prevalence much higher than in other populations.14 Similar findings have been observed among urban adults in India.29 When Adult Treatment Panel III criteria and modified waist circumference cutoffs were used, the metabolic syndrome was present in 41.1% of urban Indian adults and in 27.9% of subjects with normal plasma glucose levels. In those with elevated fasting plasma glucose, the prevalence of metabolic syndrome was >70%.Emerging Cardiac Risk FactorsAlthough conventional risk factors account for the majority of CHD risk in large populations, the identification of newer methods of risk stratification has been an area of active research. Among the many candidates, lipoprotein(a), apolipoprotein B, homocysteine, plasminogen activator inhibitor-1, fibrinogen, and C-reactive protein (CRP) have generated considerable interest. Lipoprotein(a), homocysteine, and plasminogen activator inhibitor-1 levels tend to be higher in South Asians than in white populations, although fibrinogen levels appear to be similar.14,30 These factors support a prothrombotic milieu. Microalbuminuria is recognized as an independent cardiovascular disease risk factor. In a contemporary study, urinary albumin excretion was higher and microalbuminuria more frequent in UK South Asians than in the overall population, even after adjustment for age, hypertension, and diabetes.31Altered Inflammatory Biomarkers and AdipokinesSeveral lines of evidence suggest that inflammation plays a central role in the development and progression of atherosclerosis.32–35 In addition to CRP, the prototypical biomarker of inflammation, adipose tissue–derived circulating hormones, namely, adipokines, have been proposed to link insulin resistance to atherosclerosis36,37 (Figure 2). These proinflammatory adipokines include tumor necrosis factor-α, interleukin-6, leptin, plasminogen activator inhibitor-1, angiotensinogen, resistin, and CRP. Adipose tissue is also the source of antiinflammatory and antiatherosclerotic adipokines, of which adiponectin is the best studied.37–39 Insulin-resistant states are associated with diminished adiponectin levels, and augmenting adiponectin production is viewed as a cardioprotective intervention.40Download figureDownload PowerPointFigure 2. Adipokines link insulin resistance to vascular disease. Adapted from Lau et al.37Numerous studies have suggested that altered adipokine production or action may play a role in the heightened vascular risk observed in South Asian patients. In one of the largest multiethnic studies, Anand et al41 studied CRP levels in 1250 adults of South Asian, Chinese, European, and aboriginal ancestry randomly sampled from 4 communities in Canada. The age- and sex-adjusted mean CRP levels were higher in South Asians than in Chinese and Europeans, and this effect remained significant even after adjustment for metabolic factors. CRP was independently associated with cardiovascular disease after adjustment for Framingham risk factors, atherosclerosis, anthropometric measurements, and ethnicity.Studies have demonstrated abnormalities in the adiponectin-insulin sensitivity axis in nondiabetic South Asians, which may be an important biomarker linking visceral adiposity to atherogenesis in this population. In an elegant study by Raji et al,42 adiponectin levels were found to be lower in Asian Indians than in whites, which corresponded to increased whole-body insulin resistance, impaired fibrinolysis, and altered endothelial function in this population. Low adiponectin levels in nondiabetic South Asians may not only confer increased vascular risk but also may be linked to the development of diabetes in Asian Indians.43Altered adipokines may explain why lean nondiabetic Asian Indians have decreased insulin sensitivity compared with whites and Chinese subjects. In a study by Liew et al,44 healthy, nondiabetic Asian Indians were compared with white and Chinese subjects living in Singapore with respect to insulin sensitivity and leptin levels. Indians had significantly higher fasting serum leptin and lower insulin sensitivities, and stepwise regression analysis showed that ethnicity was the only significant independent determinant variable for the differences in insulin sensitivity index. Similar observations were found by Abate and colleagues,45 who reported that plasma concentrations of the adipose tissue metabolite leptin and nonesterified fatty acids were higher in Asian Indians than in whites.Implications for Diagnosis and TreatmentAlthough it seems quite clear that South Asians are at increased risk for premature glucose intolerance and CHD, there is little evidence with regard to specific preventive and management strategies for South Asians. The INTERHEART case-control study of myocardial infarction in 52 countries concluded that in all ethnic groups, including South Asians, 9 risk factors account for >90% of the population’s attributable risk of myocardial infarction.9 These risk factors included smoking, raised apolipoprotein B/apolipoprotein A1 ratio, hypertension, diabetes mellitus, abdominal obesity, and psychosocial stress. Protective factors included daily consumption of fruits and vegetables, moderate alcohol consumption, and regular physical activity. Thus, these 9 factors warrant routine assessment and management in all subjects at risk for or with established CHD, including South Asians.Clinicians should remain aware of the increased prevalence of metabolic syndrome and glucose intolerance in South Asians, and should screen subjects accordingly. Screening methods should include measurement of waist circumference and, ideally, waist-hip ratio, rather than BMI. Assessment of fasting glucose and a complete lipid profile are essential. In subjects with features of metabolic syndrome, a strong family history of diabetes, or impaired fasting glucose, an oral glucose tolerance test should be considered. In these same patients, who may otherwise be considered at intermediate Framingham risk, measurement of CRP may prove valuable for additional risk stratification. Although complete lipoprotein profiling cannot be advocated for all South Asians, measurement of lipoprotein(a), apolipoprotein B, and HDL subtypes may be useful in determining the need for combination lipid therapy in some individuals.The therapeutic strategy likely to confer the greatest benefit to a South Asian individual is one of moderate weight loss through regular exercise and dietary restriction. Reduction of abdominal obesity through lifestyle measures can improve all components of the metabolic syndrome and likely delay the development of both diabetes and atherosclerosis. Beyond lifestyle intervention, optimal management of risk factors to evidence-based targets is essential. At present, there is no evidence to suggest that treatment targets should differ between ethnic groups. Importantly, evidence-based treatments should be optimized in South Asians at risk, including the use of aspirin, lipid-lowering agents, blood pressure control, and renin-angiotensin inhibition.DisclosuresNone.FootnotesCorrespondence to Milan Gupta, MD, 164 Queen St E, Suite 211, Brampton, ON L6V1B4 Canada. E-mail [email protected] References 1 Tuomilehto J, Ram P, Eseroma R, Taylor R, Zimmet P. Cardiovascular diseases and diabetes mellitus in Fiji: analysis of mortality, morbidity and risk factors. Bull World Health Organ. 1984; 62: 133–143.MedlineGoogle Scholar2 McKeigue PM, Miller GJ, Maromot MG. Coronary heart disease in South Asians overseas: a review. J Clin Epidemiol. 1989; 42: 597–609.CrossrefMedlineGoogle Scholar3 Harding S. Mortality of migrants from the Indian subcontinent to England and Wales: effect of duration of residence. Epidemiology. 2003; 14: 287–292.MedlineGoogle Scholar4 Sheth T, Nair C, Nargundkar M, Anand S, Yusuf S. Cardiovascular and cancer mortality among Canadians of European, South Asian and Chinese origin from 1979 to 1993: an analysis of 1.2 million deaths. Can Med Assoc J. 1999; 161: 132–138.MedlineGoogle Scholar5 Enas EA, Garg A, Davidson MA, Nair VM, Huet BA, Yusuf S. Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the United States of America. Indian Heart J. 1996; 48: 343–353.MedlineGoogle Scholar6 Gupta M, Doobay AV, Singh N, Anand SS, Raja F, Mawji F, Kho J, Karavetian A, Yi Q, Yusuf S. Risk factors, hospital management and outcomes after acute myocardial infarction in South Asian Canadians and matched control subjects. Can Med Assoc J. 2002; 166: 717–722.MedlineGoogle Scholar7 Gupta M, Singh N, Warsi M, Reiter M, Ali K. Canadian South Asians have more severe angiographic coronary disease than European Canadians despite having fewer risk factors. Can J Cardiol. 2001; 17 (suppl C): 226C.Google Scholar8 Singh N, Gupta M. Clinical characteristics of South Asian patients hospitalized with heart failure. Ethn Dis. 2005; 15: 615–619.MedlineGoogle Scholar9 Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004; 364: 937–952.CrossrefMedlineGoogle Scholar10 Patel JV, Vyas A, Cruickshank JK, Prabhakaran D, Hughes E, Reddy KS, Mackness MI, Bhatnagar D, Durrington PN. Impact of migration on coronary heart disease risk factors: comparison of Gujaratis in Britain and their contemporaries in villages of origin in India. Atherosclerosis. 2006; 185: 297–306.CrossrefMedlineGoogle Scholar11 Pais P, Pogue J, Gerstein H, Zachariah E, Savitha D, Jayprakash S, Nayak PR, Yusuf S. Risk factors for acute myocardial infarction in Indians: a case-control study. Lancet. 1996; 348: 358–363.CrossrefMedlineGoogle Scholar12 Petersen S, Peto V, Rayner M. Coronary Heart Disease Statistics. London, UK: British Heart Foundation; 2004. Available at: http://www.heartstats.org/datapage. Accessed September 7, 2005.Google Scholar13 Agyemand C, Bhopal RS. Is the blood pressure of South Asian adults in the UK higher or lower than that in European white adults? A review of cross-sectional data. J Hum Hypertens. 2002; 16: 739–751.CrossrefMedlineGoogle Scholar14 Anand SS, Yusuf S, Vuksan V, Devanesen S, Teo KK, Montague PA, Kelemen L, Yi C, Lonn E, Gerstein H, Hegele RA, McQueen M. Difference in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups (SHARE). Lancet. 2000; 356: 279–284.CrossrefMedlineGoogle Scholar15 Kulkarni HR, Nanda NC, Segrest JP. Increased prevalence of smaller and denser LDL particles in Asian Indians. Arterioscler Thromb Vasc Biol. 1999; 19: 2749–2755.CrossrefMedlineGoogle Scholar16 Bhalodkar NC, Blum S, Rana T, Bhalodkar A, Kitchappa R, Kim KS, Enas E. Comparison of levels of large and small high-density lipoprotein cholesterol in Asian Indian men compared with Caucasian men in the Framingham Offspring Study. Am J Cardiol. 2004; 94: 1561–1563.CrossrefMedlineGoogle Scholar17 Superko HR, Enas EA, Kotha P, Bhat NK, Garrett B. High-density lipoprotein subclass distribution in individuals of Asian Indian descent: the National Asian Indian Heart Disease Project. Prev Cardiol. 2005; 8: 81–86.CrossrefMedlineGoogle Scholar18 King H, Aubert RE, Herman WH. Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care. 1998; 21: 1414–1431.CrossrefMedlineGoogle Scholar19 Venkataraman R, Nanda NC, Baweja G, Parikh N, Bhatia V. Prevalence of diabetes mellitus and related conditions in Asian Indians living in the United States. Am J Cardiol. 2004; 94: 977–980.CrossrefMedlineGoogle Scholar20 Palaniappan L, Wang Y, Fortmann SP. Coronary heart disease mortality for six ethnic groups in California, 1990–2000. Ann Epidemiol. 2004; 14: 499–506.CrossrefMedlineGoogle Scholar21 Lakka HM, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E, Tuomilehto J, Salonen JT. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA. 2002; 288: 2709–2716.CrossrefMedlineGoogle Scholar22 Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P Jr., Razak F, Sharma AM, Anand SS; INTERHEART Study Investigators. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet. 2005; 366: 1640–1649.CrossrefMedlineGoogle Scholar23 McKeigue PM, Shah B, Marmot MG. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet. 1991; 337: 382–386.CrossrefMedlineGoogle Scholar24 Hodge AM, Dowse GK, Collins VR, Alberti KG, Gareeboo H, Tuomilehto J, Zimmet PZ. Abdominal fat distribution and insulin levels only partially explain adverse cardiovascular risk profile in Asian Indians. J Cardiovasc Risk. 1996; 3: 263–270.MedlineGoogle Scholar25 Banerji MA, Faridi N, Atluri R, Chaiken RL, Lebovitz HE. Body composition, visceral fat, leptin, and insulin resistance in Asian Indian men. J Clin Endocrinol Metab. 1999; 84: 137–144.MedlineGoogle Scholar26 Snehalatha C, Viswanathan V, Ramachandran A. Cutoff values for normal anthropometric variables in Asian Indian adults. Diabetes Care. 2003; 26: 1380–1384.CrossrefMedlineGoogle Scholar27 Krishnaveni GV, Hill JC, Veena SR, Leary SD, Saperia J, Chachyamma KJ, Karat SC, Fall CH. Truncal adiposity is present at birth and in early childhood in South Indian children. Indian Pediatr. 2005; 42: 527–538.MedlineGoogle Scholar28 WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet. 2004; 363: 157–163.CrossrefMedlineGoogle Scholar29 The IDF consensus worldwide definition of the metabolic syndrome. International Diabetes Federation 2005. Available at: http://www.idf.org/home. Accessed September 20, 2005.Google Scholar30 Hoogeveen RC, Gambhir JK, Gambhir DS, Kimball KT, Ghazzaly K, Gaubatz JW, Vaduganathan M, Rao RS, Koschinsky M, Morrisett JD. Evaluation of Lp(a) and other independent risk factors for CHD in Asian Indians and their USA counterparts. J Lipid Res. 2001; 42: 631–638.CrossrefMedlineGoogle Scholar31 Fischbacher CM, Bhopal R, Rutter MK, Unwin NC, Marshall SM, White M, Alberti KG. Microalbuminuria is more frequent in South Asian than in European origin populations: a comparative study in Newcastle, UK. Diabet Med. 2003; 20: 31–36.CrossrefMedlineGoogle Scholar32 Aikawa M, Libby P. Atherosclerotic plaque inflammation: the final frontier? Can J Cardiol. 2004; 20: 631–634.MedlineGoogle Scholar33 Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005; 352: 1685–1695.CrossrefMedlineGoogle Scholar34 Szmitko PE, Wang CH, Weisel RD, de Almeida JR, Anderson TJ, Verma S. New markers of inflammation and endothelial cell activation: part I. Circulation. 2003; 108: 1917–1923.LinkGoogle Scholar35 Szmitko PE, Wang CH, Weisel RD, Jeffries GA, Anderson TJ, Verma S. Biomarkers of vascular disease linking inflammation to endothelial activation: part II. Circulation. 2003; 108: 2041–2048.LinkGoogle Scholar36 Verma S, Szmitko PE, Ridker PM. C-reactive protein comes of age. Nat Clin Pract Cardiovasc Med. 2005; 2: 29–36.CrossrefMedlineGoogle Scholar37 Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines: molecular links between obesity and atherosclerosis. Am J Physiol Heart Circ Physiol. 2005; 288: H2031–H2041.CrossrefMedlineGoogle Scholar38 Verma S, Li SH, Wang CH, Fedak PW, Li RK, Weisel RD, Mickle DA. Resistin promotes endothelial cell activation: further evidence of adipokine-endothelial interaction. Circulation. 2003; 108: 736–740.LinkGoogle Scholar39 Shibata R, Sato K, Pimentel DR, Takemura Y, Kihara S, Ohashi K, Funahashi T, Ouchi N, Walsh K. Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms. Nat Med. 2005; 11: 1096–1103.CrossrefMedlineGoogle Scholar40 Despres JP, Golay A, Sjostrom L; Rimonabant in Obesity-Lipids Study Group. Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia. N Engl J Med. 2005; 353: 2121–2134.CrossrefMedlineGoogle Scholar41 Anand SS, Razak F, Yi Q, Davis B, Jacobs R, Vuksan V, Lonn E, Teo K, McQueen M, Yusuf S. C-reactive protein as a screening test for cardiovascular risk in a multiethnic population. Arterioscler Thromb Vasc Biol. 2004; 24: 1509–1515.LinkGoogle Scholar42 Raji A, Gerhard-Herman MD, Warren M, Silverman SG, Raptopoulos V, Mantzoros CS, Simonson DC. Insulin resistance and vascular dysfunction in nondiabetic Asian Indians. J Clin Endocrinol Metab. 2004; 89: 3965–3972.CrossrefMedlineGoogle Scholar43 Snehalatha C, Mukesh B, Simon M, Viswanathan V, Haffner SM, Ramachandran A. Plasma adiponectin is an independent predictor of type 2 diabetes in Asian Indians. Diabetes Care. 2003; 26: 3226–3229.CrossrefMedlineGoogle Scholar44 Liew CF, Seah ES, Yeo KP, Lee KO, Wise SD. Lean, nondiabetic Asian Indians have decreased insulin sensitivity and insulin clearance, and raised leptin compared to Caucasians and Chinese subjects. Int J Obes Relat Metab Disord. 2003; 27: 784–789.CrossrefMedlineGoogle Scholar45 Abate N, Chandalia M, Snell PG, Grundy SM. Adipose tissue metabolites and insulin resistance in nondiabetic Asian Indian men. J Clin Endocrinol Metab. 2004; 89: 2750–2755.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kokorelias K, Nelson M, Cameron J, Colquhoun H, Munce S, Hitzig S, Salbach N, Martyniuk J, Steele Gray C, Tang T, Wang R, Lindsay P, Bayley M, Kaur N and Singh H (2022) Exploring the poststroke experiences and unmet needs of South Asian communities in high-income countries: a scoping review protocol, BMJ Open, 10.1136/bmjopen-2021-059017, 12:4, (e059017), Online publication date: 1-Apr-2022. Ahmed N, Farooq J, Meo S and Pasha F (2022) Role of Phoenix dactylifera (Ajwa) on lipid profile; a randomized controlled trial, Journal of King Saud University - Science, 10.1016/j.jksus.2022.101959, 34:4, (101959), Online publication date: 1-Jun-2022. Đoàn L, Takata Y, Hooker K, Mendez-Luck C, Irvin V and Newman A (2021) Trends in Cardiovascular Disease by Asian American, Native Hawaiian, and Pacific Islander Ethnicity, Medicare Health Outcomes Survey 2011–2015, The Journals of Gerontology: Series A, 10.1093/gerona/glab262, 77:2, (299-309), Online publication date: 3-Feb-2022. Bays H, Shrestha A, Niranjan V, Khanna M and Kambhamettu L (2022) Obesity Pillars Roundtable: Obesity and South Asians, Obesity Pillars, 10.1016/j.obpill.2021.100006, 1, (10000