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Volume 1, 2016, Issue 1, Pages 24-32; Paper doi: 10.15412/J.JCC.02010106; Paper ID: 20010.
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Coronary Artery Disease among Young Indians and it's Preventive Strategy
  • 1 Department of Biostatistics and Epidemiology, Public Health College, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • 2 Department of Midwifery, Nursing and Midwifery College, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • Correspondence should be addressed to Ali Dehghani, Department of Biostatistics and Epidemiology, Public Health College, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; Tel: ; Fax: ; Email:


It is suggested that more than one fifth of world's population lives in India and an additional 15 million Indian live outside India. Early studies on migrant Indians showed increase in the prevalence of coronary artery disease (CAD) among these Indians compared to native population. Indians have three times higher risk of developing CAD compared to Chinese and are 20 times more likely to die due to CAD compared to native blacks or white South Africans. South African Indians probably constitute the largest migrant Indian population in the world. CAD is the most common cause of morbidity and mortality in this population. Ischemic heart disease is also more common in Indians in South Africa than those in India. It appears that migrant Indians have a higher incidence of vascular disease than Indians in India. This is because of combination of hyperlipidemia, hypertension and diabetes. The SHARE study demonstrated that south Asians had higher prevalence of cardio-vascular disease compared to Europeans and Chinese living in Canada. CAD among Indian was reported fifty years ago, which was confirmed later by several studies. In India, approximately 2.78 million deaths are due to cardiovascular disease, of which over 50% is due to CAD, making CAD the number one killer disease in this country. Prevalence of CAD in Indians has been shown to be escalating in an alarming proportion in the last few decades. The prevalence of heart disease in 1950s was 1.05%; this increased to 9.7% in 1990 and to 11% by 2000 in urban populations. Thus, India faces the dangerous dual epidemic of CAD and in many respects. This is due to life style changes with increased consumption of high-energy dense foods and decreased physical activity; therefore, by adopting lifestyle changes, more of CAD risk factors can be modified and thus, CAD is potentially preventable.


CAD, Young Indians, Preventive strategies, Review.


oronary artery disease (CAD) is the leading cause of morbidity and mortality in both developed and developing world, and in particular, people originating from the Indian subcontinent appear to have a particular susceptibility (1). The terms 'premature' –'early onset' and young –CAD were almost exclusively used by authors between 1970 and 1990 to distinguish impact of CAD on Indian subcontinent (2, 5). Nowadays the age range varies. For example, age of early onset of CAD in Singapore in men is less than 40 and in Baltimore, US is less than 60 years in women. Despite a growing global familiarity of these terms and associated definitions is there really any pathological basis to characterize 'premature CAD'? (Table 1 ) (5).

Table 1. The Definition of coronary artery disease (CAD) in young in different studies (1).

Matira etal (6) have reported a genetic susceptibility to CAD that appears to be dependent on the age of CAD onset amongst people living in India and they highlighted an association between gene variants of promoter region of inter lukin 6 (IL6) gene, circulating level of inflammatory markers and the presence of premature CAD (7). South African Indians probably constitute the largest migrant Indian population in the world. CAD is the most common cause of morbidity and mortality in this population. Ischemic heart disease is also more common in Indians in South Africa than those in India (8). It appears that migrant Indians have a higher incidence of vascular disease than Indians in India. This because of combination of hyperlipidemia, hypertension and diabetes. Data from the age of 50 years onward showed that the South-African Indian population, which enjoys much better economic circumstances than the indigent rural population in India, had very little life expectancy advantages. The main cause of death varies from infectious to degenerative disease. South African Indians were worse off than Indians in India beyond middle age (9). A study was done on Indian population living in metropolitan area in Durban and Natal, out of 778 subjects ages 15-69 years (408 men), a positive history of CAD was obtained from 12 percent of men and 18.9 percent of women, i.e. 15.3 percent of the whole samples (10). The prevalence of hypercholestromia, smoking and hypertension were examined for two levels of risk. Level A (≥6.5 mmol/Lit), which is conventional cut off point is regarded as the higher level of risk and level B (≥ 5.7 mmol/lit) at which the risk of CHD is higher than average according to pooling project data (11). Therefore in whole samples at the higher level of risk, 20 percent were hyper cholestromic, 25 percent were at risk from smoking, 19 percent were hypertensive and 16 percent were diabetic. An analysis of the major reversible risk factors showed that when considering hypercholesteremia, hypertension, smoking and diabetes, 52 percent had at least one major risk factor at level A and 68 percent at level B; looking at the combination of risk factors, it was found that 17 percent and 25.1 percent had two major risk factors at levels A and B respectively, with regards to combination of risk factors, hypertension and smoking were the most frequent combination in men, while in women hypertension and diabetes frequently occurred together. Investigation of minor risk factors, such as body mass index showed that 58.4 percent of women were overweight and 21.8% obese (BMI≥30). A positive history of CAD in immediate family members, viz grandparents, parents and/or siblings, was obtained in 41 percent of respondents. 30.6% of the males and 21.7% of the females were involved in sedentary work activity. It was found that in the group aged under 45 years, 14.8% of total of 540 subjects were hypercholesteremic. In the age 45 years and higher, 32.6 percent of respondent had high level of cholesterol. In younger age group there was a significant association with smoking of 10 or more cigarettes per day, similarity, there was a significant association with hypertension in younger age group. A high significant association was found between diabetes and history of CHD, similarity there was a high significant association between a raised serum triglyceride level and CAD. In this study high triglyceride level, hypercholesteremia and low level of education were significantly associated with CAD (Table 2 ).

Table 2. Prevalence (%) of risk factors in subjects with history of coronary artery disease

In India, CAD and coronary risk factors were two or three times higher among urban compared to rural subjects of India, which may be due to more sedentary behavior and greater alcohol intake among urban people. In both sex, central obesity was four times more common in urban than rural population and also there was a significant association between CHD and age, hypercholesteromia, hypertension and central obesity (12, 13). A west London cohort study comparing migrant from the Indian subcontinent of Punjab origin with their sibling in Punjab found that the West London cohort had a greater mean body mass index and higher serum cholesterol, lower HDL cholesterol level and higher fasting blood glucose level than their counterparts in India (13, 14). Patients originating from Indian subcontinent are at substantially high risk of death and further coronary events after a first myocardial infarction than are Europeans (14). This is probably due to their higher prevalence of diffuse coronary atheroma. Recent Indian studies (15, 16) show that the prevalence of coronary artery disease (CAD) in the country matches the high prevalence in the migrant Indian population (17, 18). Conventional risk factors don't explain the excess of prevalence of CAD in Asian Indian in the UK and in the USA. Some Indian studies have shown metabolic syndrome is highly prevalent among Indians in the homeland or in migrant Indian (15, 19). They found that 41.1 percent of adult population of Chennai had metabolic syndrome, increased waist circumference in 41.4 percent, hypertriglyceridemia in 45.6 percent, low HDL cholesterol in 65.5 percent, hypertension in 55.4 percent and raised fasting plasma glucose in 26.7 percent. Metabolic syndrome is more common in women than men (46.5% vs 36.4%, X2=4.6, p=0.03) and also in older people (22). Prevalence of metabolic abnormalities in urban Asian Indians appear to be similar to that Mexican American study (23). Percentage of hypertriglyceridemia, low HDL-cholesterol and hypertension were also similar in both populations. The CAD rates among overseas Asian Indians worldwide are 50-400 percent higher than people of other ethnic origin irrespective of gender, religion, or social class. India is now in the middle of a CAD epidemic with urban Indians having CAD rates similar to overseas Indians, which is four times higher than Americans. Whereas the CAD rates halved in west in the past 30 years, the rates doubled in India with no sign of a down turn yet. The average age of first myocardial infarction (MI) has decreased by 20 years in . Among Asian Indian men, about half of all MI occur under the age of 50 and 25% under the age of 40. The CAD rates among Asian Indians are at least double that of whites (24). Asian Indian residing in different countries have higher rate of incidence, hospitalization, prevalence, morbidity, mortality and case fatality from CAD than people of other ethnicities (25, 26). In the UK the prevalence of symptomatic CAD in Asian Indians is similar to that of whites (8.5% vs 8.2%) but the asymptomatic or silent CAD is higher (27). In US, the prevalence of CAD in Asian Indians is four times higher than whites (10% versus 2.5%) (17). The relative risk of CAD mortality in Asian Indians is 20-50 percent higher than whites in Canada, South Africa, 300-400 percent higher than Chinese, Canada and Singapore and 20 times higher than blacks in south Africa (28). Reported data from California among Asian Indians showed that CAD mortality among Asian Indians four times higher in men <45 years of age. The excess CAD mortality among Asian Indians is greater in woman than in men (figure 1). In the US, CAD mortality rates are two times higher in Asian Indians women ages 45 to 64 years than in whites (29). In the UK the hospitalization rate for acute MI was two times higher among Asian Indians than whites, despite a lower age and greater proportion of non-smokers among the former (30). Asian Indians undergoing coronary artery bypass grafting (CABG) have almost twice the mortality of whites (31). In the UK the CAD deaths among Asian Indians is expected to double in the next 30 years (32). In the 10 years prospective follow up of the St. James survey Trinidad, the age-standardized RR of CHD incidence in Asian Indians was two times higher than whites and seven times higher than blacks (33). In Singapore where all MI in the country are systematically entered the registry, the incidence of MI has been three times higher among Asian Indians than Chinese men and women (34, 35). In the US (California) hospitalization for CAD among Asian Indians was four times higher than whites, Japanese, Filipinas and six times higher than Chinese (36).

In rural: Despite higher rate of smoking, CAD rates in rural India are about one-half in urban India (37). A cross-sectional survey in rural areas in India revealed a CAD prevalence rate of 6 percent in rural Indians aged 35-64 years (38). This rate is two times higher than USA rates (39, 40).

The prevalence of CAD in urban India is about double (41) the rate of rural India (42) and about four times higher than US (38). The rate appears to be higher in south India, with Kerela having a prevalence of 13 percent in urban areas (43) and 7 percent in rural areas (Table 3 ).

Table 3. Prevalence of CAD in India (40, 47)

The prevalence of CAD is 10 percent in New Delhi and is 11 percent in Chennai (41, 44). Overall there has been a more three times increase from 3 percent prevalence 30 years ago in urban India (38). High rates of CAD in urban India compared to rural India suggest the importance of nutrition and environmental factors, or nurture. There is a significant higher body mass index (BMI) in urban India compared to rural areas (BMI 24 versus 20 in men and 25 versus 20 in women). There is also a higher rate of abdominal obesity among the urban population, with urban men having a waist to hip ratio (WHR) of 0.99 compared to 0.95 among rural men (Table 4 ) (45).

Table 4. Prevalence of CAD risk factors (%) in north India (48)

Among Asian Indians, as in other population, both BMI and WHR are related to CHD risk factors and maximum risk appears in apple- shaped overweight and minimum in pear-shaped individuals (46). During the past 3 decades, CAD rates doubled in , whereas these rates have halved in most developed countries especially in US. As a result, CAD rates are now four times higher in India compared to US (Table 5 ) (41).

Table 5. Cardinal features of CAD among Indians versus other populations

The excess risk of CAD in Asian Indians appears to be greater at younger ages (47). In the UK, the PR of CAD mortality in Asian Indians men compared with whites is 3.3 between the ages 20-29 as opposed to 1.36 overall (48). In Singapore, compared with Chinese, the PR of CAD mortality in Asian Indians men between ages 30-39 is 12.5 in contrast to 3.0 in individuals between the ages of 60 and 69 (49). In angiography in Malaysia, Asian Indians under 40 years of age had a fifteen times higher rate of CAD compared to Chinese and a ten times higher rate compare to Malaysians. About 25% of acute MI in India occur under the age of 40 and 50% under the age of 50 (50). One center reported a 47-fold increase in the incidence of first MI under the age of 40 in the last 20 years (51). In general, MI develops 5-10 years earlier in Asian Indians than in other population (52, 53) and it's occurrence in patients under 40 is 5-10 fold higher (54). Asian Indians compared with whites have a lower prevalence of hypertension, hyperchoesterulemia, obesity and smoking, but a higher prevalence of high triglycerides (TG), low high-density lipoprotein (HDL), glucose intolerance and central obesity. In UK hypertension is more common and less associated with greater morbidity and mortality in Asian Indians than whites but less than in blacks (55, 56).

Asian Indians with low SES have a higher prevalence of CAD and risk factors such as smoking and hypertension (56). Asian Indians have a three to four time higher odds ratio for a high-risk lipid profile after controlling for SES, age and sex (57). TC levels among Asian Indians are lower than whites (58), the levels higher than other Asian (59). A recent landmark study in Canada has found Asian Indians ethnicity to be a risk factor by itself (64). Asian Indians physicians in US have a prevalence of CAD four times higher compared to Americans (60). Numerous studies have shown Lp (a) to be a powerful risk factor among Asian Indians (61, 62). The high rate of CAD in Asian Indians is due to combination of nature (genetic predisposing) and nurture (life style factors). The nature attributed predominantly to elevated level of Lp (a) is a common but often ignored risk factor in Asian Indians with a prevalence more than 40%, elevated Lp (a) appears to be the most common risk factor in the population (Figure 1 ) (63). CAD risk among Asian Indians with TC 160 mg/dl is similar to Americans with TC 240 mg/dl (64). 25% of all deaths reported in India is due to CAD (2.4 million death) (24, 65). Indians have three times higher risk of developing CAD compared to Chinese and are 20 times more likely to die due to CAD compared to native black or white South Africans (66, 67).

Figure 1. Contribution of various risk factors for CAD among Asian Indians (24)

In India approximately 2.78 million deaths are due to cardiovascular diseases, of which 50% are due to CAD, Making CAD the number one killer in our country (68). The prevalence of heart disease in 1950's was 1.05%; this increased to 9.7% in 1990 and to 11% by 2000 in urban population (48, 69). The risk for CAD among diabetic subjects is remarkably higher compared to non-diabetic subjects. The risk of death due to CAD in diabetic subjects with one prior MI is similar to that seen in non- diabetic subjects with an earlier MI, while the risk of tripled in diabetic subjects with known MI (42). In Chennai Urban Population Study the prevalence of diabetes was 12%, whereas Chennai Urban Rural Epidemiology Study the prevalence of diabetes is 15.5%. The present prevalence is 70% higher compared to that reported in 1980's. In this study overall, 11% of total population had CAD and this total figure of CAD in the population represent a ten-fold increase in prevalence of CAD in urban Indians during the last 40 years. The prevalence of CAD was higher among diabetic subjects (21.4%) (Known diabetes 25.3% and newly diagnosed diabetes 13.1%) compared to 14.9% among subjects with normal glucose tolerance (71). Prevalence of known MI was three times higher in subjects with diabetes compared those without. The percentage of death was significantly higher among diabetic subjects (11.9%) compared to non-diabetic subjects (33%). Mortality due to cardiovascular (52.9% vs 24.2%) was higher among diabetic, compared to non-diabetic subjects (72, 73). In diabetic subjects LDL tend to get modified due to hyperglycemia and other oxidation stress and metabolic abnormalities. A study in Birmingham, USA revealed that migrant Indians have higher small dense LDL compared to their white counterparts (74). In a study in South Indians it was showed that small dense LDL level was higher in diabetic patients and even higher in diabetic with CAD (75), In CUPS study, proportion of subjects with diabetes and hypercholesteromia was higher among middle- income group compared to low income group (76, 77). In the same study, data analyzed the association of CAD with physical activity, when heavy grade activity was taken as reference, the odds ratio for CAD in the light grade activity was 2.42 for CAD (77).

The cardiovascular risk factors, which are blood pressure, blood glucose and tobacco use and blood lipids, operating a continuum, are largely preventable and often cluster together in individuals and population. Strategies for prevention must address 'multiple risk factors ' to reduce the risk across the whole population. Public health interventions which influence lifestyle behaviors through policy, public education or a combination of both have been demonstrated to yield rich dividends in reducing the risk of NCDs in population as well as in individuals. Two strategies or approaches have been conventionally advocated for CVD prevention. These are the population-based approach and the high-risk approach. The population- based approach aims at reducing the risk factor levels in the population as a whole. The high risk approach aims at identifying persons with the highest risk of disease, those with markedly elevated risk factors and also people who have had an event. These individuals are then targeted for interventions to reduce the risk factor levels (78).

Increasing physical activity and decreasing consumption of calories as well as saturated fat are the foundation of this strategy and should begin early in life. Avoidance of abdominal obesity is very important, even when BMI is normal. Every effort should be undertaken to discourage children and adults from using tobacco product (79). Well- design policy measures can be powerful tools in effecting changes in population behavior related to tobacco, alcohol control, diet and physical activity, especially among the poor and those with low level of education (80) Tobacco control requires a reduction in both demand and supply (81). It has been clearly demonstrated that countries that have implemented comprehensive bans on tobacco advertising and promotion have reduced tobacco use more quickly. Tax increase is also the single most effective intervention to reduce the demand for tobacco (78).

Atherogenic risk factor clustering is common in Indians and worsens with weight gain (82). Age-related increases in weight and waist circumferences are closely related to decrease in physical activity. Whereas daily walking of 45 to 60 minutes is sufficient to prevent weight gain, walking of five-six kilometers per week is necessary for weight loss. However, even walking two or three kilometers (1 hour) per week produces a favorable risk factors profile, especially fibrinogen and insulin levels (83). With urbanization, manual work decreases. To maintain physical activity, leisure time activity has to be increased. These need safe, open spaces with fresh air and recreational facilities. There is clear scientific evidence that policy and environmental changes increase the physical activity levels of the entire population. Promoting increase use of walking and bicycling for transportation, though dedicate, safe, well-networked walking and cycling paths, and making communities walkable should be high national priority in urban design. Staircase need to be well-lit, painted, and pleasant and well maintained to be used more often. Simple motivation signs at the bottom of staircase promote its use in workplaces, public places and educational institutions. India has to take this into consideration. Roads with pedestrian and bicycle paths, along with play grounds and parks have to be integral part of a model city. There is a critical need for policy-level facilitation to make physical activity in daily living in all age groups in all sections of the society accessible, affordable, available, desirable and safe.

There is a strong rationale for policy interventions to enhance the supply of healthier food choices and curtail the availability of unhealthy food. The consumption of fresh fruit and vegetables, whole grains, whole pulses, nuts and fish needs to be increased. Saturated fats, salt and refined carbohydrates need to be decreased and artificial trans- fats need to be eliminated. Food prices are critical determinants of food we eat. What type of food people, families and communities buy and consume is determined by the relative food pricing in the market (78). Systematically altering the relative prices of different food stuffs will favorably affect food consumption which will bring down obesity, blood pressure, serum cholesterol and blood glucose at population level and thereby saves millions of people from chronic diseases. Food prices together with the shopping environment significantly contribute towards people becoming overweight and obese (84). The National Cholesterol Educational Program (NECP) III recommends > 50 percent of the total calories from carbohydrates, < 20 percent from protein and 25 to 35 percent from fat. Diets of any type containing more energy than needed or expanded will lead to obesity and dyslipidemia. Saturated Fat (SAFA): The quality of the fat is perhaps more important than the quantity. Saturated fat intake is the principle determinant of the TC and CAD. Food containing SAFA should be severely restricted to limit the meat, coconut (meat, milk and oil) palm oil, butter, ghee (clarified butter) vanaspati (vegetable ghee ), and most diary and bakery products.

Consumption of TRUFA, formed by the partial hydrogenation of vegetable oils increases LDL and decreases HDL, resulting in higher TC/HDL ratio. The major sources of TRUFA include vanaspati, margarines, vegetable shortening, biscuits, cake, donuts and white bread and virtually all "crispy foods". SAFA calories should not be replaced by TRUFA calories.

Substitution of 1 percent carbohydrate calories by SAFA increases TC by 1.5 mg/DL whereas PUFA and MUFA lower it by 0.5 mg/dL. Replacing SAFA with MUFA and PIFA may be more effective in preventing CAD than reducing overall fat intake. The NCEP III has recommended up to 20 percent of total calories from MUFA. Since all fats are high in calories, the addition of MUFA should be at the expense of SAFA and carbohydrates. Olive oil and Canola oil are high in MUFA. Nuts and avocado are excellent source of MUFA and are recommended provided the quantity is no more than 30 grams. Meats are high in MUFA but also high in SAFA and should be used sparingly.

Reuse of such oil may be particularly dangerous. The repeated use of such oil is a cause of concern in India where this practice is common. The consumer needs to be educated about the atherogenic and anti-atherogenic effects of various cooking oils, as well as animal and vegetable ghee. There is a little awareness and even some controversy about the atherogenic effects of certain foods and oils, especially in regions where sale or consumption of such products has profound impact on the regional economy.

About 50 percent of Indians are vegetarians, but their rates of diabetes and Cad are as high non-vegetarians. This phenomenon is due to contaminated vegetarianism, wherein vegetarians consume liberal amounts of butter, ghee, cheese, dairy, and bakery products, all of which are major sources of SAFA and/or TRUFA. Contrary to popular belief, dairy products (and meat) are major sources of SAFA. Recent research indicates that a diet very low in fat and very high in carbohydrate can aggravate dislipidemia by increasing TG and decreasing HDL levels. There appear to be threshold carbohydrate consumption. Intake of carbohydrate >282g/day often leads to high TG and atherogenic dyslipidemia (24).


Therefore, India faces the dangerous dual epidemic of CAD and in many respects this is due to life style changes with increased consumption of high energy dense foods and decreased physical activity. Thus, by adopting lifestyle changes, more CAD risk factors can be modified and thus, CAD is potentially preventable.

Funding/ Support

My special thanks to Dr Shridhar Dwivedi who has directed me for preparing this review.


This work was carried out in collaboration among all authors.


The authors declared no potential conflicts of interests with respect to the authorship and/or publication of this paper.


1. Patel JV, Dwivedi S, Hughes EA, Lip GY. Premature coronary artery disease: an inferred cardiovascular variant or a South Asian genetic disorder? THROMBOSIS AND HAEMOSTASIS-STUTTGART-. 2008;99(6):991. [View at Google Scholar]; [View at PubMed].

2. Rastogi SK. Myocardial infarction in young adults. (A study of 28 cases). Indian heart journal. 1968 Jul;20(3):289-95. PubMed PMID: 5705267. Epub 1968/07/01. eng. [View at Google Scholar]; [View at PubMed].

3. Antani J. A comparative clinical study of ischaemic heart disease in the young and the elderly. Indian heart journal. 1973;25(3):157-60. [View at Google Scholar].

4. Dwivedi S, Somani P, Gode K. Risk factors in patients of coronary artery disease. Indian J Preventive Social Medicine. 1975;6:139-45. [View at Google Scholar].

5. Iribarren C, Go AS, Husson G, Sidney S, Fair JM, Quertermous T, et al. Metabolic syndrome and early-onset coronary artery disease: is the whole greater than its parts? Journal of the American College of Cardiology. 2006;48(9):1800-7. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

6. Maitra A, Shanker J, Dash D, John S, Sannappa PR, Rao VS, et al. Polymorphisms in the IL6 gene in Asian Indian families with premature coronary artery disease–the Indian Atherosclerosis Research Study. Thrombosis and haemostasis. 2008;99(5):944-50. [View at Google Scholar]; [View at PubMed].

7. Marcucci R, Paniccia R, Antonucci E, Poli S, Gori AM, Valente S, et al. Residual platelet reactivity is an independent predictor of myocardial injury in acute myocardial infarction patients on antiaggregant therapy. Thrombosis and haemostasis. 2007;98(4):844-51. [View at Google Scholar]; [View at PubMed].

8. Flisher AJ, Parry CD, Bradshaw D, Juritz JM. Seasonal variation of suicide in South Africa. Psychiatry Research. 1997;66(1):13-22. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

9. Walker A. Studies bearing on coronary heart disease in South African populations. South African medical journal= Suid-Afrikaanse tydskrif vir geneeskunde. 1973;47(3):85-90. [View at Google Scholar]; [View at PubMed].

10. Rose GA, Blackburn H, Gillum R, Prineas R. Cardiovascular survey methods: Geneva, Switzerland; WHO; 1982. [View at Google Scholar].

11. Group PPR. Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events: final report of the Pooling Project. Journal of chronic diseases. 1978;31(4):201-306. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

12. Singh RB, Sharma JP, Rastogi V, Raghuvanshi RS, Moshiri M, Verma SP, et al. Prevalence of coronary artery disease and coronary risk factors in rural and urban populations of north India. European heart journal. 1997 Nov;18(11):1728-35. PubMed PMID: 9402447. Epub 1997/12/24. eng. [View at Google Scholar].

13. Bhatnagar D, Anand IS, Durrington PN, Patel DJ, Wander GS, Mackness MI, et al. Coronary risk factors in people from the Indian subcontinent living in west London and their siblings in India. Lancet (London, England). 1995 Feb 18;345(8947):405-9. PubMed PMID: 7853948. Epub 1995/02/18. eng. [View at Google Scholar].

14. Shaukat N, Lear J, Lowy A, Fletcher S, De Bono D, Woods K. First myocardial infarction in patients of Indian subcontinent and European origin: comparison of risk factors, management, and long term outcome. Bmj. 1997;314(7081):639. [View at Google Scholar].

15. Ramachandran A, Snehalatha C, Latha E, Satyavani K, Vijay V. Clustering of cardiovascular risk factors in urban Asian Indians. Diabetes care. 1998;21(6):967-71. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

16. Deepa R, Shanthirani C, Premalatha G, Sastry N, Mohan V. Prevalence of insulin resistance syndrome in a selected south Indian population--the Chennai urban population study-7 [CUPS-7]. Indian Journal of Medical Research. 2002;115:118. [View at Google Scholar].

17. Enas E, Garg A, Davidson M, Nair V, Huet B, Yusuf S. Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the United States of America. Indian heart journal. 1995;48(4):343-53. [View at Google Scholar]; [View at PubMed].

18. McKeigue P, Shah B, Marmot M. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. The Lancet. 1991;337(8738):382-6. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

19. Misra A, Vikram NK. Insulin resistance syndrome (metabolic syndrome) and Asian Indians. CURRENT SCIENCE-BANGALORE-. 2002;83(12):1483-96. [View at Google Scholar].

20. Tai E, Lim S, Chew S, Tan B, Tan C. Homeostasis model assessment in a population with mixed ethnicity: the 1992 Singapore National Health Survey. Diabetes research and clinical practice. 2000;49(2):159-68. [View at Publisher]; [View at Google Scholar]; [View at Scopus].

21. Forouhi N, Jenkinson G, Thomas EL, Mullick S, Mierisova S, Bhonsle U, et al. Relation of triglyceride stores in skeletal muscle cells to central obesity and insulin sensitivity in European and South Asian men. Diabetologia. 1999;42(8):932-5. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

22. Ramachandran A, Snehalatha C, Satyavani K, Sivasankari S, Vijay V. Metabolic syndrome in urban Asian Indian adults—a population study using modified ATP III criteria. Diabetes research and clinical practice. 2003;60(3):199-204. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

23. Meigs J, Haffner S, Williams K, Nathan D, D'Agostino R, Wilson P, editors. Prevalence of the metabolic syndrome by NCEP-ATP3 criteria in the San Antonio and Framingham offspring studies. Diabetes; 2002: AMER DIABETES ASSOC 1660 DUKE ST, ALEXANDRIA, VA 22314 USA. [View at Google Scholar].

24. Rao GH, Thanikachalam S. Coronary Artery Disease: Risk Promoters, Pathophysiology, and Prevention: Jaypee Brothers Medical Publishers; 2005. [View at Google Scholar].

25. Enas EA, Yusuf S, Mehta J. MEETING OF THE INTERNATIONAL WORKING GROUP ON CORONARY ARTERY DISEASE IN SOUTH ASIANS 24 MARCH 1996, ORLANDO, FLORIDA, USA. Indian heart journal. 1996;48(6):727-32. [View at Google Scholar].

26. Enas EA, Senthilkumar A. Coronary artery disease in Asian Indians: an update and review. Coron Artery Dis. 2005;3:21-57. [View at Google Scholar].

27. McKeigue P, Ferrie J, Pierpoint T, Marmot M. Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia. Circulation. 1993;87(1):152-61. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

28. Jha P, Enas E, Yusuf S. Coronary Artery Disease in Asian Indians: Prevalence and Risk Factors. Asian American and Pacific Islander journal of health. 1992;1(2):163-75. [View at Google Scholar]; [View at PubMed].

29. Wild SH, Laws A, Fortmann SP, Varady AN, Byrne CD. Mortality from coronary heart disease and stroke for six ethnic groups in California, 1985 to 1990. Annals of epidemiology. 1995;5(6):432-9. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

30. Wilkinson P, Sayer J, Laji K, Grundy C, Marchant B, Kopelman P, et al. Comparison of case fatality in south Asian and white patients after acute myocardial infarction: observational study. Bmj. 1996;312(7042):1330-3. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

31. Zindrou D, Bagger JP, Smith P, Taylor KM, Ratnatunga CP. Comparison of operative mortality after coronary artery bypass grafting in Indian subcontinent Asians versus Caucasians. The American journal of cardiology. 2001 Aug 1;88(3):313-6. PubMed PMID: 11472718. Epub 2001/07/27. eng. [View at Google Scholar]; [View at PubMed].

32. Lowy A, Woods K, Botha J. The effects of demographic shift on coronary heart disease mortality in a large migrant population at high risk. Journal of Public Health. 1991;13(4):276-80. [View at Google Scholar].

33. Miller GJ, Beckles GL, Maude GH, Carson DC, Alexis SD, Price S, et al. Ethnicity and other characteristics predictive of coronary heart disease in a developing community: principal results of the St James Survey, Trinidad. International journal of epidemiology. 1989;18(4):808-17. [View at Publisher]; [View at Google Scholar]; [View at Scopus].

34. Bee K. The Health of Singaporeans. Singapore: Research and Evaluation Department, Ministry of Health. 1993. [View at Google Scholar].

35. Lee J, Heng D, Chia KS, Chew SK, Tan BY, Hughes K. Risk factors and incident coronary heart disease in Chinese, Malay and Asian Indian males: the Singapore Cardiovascular Cohort Study. International journal of epidemiology. 2001;30(5):983-8. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

36. Heng D, Lee J, Chew S, Tan B, Hughes K, Chia K. Incidence of ischaemic heart disease and stroke in Chinese, Malays and Indians in Singapore: Singapore Cardiovascular Cohort Study. Annals of the Academy of Medicine, Singapore. 2000;29(2):231-6. [View at Google Scholar]; [View at PubMed].

37. Klatsky AL, Tekawa I, Armstrong MA, Sidney S. The risk of hospitalization for ischemic heart disease among Asian Americans in northern California. American journal of public health. 1994;84(10):1672-5. [View at Publisher]; [View at Google Scholar].

38. Gupta R, Rao G. Coronary heart disease epidemiology in India: the past, present and future. Coronary Artery Disease in South Asians New Delhi: Jaypee. 2001:6-28. [View at Google Scholar].

39. Reddy K. Rising burden of cardiovascular disease in India. Coronary artery disease in Indians: a global perspective Mumbai: Cardiological Society of India. 1998:63-72. [View at Google Scholar].

40. Dewan B, Malhotra K, Gupta S. Epidemiological study of coronary heart disease in rural community in Haryana. Indian heart journal. 1974;26(2):68-78. [View at Google Scholar]; [View at PubMed].

41. Enas E. Coronary artery disease epidemic in Indians: a cause for alarm and call for action. Journal of the Indian Medical Association. 2000;98(11):694-5, 7-702. [View at Google Scholar].

42. Chadha S, Radhakrishnan S, Ramachandran K, Kaul U, Gopinath N. Epidemiological study of coronary heart disease in urban population of Delhi. The Indian journal of medical research. 1990;92:424-30. [View at Google Scholar].

43. Gupta R, Prakash H, Majumdar S, Sharma S, Gupta V. Prevalence of coronary heart disease and coronary risk factors in an urban population of Rajasthan. Indian heart journal. 1994;47(4):331-8. [View at Google Scholar].

44. Begom R, Singh R. Prevalence of coronary artery disease and its risk factors in the urban population of South and North India. Acta cardiologica. 1994;50(3):227-40. [View at Google Scholar].

45. Reddy K, Shah P, Shrivastava U, Prabhakaran D, Joshi M, Puri S. Coronary heart disease risk factors in an industrial population of north India. Can J Cardiol. 1997;13(Suppl B):26B. [View at Google Scholar].

46. Prabhakaran D, Shah P, Joshi M, Puri S, Reddy K. Generalized obesity is also an important coronary heart disease risk factor in Indians (Abstr). Indian heart journal. 1997;49:619. [View at Google Scholar].

47. Enas EA. Avoiding premature coronary deaths in Asians in Britain. Guidelines for pharmacological intervention are needed. BMJ: British Medical Journal. 1996;312(7027):376. [View at Google Scholar]; [View at PubMed].

48. Balarajan R. Ethnic differences in mortality from ischaemic heart disease and cerebrovascular disease in England and Wales. Bmj. 1991;302(6776):560-4. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

49. Hughes K, Yeo P, Lun K, Thai A, Sothy S, Wang K, et al. Cardiovascular diseases in Chinese, Malays, and Indians in Singapore. II. Differences in risk factor levels. Journal of epidemiology and community health. 1990;44(1):29-35. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

50. Bahuleyan C. Hospital data on coronary heart disease from North Kerala. Cardiovascular Disease Prevention: Trivandrum Medical College. 1996:54-9. [View at Google Scholar].

51. Mammi M, Pavithran K, Abdu RP, Pisharody R, Sugathan K. Acute myocardial infarction in north Kerala--a 20 year hospital based study. Indian heart journal. 1990;43(2):93-6. [View at Google Scholar]; [View at PubMed].

52. Negus BH, Willard JE, Glamann DB, Landau C, Snyder RW, Hillis LD, et al. Coronary anatomy and prognosis of young, asymptomatic survivors of myocardial infarction. The American journal of medicine. 1994;96(4):354-8. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

53. Zimmerman FH, Cameron A, Fisher LD, Grace N. Myocardial infarction in young adults: angiographic characterization, risk factors and prognosis (Coronary Artery Surgery Study Registry). Journal of the American College of Cardiology. 1995;26(3):654-61. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

54. Hughes L, Raval U, Raftery E. First myocardial infarctions in Asian and white men. BMJ. 1989;298(6684):1345-50. [View at Publisher]; [View at Google Scholar]; [View at PubMed].

55. Boos CJ, Lane DA, Karpha M, Beevers DG, Haynes R, Lip GY. Circulating endothelial cells, arterial stiffness, and cardiovascular risk stratification in hypertension. CHEST Journal. 2007;132(5):1540-7. [View at Publisher]; [View at Google Scholar]; [View at Scopus].

56. Cappuccio FP, Cook DG, Atkinson RW, Strazzullo P. Prevalence, detection, and management of cardiovascular risk factors in different ethnic groups in south London. Heart. 1997;78(6):555-63. [View at Publisher]; [View at Google Scholar].

57. Gupta R, Gupta V, Ahluwalia N. Educational status, coronary heart disease, and coronary risk factor prevalence in a rural population of India. Bmj. 1994;309(6965):1332-6. [View at Publisher]; [View at Google Scholar].

58. Whitty CJ, Brunner EJ, Shipley MJ, Hemingway H, Marmot MG. Differences in biological risk factors for cardiovascular disease between three ethnic groups in the Whitehall II study. Atherosclerosis. 1999;142(2):279-86. [View at Publisher]; [View at Google Scholar]; [View at PubMed]; [View at Scopus].

59. Krishnaswarmi S, Prasad N, Jose V. A study of lipid levels in Indian patients with coronary heart disease. Int J Cardiol. 1989;24:337-45. [View at Google Scholar]; [View at PubMed].

60. Chen Z, Peto R, Collins R, MacMahon S, Lu J, Li W. Serum cholesterol concentration and coronary heart disease in population with low cholesterol concentrations. Bmj. 1991;303(6797):276-82. [View at Publisher]; [View at Google Scholar];