Medical, Socialogical and environmental issues in cardiovascular disease epidemiology, prevention and rehabilitation.
Thomas A. Gaziano, MD MSc
Boston University, Boston USA
At the beginning of the 20th century, cardiovascular disease (CVD) was responsible for less than 10% of all deaths worldwide. Today, that figure is about 30% and CVD is the leading cause of death worldwide with about 80% of the burden now occurring in developing countries (Figure 1).1-3 This issue of Cardiology Rounds explains the epidemiological transition that has made CVD the leading cause of death in the world, assesses the status of the transition by region, and shows the regional differences in the burden of CVD. Further, this issue reviews the cost-effectiveness of various interventions addressing the most relevant causes of CVD morbidity and mortality.
Figure 1: CVD Compared to Other Causes of Death Worldwide
  • CVD 30%
  • Infections 19%
  • Other 17%
  • Cancer 13%
  • Injuries 9%
  • Respiratory 6%
  • Maternal / Perinatal 6%
Over the last two centuries, the industrial and technological revolutions and the economic and social transformations associated with them have resulted in a dramatic shift in the causes of illness and death. Prior to 1900, infectious diseases and malnutrition were the most common causes of death. With improved nutrition and public health measures, they have gradually been supplanted by CVD and cancer deaths in most high-income countries. Omran developed an excellent model of the epidemiological transition dividing the transition into three basic stages: pestilence and famine, receding pandemics, and degenerative and man-made diseases (Table 1).1-4 Olshansky and Ault added a fourth stage, delayed degenerative diseases.5
Stages of The Epidemiological Transition and its Global Status, by Region
Stage 1: Pestilence and famine
  • Description: Predominance of malnutrition and infectious diseases
  • Life expectancy: 35 years
  • Dominant form of CVD: rheumatic heart disease, cardiomyopathy due to infection and malnutrition. % of deaths due to CVD: 5-10
  • % of the world’s population in this state: 11
  • Region affected: SSA, parts of all regions excluding high-income regions
Stage 2: Receding pandemics
  • Description: Improved nutrition and public health leads to increase in chronic diseases, hypertension
  • Life expectancy: 50 years
  • Dominant form of CVD: Rheumatic valvular disease, IHD, hemorrhagic
  • % of deaths due to CVD: 15-35
  • - % of the world’s population in this stage: 38
  • Region affected: SAR, southern EAP parts of LAC
Stage 3: Degenerative and man-made diseases
  • Description: Increased fat and caloric intake, widespread tobacco use, chronic disease deaths exceed mortality from infections and malnutrition
  • Life expectancy: 60 years
  • Dominant form of CVD: IHD, stroke (ischemic and hemorrhagic)
  • % of deaths due to CVD: greater than 50
  • % of the world’s population in this stage: 35
  • Region affected: ECA, northern EAP, LAC, MNA, and urban parts of most low-income regions (especially India)
Stage 4: Delayed degenerative diseases
  • Description: CVD and cancer are leading causes of morbidity and mortality, prevention and treatment avoids death and delays onset; age-adjusted CVD declines
  • Life expectancy: greater than 70 years
  • Dominant form of CVD: IHD, stroke (ischemic and hemorrhagic), CHF
  • % of deaths due to CVD: less than 50
  • % of the world’s population in this stage: 15
  • Region affected: High-income countries, parts of LAC
The stage of pestilence and famine is characterized by the predominance of malnutrition and infectious disease and by the relative infrequency of CVD. In this situation, CVD is responsible for only ~ 10% of deaths, mostly attributed to rheumatic heart disease and cardiomyopathies due to infection and malnutrition.
The stage of receding pandemicsis marked by increases in wealth that lead to better availability of food, improved sanitation, and access to vaccines and antibiotics. The results are lower rates of communicable, maternal, perinatal, and nutritional diseases, and an increase in cardiovascular risk factors, particularly hypertension. These changes, along with increased lifespan, eventually lead to a greater incidence of CVD, particularly hemorrhagic stroke.
The stage of degenerative and man-made diseasesis characterized by dramatic lifestyle changes in diet, activity levels, and smoking that set the stage for the emergence of atherosclerosis. The average lifespan increases to beyond 50 years and mortality from CVD, in particular, and other non-communicable diseases now exceeds mortality from malnutrition and infectious diseases. The predominant form of CVD is coronary heart disease (CHD), but ischemic stroke also emerges as a significant cause of mortality and morbidity.
In the stage of delayed degenerative diseases, CVD and cancer continue to be the major causes of morbidity and mortality. Due to widespread primary and secondary prevention efforts, however, the age-adjusted CVD mortality tends to decline. Congestive heart failure (CHF) prevalence increases due to improved survival of those with ischemic heart disease and life expectancy increases to greater than 70 years.
New trends suggest that the United States (USA) could be entering a fifth as-yet-unnamed phase of the epidemiologic transition, characterized by an epidemic of obesity. Although rates of CVD fell 2% to 3 % per year through the 1970s and 1980s in most developed countries, the rate of decline has slowed. In the USA, physical activity continues to decline as total caloric intake increases. Overweight and obesity are escalating at an alarming pace, while rates of type 2 diabetes, hypertension, and lipid abnormalities associated with obesity are on the rise. This trend is not unique to developed countries only. According to the World Health Organization (WHO), more than 1 billion adults worldwide are overweight and 300 million are clinically obese. Even more disturbing are increases in childhood obesity, leading to large increases in diabetes and hypertension. If these trends continue, age-adjusted CVD mortality rates could increase in the USA and other countries in the coming years.
While countries tend to enter these stages at different times, the progression from one stage to the next tends to proceed in a predictable manner, with both the rate and the nature of CVDs changing over the course of the transition. The USA and most other developed economies, for example, spent most of their early history in the first stage and then progressed through the next 3 stages over the course of the last century and a half.
Japan is unique among high-income countries because the transition started later, but proceeded much more rapidly. In the early part of the 20th century, stroke rates increased dramatically, eventually becoming the highest in the world by the middle of the century. CHD rates in Japan, however, have not risen as sharply as in other industrialized countries and have remained lower. Since the 1970s, stroke rates have declined dramatically, but there are indications of a possible recent increase in CHD. The historically lower heart disease rates may be at least partly attributable to genetic factors, but it is more likely that the average plant-based, low-fat diet and resultant low cholesterol levels have played a more important role. If CHD is increasing, it could be related to changes in dietary habits that Japan is currently experiencing with increased dairy and fat consumption.6
The World Bank groups countries based on economic and geographic variation. The high-income countries are those with a gross national income (GNI) per capita of greater than or equal to $9,200. The rest of the low- and middle-income countries are divided according to geographic region. The 6 developing regions are:
  • East Asia and the Pacific (EAP) with China representing the bulk of its population
  • Europe and Central Asia (ECA)
  • Latin America and the Caribbean (LAC)
  • Middle East and North Africa (MNA)
  • South Asia (SAR) with India as its largest member
  • Sub-Saharan Africa (SSA).
The stage of the transition for each region varies widely (Table 1). With roughly 840 million people, the USA and the other established market economy countries currently comprise a little more than 15% of the world’s population. Rapid declines in CHD and stroke rates since the early 1970s indicate that these countries are in the fourth phase of the epidemiologic transition, the stage of delayed degenerative diseases. In these countries, CHD rates tend to be higher than stroke rates and overall CVD deaths are about 30% of the total with a rate of 320 deaths per 100,000 population.
As a result of the epidemiological transition outlined above, CVD is the leading cause of death in all World Bank developing regions, with the exception of SSA.1 Most developing regions appear to be following a similar pattern as developed countries with an initial rise in stroke (EAP and SSA) and then a predominance of CHD; however, the transition has occurred at a more compressed rate than in the high-income countries. Between 1990 and 2020, CHD alone is anticipated to increase by 120% for women and 137% for men in developing countries, compared to age-related increases of between 30% and 60% in developed countries.7 The INTERHEART study suggests that the same risk factors found in the developed countries also appear to account for the rapid increase in the developing countries.8 This case-control study, conducted in 52 countries with over 15,000 cases of myocardial infarction (MI), demonstrated that smoking, diabetes mellitus, hypertension, abdominal obesity, dyslipidemia, physical inactivity, and poor fruit and vegetable intake had a population attributable risk (PAR) of 90%. The PAR for current and past smokers was 36%.
The EAP region appears to be straddling the second and third stages with apparent regional differences in CVD rates. A north/south gradient has emerged, with higher CVD rates in northern China than in southern China. The ECA region is firmly at the peak of the third transition stage with CVD representing 60% of all deaths. Croatia, Belarus, and the Ukraine saw an increase of 40% to 60% in CHD death rates between 1988-98 (Figure 2). The ECA region has a rate of 690 CVD deaths per 100,000, more than double that of the high-income countries. Within the region of the MNA, the majority of the Middle Eastern crescent appears to be entering the third stage of the epidemiologic transition; increasing economic wealth has been accompanied by a rapid increase in CVD. As a whole, the LAC region also seems to be in the third stage, but this region, as defined by the World Bank, includes all of South America. Residents of some of these countries are still at risk of contracting malaria and dengue fever; as a result, those portions of the region are still in the first transitional phase. Despite large regional variations, HIV/AIDS-plagued SSA remains largely in the first phase of the epidemiologic transition. Heterogeneity is also apparent throughout the rest of the developing world - even within countries (eg, some regions of India appear to be in the first phase of the transition, whereas others are in the second or even the third phase).
Figure 2: Percentage change in ischemic heart disease death rates in people age 35-74, 1988-98, selected countries
  • Croatia: male  63%  / female  61%
  • Kazakhstan:  male 56%  / female  36%
  • Belarus:  male  53%  / female  30%
  • Ukraine:  male  49%  / female  33%
  • Romania: male  26%  / female  26%
  • Japan: male  -10%  / female  -8%
  • Hungary: male  -2%  / female  2%
  • Greece: male  -15%  / female  -11%
  • Portugal: male  -29%  / female  -19%
  • USA: male  -29%  / female  -30%
  • Netherlands: male  -29%  / female  -39%
  • Sweden: male  -40%  / female  -43%
  • Luxembourg: male  -20%  / female  -43%
  • Australia: male  -52%  / female  -46%
  • Denmark: male  -46%  / female  -49%

While no detailed data exist on the direct economic burden of the individual risk factors, the costs of CVD treatment in developing countries is significant and appears similar to that in developed countries. In South Africa, for example, 2% to 3% of the gross domestic product (GDP) was devoted to the direct treatment of CVD or roughly 25% of the South African healthcare expenditures.9  An indication of possible future expenditures in developing countries is also provided by current expenditures in developed countries. For example, the USA spent an estimated $368 billion relating to direct and indirect costs of CVD in 2004.10 In 1998, US$109 billion was spent on hypertension, or about 13% of the healthcare budget.11 In 2004, an estimated $26 billion was spent for the care of CHF patients. Studies are limited, but suggest that obesity related diseases are responsible for 2% to 8% of all healthcare expenditures in developed countries.12

While the disease burden and the social costs of CVD are high, the resources devoted towards healthcare are extremely scarce. The GNI per capita of developed countries ($27,000) is nearly 25-fold that of developing countries ($1,100). Further, developed countries devote twice as much of its GNI (10%) to healthcare compared to low- and middle-income countries (6%). This results in about a 40-fold difference between developed and developing countries in funds devoted to healthcare.13 This is further compounded by the fact that a high proportion of the CVD burden occurs earlier among adults of working age in developing countries. In 5 of the countries surveyed (Brazil, India, China, South Africa and Mexico), conservative estimates indicated that at least 21- million-years of future productive life are lost because of CVD each year.7
There are many interventions with strong evidence for significant reductions in morbidity and mortality associated with CVD, but few intervention trials have been carried out solely in developing countries. As a result, estimates of cost effectiveness ratios have been extrapolated to the developing world based on changes in key input prices.14 This process is limited, however, by the fact that both the underlying epidemiology and the costs can be quite different across countries and regions. The following section reviews results of interventions based on models using prices and epidemiological data from the World Bank developing regions. The analyses comply with the Disease Control Priorities Project (DCPP) Guidelines for Authors of July 2003.15 Only the costs related to the intervention itself and CVD events are included in the model. Costs include personnel salaries, healthcare visits, diagnostic tests, and hospital stays, according to DCPP September 2004 draft of unit costs.16  Indirect costs, such as work loss or family assistance, are not included in the analysis. Drug costs are from the International Drug Price Indicator Guide.17 All costs unless otherwise specified are in $US. For a detailed explanation of the methods for the following analyses, please refer to the DCPP Working Papers Series on Cardiovascular Disease.18 Results are reported in costs per quality-adjusted life-year (QALY) gained. This section reviews only drug-related interventions; however, smoking cessation interventions through taxation policies, physician education, and advertising regulations are also extremely cost-effective.
Acute MI
Four incremental strategies were evaluated for the treatment of acute MI (AMI) and compared to a strategy of no treatment as a base case. The 4 strategies were: aspirin (ASA); ASA and beta-blocker (BB[atenolol]); ASA, BB, and streptokinase (SK); and ASA, BB, and tissue plasminogen activator (t-PA). Doses for the ASA and SK were those used in ISIS-2. The BB regimen was that of ISIS-1 and the t-PA dosing was that used in GUSTO-I. All patients receiving the medications had relative risk reductions in the risk of dying from AMI. Patients receiving the thrombolytics also faced the complication of increased risks of major bleeds and hemorrhagic strokes. Two further sensitivity analyses were completed comparing SK in those aged over 75-years and those aged less than 75-years, and whether or not patients received the intervention more than 6 hours or less than 6 hours from onset of symptoms, since treatment effectiveness diminishes over time. The incremental cost per QALY gained for both ASA and BB interventions was less than $25 for all 6 regions. Costs per QALY gained for SK were between $630-$730 across the regions. ICERs for t-PA were around $16,000/QALY gained compared to SK. Minor variations occurred between regions due to small differences in follow-up care based on regional costs. Giving SK in less than 6 hours reduces the incremental cost per QALY gained to around $500 compared to over $1200 per QALY gained if given after more than 6 hours. Equivalent effects are seen when SK is given to those aged less than 75 ($600/QALY) compared to those aged greater than 75 ($1300/QALY). Other criteria that would improve the cost-effectiveness of thrombolytics, but were not analyzed include location of the infarct (anterior) or the presence of a new left bundle branch block.
Secondary prevention
Four incremental strategies were evaluated for the treatment of acute MI (AMI) and compared to a strategy of no treatment as a base case. The 4 strategies were: aspirin (ASA); ASA and beta-blocker (BB[atenolol]); ASA, BB, and streptokinase (SK); and ASA, BB, and tissue plasminogen activator (t-PA). Doses for the ASA and SK were those used in ISIS-2. The BB regimen was that of ISIS-1 and the t-PA dosing was that used in GUSTO-I. All patients receiving the medications had relative risk reductions in the risk of dying from AMI. Patients receiving the thrombolytics also faced the complication of increased risks of major bleeds and hemorrhagic strokes. Two further sensitivity analyses were completed comparing SK in those aged over 75-years and those aged less than 75-years, and whether or not patients received the intervention more than 6 hours or less than 6 hours from onset of symptoms, since treatment effectiveness diminishes over time. The incremental cost per QALY gained for both ASA and BB interventions was less than $25 for all 6 regions. Costs per QALY gained for SK were between $630-$730 across the regions. ICERs for t-PA were around $16,000/QALY gained compared to SK. Minor variations occurred between regions due to small differences in follow-up care based on regional costs. Giving SK in less than 6 hours reduces the incremental cost per QALY gained to around $500 compared to over $1200 per QALY gained if given after more than 6 hours. Equivalent effects are seen when SK is given to those aged less than 75 ($600/QALY) compared to those aged greater than 75 ($1300/QALY). Other criteria that would improve the cost-effectiveness of thrombolytics, but were not analyzed include location of the infarct (anterior) or the presence of a new left bundle branch block.
In India, per capita consumption of major fats and oils has increased significantly during the last 30 years.42 In 1958 it was 5.62 Kg per year which increased to 5.79 in 1961, 5.23 in 1966, 5.85 in 1971, 5.21 in 1976, 6.48 in 1981 and 6.97 in 1986 (r=0.64, p=0.168). This consumption is much lower than in EEC countries (38.98), USA (39.72), Canada (34.83) and Japan (19.84). However, diet of 17% of rural poor does not include any edible oil and about 5% of the population consumes nearly 40% of the available fat, hence the increase in the fat consumption is mainly in urban middle and upper classes where CHD is rampant. Reliable data regarding the consumption of Indian ghee (clarified butter) are not available as this fat is produced and consumed as a household item. It has been reported that 27.5% of the total milk production is utilized for its production and in 1990, 750 thousand tonnes of Indian ghee was consumed, i.e., 0.91 kg/person/year.42
An important and unstudied aspect of the fat intake is effect of various Indian cooking habits on fatty acid composition. Shallow-frying, which is widely prevalent in Indian kitchens, can lead to oxidation of fatty acids and formation of cholesterol oxides which are toxic to arterial endothelium.43 Deep-frying increases the temperature of oils to very high levels and can change chemical composition of the fats. Trans-fatty acid composition of various Indian fats is not well defined although it has been reported in high amounts in hydrogenated oils.43
WHO has estimated that at present tobacco causes 2.5 million premature deaths per annum world-wide that increased more than ten-fold since 1950.1 The mortality from tobacco will rise to 3.0 million during the 1990's and to 10 million in 2020's.1 With consumption projected to rise still further, the actual figures may be greater. According to World Bank, tobacco related pulmonary and cardiovascular diseases have become major community health problems in South Asia. Tobacco is already killing more than these estimates and GBD Study has reported that in the year 2000, tobacco caused 4.9 million deaths of the total 55.8 million deaths per annum worldwide.4

Cigarette and tobacco smoke is known to contain many toxic and vasoactive substances. Bidi (tobacco rolled in Diospyrus melanoxylon leaf) is the commonest form of tobacco smoked in India. Studies have shown that bidi smokers face similar risk of hypertension and CHD as cigarette smokers despite the fact that tobacco content is less than a quarter. This may be because of smoking habits- as bidi smoke is required to be inhaled more frequently per minute than a cigarette to keep it burning- as well as reason that bidi may contain yet unidentified toxic substances per unit weight.44

The smoking habit became epidemic with the growth of the cigarette-manufacturing industry. It is thus a recent, widespread and unnatural behaviour, compared to older ones. In the whole population smoking should be reduced in amount and in frequency with the final aim of eliminating the habit completely. Low-tar, low-nicotine cigarettes offer no alternative solution to the abandonment of smoking so far as the heart is concerned. Habits of smoking and use of smokeless tobacco consumption need to be curtailed. The problem of environmental tobacco exposure cannot be underestimated.4 One of the most convincing studies of the harmful effect of passive smoking was conducted in China among non-smoking women with CHD and matched controls. A nearly 2-fold greater odds of CHD among women who were exposed to tobacco at work persisted after adjustment for other risk factors, and a linear trend with the amount of tobacco exposure was observed.45

In both urban and rural subjects in India smoking and tobacco use is widely prevalent. Our studies have shown that 39% urban men26 and 51% rural men35 in Rajasthan either smoked or consumed tobacco in some form. Other Indian epidemiological studies report smoking prevalence in adult men between a low of 10% (rural Punjab)34 to a high of 80% (rural Haryana).31 Smoking rates are significantly lower in women but consumption of tobacco in other forms is highly prevalent.46

Tobacco production which is surrogate for its consumption is increasing at a very high rate in India. According to Economic Survey of India39 (1994-95), tobacco production registered a growth of 2.4% in 1991-92, 5.9% in 1992-93 and 21.3% in 1993-94. The tobacco production was 75.5 thousand tonnes in 1971, 100.2 in 1981, 91.9 in 1986, 115.8 in 1991 and 124.2 in 1993. According to Human Development Report,40 in India tobacco consumption per adult person per year in kg was 0.7 in 1974-76, 0.8 in 1990 and is projected to increase to 0.9 in the year 2000. This is in contrast to established market economies where there is a decline in cardiovascular disease mortality and the tobacco consumption (kg/year) is projected to decline from 2.9 in 1974-76 to 2.2 in 1990 and 1.8 in the year 2000. Epidemiological studies in India confirm that smoking is an independent risk factor for CHD. We reported a multivariate odds ratio of 2.50 (95% confidence interval 1.09-5.73) for smoking and electrocardiographic Q-wave prevalence in rural men,47 and 1.23 (0.79-1.93) in urban men.26 Pais et al reported similar odds for bidi-smoking and CHD risk in a case-control study.48 Smoking is also an independent risk factor for hypertension.49

Tobacco is an important component all CHD prevention and control programs. In India also, the present findings emphasise that tobacco avoidance and cessation must be an important component of CHD prevention strategies.
Table 5: Indian Hypertension Prevalence Studies (BP160/95)50,51
First Author Year Age-Group Place Sample Size Prevalence (%±SE)
Dotto BB 1949 18-50 Calcutta 2500 1.24±0.2
Dubey VD 1954 18-60 Kanpur 2262 4.24±0.4
Sathe RV 1959 20-80 Bombay 4120 3.03±0.3
Mathur KS 1963 20-80 Agra 1634 4.35±0.5
Malhotra SL 1971 20-58 Railways 4232 9.24±0.4
Gupta SP 1978 20-69 Rohtak 2023 6.43±0.5
Dalal PM 1980 20-80 Bombay 5723 15.52±0.5
Sharma BK 1985 20-75 Ludhiana 1008 14.08±1.1
Chadha SL 1990 25-69 Delhi 13134 11.59±1.0
Gupta R 1995 20-80 Jaipur 2212 10.99±0.7
Thakur K 1999 30-80 Chandigarh 1727 13.11±1.0
Shah VV 1959 30-60 Bombay 5996 0.52±0.1
Padmavati S 1959 20-75 Delhi 1052 1.99±0.4
Gupta SP 1977 20-69 Haryana 2045 3.57±0.4
Wasir 1983 20-69 Delhi 905 5.41±0.8
Baldwa VS 1984 21-60 Rajasthan 912 5.59±0.8
Sharma BK 1985 20-75 Punjab 3340 2.63±0.3
Kumar V 1991 21-70 Rajasthan 6840 3.83±0.2
Joshi PP 1993 16-60 Maharashtra 448 4.02±0.9
Chadha SL 1989 25-69 Haryana 1732 3.58±0.5
Jajoo UN 1993 20-69 Maharashtra 4045 3.41±0.3
Gupta R 1994 20-80 Rajasthan 3148 7.08±0.5
Studies that report prevalence of hypertension in Indian populations have been reviewed.50,51 Epidemiological studies to determine blood pressure (BP) norms in Indians were performed in early 40's and 50's using ill-defined methodology. Uniformity was achieved after publication of a WHO report on proper measurement techniques of BP and criteria for diagnosis of hypertension in 1959. 52 Accordingly hypertension was defined as systolic BP >160 mm Hg and/or diastolic BP >95 mm Hg, or those on medical treatment for high BP and most Indian studies used these guidelines (Table 5). In urban populations earlier studies of Dotto (1949)53, Dubey (1954)54 and Sathe (1959)55 showed hypertension prevalence of 1.24%, 4.24% and 3.03% in populations of Calcutta, Kanpur and Bombay respectively. Later studies that also used WHO guidelines have shown a steadily increasing trend in hypertension prevalence. Recent studies from Ludhiana,56 Jaipur57 and Mumbai58 show prevalence of more than 10%. The prevalence of hypertension defined by JNC-V criteria also shows a steep increase from 6.2% in 1959 (Delhi)22 to 30.9% in 1995 (Jaipur)57 and 43.0% in 1999 (Mumbai)59. In rural populations also there is a steady increase in prevalence of hypertension. Padmavati (1959)22 in Delhi reported prevalence of 1.99%, Shah (1959)60 in Bombay reported a prevalence of 0.52% and Gupta (1977)29 in Haryana reported a prevalence of 3.57%.
Table 6: Recent Indian Hypertension Prevalence Studies (BP 140/90)
First Author Year Age-Group Place Sample Size Prevalence (%)
        Men Women Men Women
Gupta R57 1995 20-75 Jaipur 1415 797 29.5 33.5
Gupta PC58 1999 18-60 Mumbai 40067 59522 43.8 44.5
Joseph A64 2000 20-89 Trivandrum 76 130 31.0 41.2
Anand MP65 2000 30-60 Mumbai 1521 141 34.1*  
Mohan V27 2001 20-70 Chennai 518 657 14.0*  
Gupta R28 2002 20-75 Jaipur 550 573 36.4 37.5
Gupta R61 1994 20-75 Rajasthan 1982 1166 23.7 16.9
Malhotra 1999 16-70 Haryana 2559   3.0 5.8#
*Gender-specific data not available. #Prevalence rates based on multiple examinations.
Subsequent studies have shown gradually increasing hypertension prevalence in rural areas of India. Recent studies in North India have reported a higher prevalence of 7.08% in Rajasthan.61 In South India the prevalence has been reported as high as 17.8% in recent years.62 Thus, there has been a significant increase in hypertension prevalence in India since the 1950's. The increase is significantly more in urban subjects than in the rural and is associated with a significant increase in mean systolic BP.

The prevalence of hypertension defined by US Fifth Joint National Committee and World Health Organisation criteria has been reported among some urban Indian populations (Table 6).63 Gupta et al (1995)57 reported hypertension in Jaipur in 30% men and 33% women aged >20 years. Gupta et al (1999)58 reported hypertension in 44% men and 45% women in Mumbai, Joseph et al (2000)64 reported it in 31% men and 41% women in Trivandrum, while Mohan et al (2001)27 reported an age-adjusted prevalence of 14% in Chennai. Gupta et al (2002)28 reported its prevalence in 36% men and 37% women in Jaipur. Anand (2000)65 reported hypertension in 34.1% middle-class executives in Mumbai but after multiple blood pressure measurements it was confirmed in 26.8% male and 27.6% female officers. These findings are in consonance with other regions of Asia where it has been reported that, at any one time, about half of all individuals have high blood pressure.2

Among the rural populations hypertension prevalence using recent criteria was reported by Gupta et al (1994)61 in subjects aged >20 years. Hypertension was present in 24% men and 17% women. Prevalence of hypertension diagnosed on the basis of multiple blood pressure measurements was reported by Malhotra et al (1999)66 who reported it in 3.5% men and 5.8% women in Haryana adults aged 16-70 years; this low prevalence was attributed to very low body-mass index in this population.

Is hypertension prevalence increasing in India? Meta-analysis of previous Indian prevalence studies has shown that there has been a significant increase in hypertension in both urban and rural areas (Tables 5,6). This increase is associated with increasing mean systolic blood pressure levels. These studies were widely distributed in time and the methodologies were different. Observer bias cannot be excluded.

We performed successive cross sectional studies to determine the change in blood pressure levels and hypertension prevalence in Jaipur.28 In 1995, the overall prevalence of hypertension in adults >20 years was 30% in men and 33% in women while in 2002 the age-adjusted prevalence was 30% in men and 34% in women (p=n.s.). These results show that over a short-term of 7 years there is no significant change in hypertension prevalence in an urban Indian population. The mean blood pressure levels also did not change although the blood pressure distribution curves showed increased variance suggesting more severe hypertension.67 Possibly a longer time is needed to effect changes in a given population. Prospective cohort studies within a population are needed to answer these questions as multiple factors are involved in hypertension variation in epidemiological studies. Hypertension increase in India correlates strongly with increasing CHD prevalence (r=0.88) and identifies it as a risk factor of importance.36
The epidemiological studies of cholesterol measurement in India are hampered by lack of uniform assay technique which have resulted in large variation in measured levels. However, cholesterol levels measured by enzyme-based assays have shown an increase as seen in recent studies in urban populations (Table 7).68
Padmavati et al performed a study of dietary fat and serum cholesterol levels among industrial workers aged 18-60 years and in rural subjects aged 10-60 years in Delhi in 1958.22 Cholesterol was measured by the now obsolete chemical iron-reagent method. In subjects <40 years the average serum cholesterol was 168 mg/dl in industrial workers, 180 mg/dl in rural males and 174 mg/dl in rural females. In subjects >40 years the corresponding levels were 169.0, 192.4 and 182.4 mg/dl. In high-income subjects in Delhi mean cholesterol was 220 mg/dl in men <40 years and 256 mg/dl in >40 years. Barrington et al69 measured cholesterol in 279 subjects in South India to determine reference ranges. Mean levels were 185 mg/dl (range 115-255 mg/dl).
Table 7: Cholesterol Levels in India
First Author Year Age-Group Place Sample Size Cholestrol mg/dl
Padmavati S22 1958 10-60 Delhi 197 142.6
Padmavati S22 1959 10-60 Delhi 100 230.4
Barrington H69 1980 20-70 Vellore 279 185.0
Gandhi BM70 1982 20-70 Delhi 200 157.0±29
Vasisth S71 1990 30-70 Delhi 186 198.1±30
Reddy KS72 1992 25-64 Delhi 1581 196.6±37
Gupta R74 1994 20-60 Jaipur 210 191.4±53
Gopinath N73 1994 25-64 Delhi 1345 199.0±39
Gupta R79 1997 20-80 Jaipur 199 175.8±43
Gupta R28 2002 20-80 Jaipur 1123 196.1±42
Padmavati S22 1958 10-60 Delhi 269 179.6
Reddy KS72 1992 25-64 Delhi 302 180.4±30
Gopinath N73 1994 25-64 Haryana 323 177.0±26
Gupta R79 1994 20-80 Rajasthan 300 169.4±39
Gandhi estimated cholesterol lipoproteins in 201 urban Delhi subjects in 1982 using enzyme-based assays.70 The mean serum cholesterol was 157±29 mg/dl, 160±29 in males and 150±25 in females. Vashisth et al reported cholesterol lipoprotein levels in a case-control study of CHD patients in 1990.71 In the control group (n=186) mean cholesterol was 198 mg/dl. Reddy et al studied 1581 urban and 302 rural subjects aged 35-64 years in Delhi in 1992.72 The mean total cholesterol was 196±37 mg/dl in urban and 180+30 mg/dl in rural subjects. Gopinath et al reported lipoprotein cholesterol values in 1345 urban and 323 rural subjects aged 25-64 years in 1994.73 The mean total cholesterol in normal subjects was 199 mg/dl in urban and 177 mg/dl in rural subjects while the corresponding values in CHD patients were 210 mg/dl and 169 mg/dl in urban and rural subjects. Gupta et al reported a mean cholesterol level of 191±53 mg/dl in a cohort of 210 adult men of higher social class in Jaipur.74 In Rajasthan rural men the mean cholesterol was 165.2±37 mg/dl and in urban it was 175.8±43 mg/dl.75

Levels of high density lipoprotein (HDL) cholesterol have been reported in recent studies. Gandhi reported mean HDL cholesterol of 31±11 mg/dl in Delhi subjects in 1982.70 Gopinath et al reported HDL cholesterol of 56±13 mg/dl in urban and 51±9 mg/dl in rural subjects.73 Reddy et al reported higher HDL cholesterol in rural (43.9±7 mg/dl) than in urban subjects (42.7±9 mg/dl).72 Gupta et al reported HDL cholesterol of 44.1±13 in rural and 43.1±12 mg/dl in urban men (p=n.s.).75

Prevalence of dyslipidemias has not been adequately reported from India. Confusion exists about the population norms in absence of prospective studies. We used the US National Cholesterol Education Program guidelines to classify dyslipidemia among men in Rajasthan (rural=202, urban=199).34 High-risk and borderline-high cholesterol >200 mg/dl was in 24.2% and low HDL cholesterol (<35 mg/dl), which was the most prevalent dyslipidemia, in 30%.75 Reddy et al have reported prevalence of hypercholesterolaemia (>200 mg/dl) in industrial, urban and rural populations in Delhi.72 In men the prevalence was 30.9%, 36.8%, and 16.3% and in women it was 21.7%, 39.7% and 16.3% respectively.

The increase in total cholesterol levels in urban Indians is in contrast to declining mean population cholesterol in USA. Secular tends in the age-adjusted mean serum cholesterol levels of adults aged 20-74 years have been reported. In 1962 the mean cholesterol was 217 mg/dl in men and 223 mg/dl in women. It was 214 mg/dl and 216 mg/dl in 1974, 211 mg/dl and 215 mg/dl in 1980 and 206 mg/dl and 208 mg/dl in 1991 for males and females respectively.76 A similar declining trend in mean cholesterol is seen in North American and Western European cohorts of Seven Countries Study.77

On the other hand in many developing countries of Asia, trends similar to India are seen. In China mean cholesterol are 175.2+38 mg/dl with a significant rural urban difference as in India. In Taiwan mean cholesterol levels range from 110 to 180 mg/dl and in Singapore it is 220 mg/dl.78 Increasing population cholesterol levels in India and a rural-urban gradient reiterates its importance in CHD epidemic in India.
The prevalence of non-insulin dependent diabetes mellitus (NIDDM), a strong risk factor for CHD, varies in different geographic regions and in different ethnic groups in India.79 At the turn of the century diabetes was uncommon in India and was present in higher socio-economic groups but it has been realised that Indians and south Asians as an ethnic group have a high risk of developing diabetes.80 The first authentic data on the prevalence of NIDDM in India was a result of a multicentric study conducted by the Indian Council of Medical Research in early seventies and reported a prevalence of 3.0% in urban and 1.3% in rural populations.79 Verma et al reported prevalence of known diabetes as 3.1% in an affluent locality of Delhi. Self reported diabetes was seen in 1.03% urban subjects and 0.19% rural subjects in our studies from Rajasthan.81 Ramachandran et al82 using the WHO criteria found a prevalence of 5% in an urban township in South India. In another study Ramachandran et al found an age-adjusted prevalence of 8.2% in urban populations and 2.4% in rural subjects in South India.82 This study, while showing a wide difference in the prevalence of diabetes in urban and rural populations, also highlighted the fact that diabetes was as common in urban Indians as in emigrant Indians.79 Prevalence of impaired glucose tolerance which may be a precursor of diabetes was equal in urban and rural subjects showing that Indians have a genetic predisposition for diabetes.82 In the Indian national diabetes survey the age-adjusted prevalence of diabetes diagnosed by oral glucose-tolerance test was 13.5% in Chennai, 12.4% in Bangalore, 16.6% in Hyderabad, 11.7% in Calcutta, 9.3% in Mumbai and 11.6% in Delhi.83

Insulin resistance state has been recognized as a risk factor of importance in CHD among South Asians living in Britain.79,84 Features of this syndrome include resistance to insulin-stimulated glucose uptake, central obesity, glucose intolerance, hyperinsulinemia, hypertension, increased VLDL triglyceride, decreased HDL cholesterol, increased IDL and small dense particles in LDL fraction. McKeigue et al84 explained the high incidence of CHD mortality in South Asians settled in Britain on the basis of a greater prevalence of diabetes as compared to the British (20% vs. 5%) and insulin resistance. He noted that mean fasting and post-load insulin levels were higher in South Asians than in Europeans, and the elevated insulin levels were generally associated with components of insulin resistance syndrome. Enas et al85 studied CHD and its risk factors in first-generation immigrant Asian Indians to the USA and reported that age-adjusted prevalence was three times more in Asian men as compared to Framingham Offspring Study (7.2% vs. 2.5%), this was associated with a greater prevalence of diabetes, low HDL cholesterol and hypertriglyceridemia- all components of insulin resistance syndrome. Many smaller studies report a high prevalence of insulin resistance in emigrant South Asians.86

Accompaniments of insulin resistance syndrome, viz., truncal obesity, low HDL cholesterol levels, high triglyceride levels and hypertension, are widely prevalent in India. Reddy et al72 reported high prevalence of truncal obesity (waist hip ratio (WHR); men >0.95, women >0.85) in both urban subjects (men 39.1%, women 70.9%) as well as rural subjects (men 32.4%, women 42.3%) in Delhi. Epidemiological studies in Indian rural men showed that prevalence of CHD was significantly more when WHR was >0.88.35 In urban men and women WHR >0.85 was associated with higher systolic and diastolic BP.87 Pais et al88 performed a case-control study of acute myocardial infarction in Bangalore and found that WHR was an independent coronary risk factor. Serum triglyceride levels, which is part of the insulin resistance syndrome, show a significant increase over the years in Indian urban populations (Table 8). Deepa et al89 determined insulin resistance in selected Chennai urban population using HOMA method. Prevalence of insulin resistance among adults was 11.2%. Mishra et al86 have recently reviewed the epidemiology of insulin resistance syndrome in India. Multiple small studies have reported that the prevalence of insulin resistance varied from 5% to 60% depending on the criteria used. This is more than in other ethnic groups.
Table 8: Triglycerides in Indian Urban Subjects
First Author Year Age-Group Place Sample Size Triglycerides mg/dl
Gandhi BM70 1982 20-70 Delhi 200 124.0±29
Vasisth S71 1990 30-70 Delhi 186 128.1±30
Reddy KS72 1992 25-64 Delhi 1581 110.2±45
Gopinath N73 1994 25-64 Delhi 1345 131.0±54
Gupta R79 1997 20-80 Jaipur 199 126.1±55
Gupta R28 2002 20-80 Jaipur 1123 144.6±70
Metabolic syndrome has recently been defined by the US National Institutes of Health using clinical and biochemical criteria that include truncal obesity, high normal blood pressure, impaired fasting glucose or diabetes, low HDL cholesterol and borderline high triglycerides.90 Using these criteria, in an urban Indian population the age-adjusted prevalence has been reported as 24.9%, 18.4% in men and 30.9% in women.91 This prevalence is comparable to that in developed countries where the prevalence has been reported as about 25%.92 An excess of this syndrome in native Indians needs more studies although it is speculated that this may be a major coronary risk factor in Indians.78,86,91
Lipoprotein(a) consists of an LDL bound by a disulfide bond to apo(a). Apo(a) is a hydrophilic glycoprotein of the plasminogen family. These unique features give Lp(a) potential atherogenic and thrombogenic roles. Serum levels of Lp(a) correlate directly with the presence, extent, severity and lesion score on coronary angiogram, and family history of premature CHD. In a study in Singapore, mean Lp(a) levels were three-fold higher in Asian Indians as compared to Singapore Chinese (20 mg/dl vs. 7 mg/dl).93 The Coronary Artery Disease in Indians Study94 found that Lp(a) levels in Indians were significantly greater than Caucasians. Proportion of persons with Lp(a) >30 mg/dl was 25% in South Asians, 19% in Caucasians and 8% in Mexican Americans. In a case-control study, Bhatnagar et al found that Lp(a) levels were high in South Asians living in Britain as well as in their siblings in Punjab.95 Many small case-control studies have emphasised the importance of Lp(a) in India96 but prospective studies need to be performed.

Small studies of other risk factors for atherosclerosis have been done in India. Case-control studies of genetic influences, antioxidant defense mechanisms, thrombogenic risk factors (fibrinogen), and infections (cytomegalovirus) have been performed. Environmental pollution can influence CHD prevalence. Thus, there is a need for more epidemiological and case-control studies to determine the importance of these and other coronary risk factors.
More than 100 genes have been identified to be important in evolution of atherosclerosis and its complications such as acute coronary syndromes and stroke (Table 9). A large Japanese case-control study recently reported that connexin-37, plasminogen-activator inhibitor type-1, and stromelysin genes may prove reliable in predicting risk of myocardial infarction.97 The European GENECARD sib-pair analysis study reported that classical remediable risk factors (smoking, hypertension, lipid abnormalities, and diabetes) are highly prevalent in familial premature CHD and a major contribution of genes acting in absence of these risk factors was unlikely.98

In India some case-control studies have reported influence of specific genes using a case-control design. No correlation was found for angiotensin converting enzyme genotypes (ACE gene polymorphism),99 methylene tetra-hydro folate reductase (MTHFR) gene,100 or various genes of apolipoprotein E.101 Using mitochondrial genetic analyses technique Roychaudhary et al reported that there was no fundamental dissimilarities among various Indian tribals and other subgroups.102 To determine genetic influence is cumbersome and may not yield positive conclusions in population studies.103 However, larger studies are needed to more specifically determine the genetic influences among Indians and other south Asian groups.
Table 9: Genes and Polymorphisms Implicated in Coronary Heart Disease
Angiotensin converting enzyme Insulin receptor substrate-1
Angiotensin II receptor type I Interleukin-10
Angiotensinogen Interleukin-1a
Apolipoprotein A-1 Interleukin-1b
Apolipoprotein B Interleukin-6
Apolipoprotein C-III Leptin
Apolipoprotein E Lipoprotein lipase
ATP Binding casette transported Low-density lipoprotein receptor related protein
Atrial natriuretic peptide Lp(a) lipoprotein
ANP clearance receptor Manganese superoxide dismutase
B2-adrenergic receptor Matrix Gla protein
B3-adrenergic receptor Metalloproteinase-1 (collagenase)
B-fibrinogen Metalloproteinase-12 (macrophage elastase)
CD14 receptor Methionine synthase
CC chemokine receptor 2 Methylenetetrahydrofolate reductase
Cholesterol ester transfer protein Monocyte chemoattractant protein 1
Coagulation factor V P22
Coagulation factor VII Neuropeptide Y
Coagulation factor XII Paroxanase
Coagulation factor XIII A subunit Platelet endothelial cell adhesion molecule CD31
Connexin 37 Peroxisome proliferator activated receptor a
Endothelial nitric oxide synthase Peroxisome proliferator activated receptor g2
Endothelin-1 Plasminogen activator inhibitor type 1
E-selectin Platelet activating factor acetylhydrolase
Extracellular superoxide dismutase Prothrombin
Fatty-acid binding protein 2 P-selectin
Fractalkine receptor Scavenger receptor B1
Glycoprotein Ia Serotonin receptor 2a
Glycoprotein Iba Stromelysin-1
Glycoprotein IIIa Thrombomodulin
Glycoprotein PC-1 Thrombopoetin
G protein B3 subunit Thrombospondin 1, thrombospondin 4
Hemachromatosis associated protein Tissue factor pathway inhibitor
Hepatic lipase Transforming growth factor b1
Insulin receptor substrate Tumor necrosis factor a
Insulin receptor gene Von Willebrand factor
The study of urban-rural and geographic differences can provide useful information regarding pathogenesis of CHD in an ethnic group.78,104 The prevalence of CHD is low in rural populations of India and has not changed significantly over the years.12 The prevalence is significantly more and increasing in urban Indians. To examine whether there are important risk factor differences in urban as compared with rural populations, some studies have been performed.

In hospital based studies, a higher prevalence of CHD in urban Indians was initially reported in 1950's. Epidemiological studies in Agra,21 Delhi22 and Chandigarh24 in1960s confirmed the high prevalence in urban subjects.12 In a case-control study, Bordia et al (1974),105 determined prevalence of coronary risk factors in urban and rural subjects. In rural subjects smoking was a more important risk factor as compared to urban subjects where sedentary lifestyle, obesity and hypercholesterolaemia were important. Gupta et al (1975),29 Chadha et al (1997),106 Reddy et al (1997),72 and Gupta et al (1997)81 performed comparison of CHD and risk factor prevalence in urban and rural populations of Northern India using similar epidemiological tools (Figure 3). CHD prevalence in urban subject was twice that of the rural. Greater prevalence of major coronary risk factors- sedentary lifestyle, obesity, truncal obesity, hypertension, high cholesterol, low HDL cholesterol, and diabetes was observed in urban subjects in these studies. This has important public health connotation as control of these risk factors could lead to control of the cardiovascular disease epidemic in India.8
Figure 3: Urban-rural differences in coronary risk factor prevalence in Indian men. Data from the Jaipur Heart Watch-1 Study in Rajasthan.79 Similar results have been reported in studies from Haryana and Delhi by Gupta et al, 22 Chadha et al,25 Reddy et al72 and Gopinath et al.73
There in a need to develop models for cardiovascular surveillance in India.107 To be applicable on a large scale these have to be a user friendly, inexpensive and representative of the population being studied. Data must be collected, analysed and used in a regular and systematic way. The interval between the episodes of data collection may vary depending on the different measurements involved and the infrastructure available to conduct surveys. Surveillance involves commitment to data collection on an ongoing basis, as well as the use of data for public health. Four considerations guide the choice of risk factors for inclusion in surveillance activities: (i) the significance of the risk factor for public health in terms of nature and severity of the morbidity, disability and mortality of the non-communicable diseases with which it is associated; (ii) cost of collecting valid data on a long-term and repeated basis; (iii) availability and the strength of evidence that intervening on the risk factor will change it and reduce the non-communicable disease in the community; and (iv) ability to measure the risk factor burden uniformly in different settings to ensure comparability and to measure changes over time.
Table 10: Age-adjusted Coronary Risk Factor Prevalence in an urban Indian
population in the years 1995 (JHW-1) and 2002 (JHW-2)28
Risk Factors Males Females
Smoking/tobacco 548/1415 (38.7) 196/550 (35.6) 149/797 (18.7) 69/573 (12.1)
Leisure-time physical inactivity 1003/1415 (70.9) 338/550 (61.5) 577/797 (72.4) 362/573 (63.2)
Diabetes (History) 15/1415 (1.1) 42/550 (7.6)* 8/797 (1.0) 49/573 (8.6)*
Obesity (BMI >27 Kg/m2) 158/1415 (11.2) 123/550 (22.3)* 105/797 (13.2) 170/573 (29.7)*
Truncal obesity Males >0.9, Females >0.8 128/250 (51.2) 280/550 (50.9) 131193 (67.9) 388/573 (67.8)
Diabetes (History or fasting glucose >125 mg/dl) - 72/550 (13.1) - 65/573 (11.3)
Hypertension (>140/90) 417/1415 (29.5) 165/550 (30.0) 267/797 (33.5) 174/573 (30.3)
Total Cholesterol
High cholesterol >200 mg/dl
49/199 (24.6)
183/532 (34.4)*
22/98 (22.5)
243/559 (43.5)*
LDL cholesterol
High LDL cholesterol >130 mg/dl
44/199 (22.1)
182/532 (34.2)*
28/98 (28.6)
254/559 (45.4)*
HDL cholesterol
Low HDL cholesterol >40 mg/dl
86/199 (43.2)
284/532 (53.4)*
45/98 (45.9)
303/559 (54.2)*
High triglycerides (>150) mg/dl
53/199 (26.6)
163/532 (30.6)*
28/98 (28.6)
160/559 (28.7)*
Numbers in parentheses are percent.
To determine trends of coronary risk factors, as part of cardiovascular risk surveillance, we performed successive surveys in Jaipur urban population, Jaipur Heart Watch-1 in 1993-9426 and Jaipur Heart Watch-2 in 2000-01.28 Subjects aged >20 years in randomly selected municipal blocks using Voters' Lists for enrolment were examined. We obtained details of smoking or tobacco use, physical activity, hypertension, diabetes and dyslipidemias. In the first study 2112 subjects (1415 men, 797 women) were examined. In the second study 1123 subjects (550 men, 573 women) were examined. Age-standardised comparison of coronary risk factors in JHW-1 and JHW-2 is shown in Table 10. The table shows that the prevalence of smoking, leisure-time physical inactivity, truncal obesity, and hypertension have not increased significantly over a period of about eight years. There is a significantly increased prevalence of diabetes (diagnosed by history), obesity, and all the types of dyslipidaemias in both males and females.

These results can not be compared with previous Indian studies. There is no study that has systematically examined changes in multiple coronary risk factors in a similar population over a time period. Ramachandran et al82 reported an increasing prevalence of impaired glucose tolerance and diabetes in Chennai urban residents in south India.

Secular trends in coronary risk factors are available from various cohorts of Seven Countries Study.77 Koga et al reported that in years 1958, 1977 and 1989 in a Japanese rural population there was a significant increase in total cholesterol levels (150+41, 161+32 and 188+37), overweight and obesity (8%, 11%, 18%), and diastolic hypertension (8%, 20%, 13%) while the prevalence of smoking and isolated systolic hypertension declined. In rural and urban Yugoslavian cohorts there was a declining trend in cigarette smoking on one hand and increase in mean levels of systolic blood pressure and cholesterol on the other associated with an increase in consumption of meats, eggs, dairy products, fats and oils and desserts. In urban areas of Greece from 1968 to 1988 there was increase in body-mass index, blood pressure, cholesterol levels and diabetes, but the dietary consumption of vegetables and fruits, olive oil and bread also increased associated with a decline in CVD mortality. On the other hand in developed countries cohorts of the Seven Countries Study in Netherlands, Italy, North America and Finland there has been a decline in CHD mortality associated with a declining trend in smoking, hypertension, and cholesterol levels.77 Increasing population levels of major coronary risk factors in India highlights importance of universally tried and tested measures in controlling the CHD epidemic.38
WHO estimates that death attributable to cardiovascular diseases have increased in parallel with the expanding population in India. Cardiovascular diseases now account for a large proportion of disability adjusted life years lost in India as well as other developing countries.1-4 The CHD rate in India is expected to rise in parallel with the increase in life expectancy secondary to increases in per capita income and declining infant mortality. The average life expectancy has increased from 41 years in the years 1951 to 1961, to 61.4 years in the years 1991 to 1996 and is projected to reach 72 years by 2030, which could lead to large increases in CHD prevalence. By contrast, in the UK and Canada, although the CHD mortality rate of Indians compared with other populations remains high, a decline in CHD have been observed over the past 10 years. These data indicate that the high rates of CHD with economic changes are reversible and perhaps even avoidable. Therefore, lessons learnt from migrant Indians may be helpful in developing prevention strategies for the Indian subcontinent.8,78,80

Because of the importance of cardiovascular disease and CHD in overall mortality statistics in India it is important that a national surveillance program be started. This is all the more important because CHD is a preventable diseases and mortality from acute coronary events can be delayed or even prevented by suitable primary and secondary prevention effort.108 Sadly, the initiative is lacking in India due to a variety of social and economic reasons that are determinants of improper health behaviour among Indians.76 (Table 11).
Table 11: Determinants of Health Behaviour among Indians
Educational status, illiteracy
Family structure, breakdown of traditional family systems
Peer influence, improper guidance
Caste system and social hierarchy
Lack of media awareness
Lack of motivation to change
Periodic workshops for development of strategies to tackle the growing menace of cardiovascular diseases should be organised at national level. Following are the suggested objectives for the meetings:
1 To examine the trends in levels of cardiovascular disease mortality and morbidity in the Indian population and in selected sub-populations. Start from the available data from Registrar General of India database. Find out faults in the data and develop methodology to correct the discrepancies. A lot of effort is already ongoing in this direction. This exercise would help the effort in gathering more data.
2 To describe trends in levels of cardiovascular risk factors. Both behavioural (e.g., diet, exercise and tobacco use) and physiological (e.g., serum lipids, blood pressure, obesity and diabetes) risk factors should be assessed. These trends need to be examined for the population as a whole and also in high-risk groups (urban population, etc.). A lot of existing data needs to be re-examined and validated.
3 To estimate trends in levels of cardiovascular health services, including primary prevention, secondary prevention, and rehabilitation. This would estimate the disparities in health care.
4 To develop effective strategies for cardiovascular prevention programs.
International agencies including the WHO have recommended that a national surveillance system for cardiovascular diseases should be developed.107,109 American National Institutes of Health provides two key issues in development of surveillance programs: (i) provide adequate data to monitor levels and trends in population subgroups, as defined by race/ethnicity, socioeconomic status and geography; and (ii) allow differences within the population in mortality, morbidity, incidence, and risk factor levels to be better understood. Increasing burden of non-communicable disease in South Asia has attracted attention of international policymakers also.4,110
Table 12: Information sources for surveillance
Source Information
Surveys Population based data
Disease registries Incidence and case-fatality
Administrative data Birth, death data
Insurance claims
Medication use, etc.
Aggregate consumption data Per capita consumption and economic activity indicators
Hospital activity data Morbidity and health services indicators
In India there is a serious lack of standardised data for policy makers. There has been no national effort to assess the burden of non-communicable diseases especially cardiovascular diseases in the past. Prevalence studies as reported in the earlier part of this article are sporadic and are not driven by a national policy but are result of efforts by an individual investigator. There is an urgent need for a national surveillance system for determining the extent, burden and trends of different cardiovascular diseases in this country. A system that incorporates practitioners of medicine working with the community at various levels of health-care is suggested. Various information sources for surveillance are shown in Table 12. A serious effort is required in India to collate this sort of data for cardiovascular diseases in different states of the country. This should be done along with the existing national health services framework. Efforts to create a new network are under way but are likely to be more expensive and may not be an immediate solution to the problem. We believe that cardiovascular diseases have been long neglected in this country and unless a serious surveillance and prevention effort is initiated as quickly as possible we shall see more numbers of our young people succumb to this deadly malady.
1. Murray CJL, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet 1997 349:1269-1276
2. Rodgers A, Lawes C, MacMahon S. Reducing the global burden of blood pressure related cardiovascular disease. J Hypertens 2000; 18(Suppl 1):S3-S6
3. Reddy KS. Why is preventive cardiology essential in the Indian context? In: Wasir HS. Editor. Preventive Cardiology: An Introduction. New Delhi. Vikas Publishing. 1991; 1-14
4. Ezzati M, Lopez AD, Rodgers A, Hoorn SV, Murray CJL, and the Comparative Risk Assessment Collaborating Group. Selected major risk factors and global and regional burden of disease. Lancet 2002; 360:1347-1360
5. Omran AR. The epidemiological transition: a theory of the epidemiology of population change. Milbank Mem Fund Q 1971; 49:509-538
6. Gupta R. Epidemiological transition and increase in coronary heart disease in India. South Asian J Prev Cardiol 1997 1:14-22
7. Yusuf S, Reddy KS, Ounpuu S, Anand S. Global burden of cardiovascular diseases: Part I: General considerations, the epidemiological transition, risk factors and impact of urbanisation. Circulation 2001; 104:2746-2753
8. Gupta R, Jain P, Kaul U, Reddy KS, Kumar A. Prevention of coronary heart disease in India: Cardiological Society of India guidelines. South Asian J Prev Cardiol 2001; 5:45-60
9. Marmot MG. Coronary heart disease: rise and fall of a modern epidemic. In Marmot MG, Elliot P. Editors. Coronary heart disease epidemiology. Oxford. Oxford University Press. 1992; 3-19
10. Hegde BM. Angina: an Indian disease. J Assoc Phys India 1999; 47:440-441
11. Gupta R. Ayurveda, cholesterol and coronary heart disease. South Asian J Prev Cardiol 2002; 6:51-75
12. Gupta R. Coronary heart disease epidemiology in India: the past, present and the future. In: Rao GHR, Kakkar VV. Editors. Coronary artery disease in South Asians. New Delhi. Jaypee Brothers. 2001; 6-28
13. Sapru RP. An overview of cardiovascular diseases in India. In Wasir HS. Editor. Preventive Cardiology: An Introduction. New Delhi. Vikas Publishing. 1991; 69-86
14. Mammi MVI, Pavithran K, Rahiman PA, Pisharody R, Sugathan K. Acute myocardial infarction in North Kerala- a 20 year hospital based study. Indian Heart J 1991; 43:93-96
15. Gupta R, Gupta LP. An eight year review of medical diseases in rural Rajasthan. J Assoc Phys India. 1993; 41:711-712
16. Praveen K, Haridas KK, Prabhakaran D, Xavier D, Pais P, Yusuf S for CREATE Registry. Patterns of acute coronary syndromes in India: The CREATE Registry. Indian Heart J 2002; 54:477
17. Canto JG, Zalenski RJ, Ornato JP, et al. Use of emergency medical services in acute myocardial infarction and subsequent quality of care: observations from the National Registry of Myocardial Infarction-2. Circulation 2002: 106:3018-3023
18. Ramana GNV, Sastry JG, Peters D. Health transition in India: Issues and challenges. Natl Med J India 2002; 15(Suppl 1): 37-
19. Gupta R, Gupta VP. Meta-analysis of coronary heart disease prevalence in India. Indian Heart J 1996; 48:241-245
20. Krishnaswamy S. Prevalence of coronary artery disease in India. Indian Heart J 2002; 54:103-104
21. Mathur KS. Environmental factors in coronary heart disease. An epidemiological survey at Agra (India). Circulation 1960; 21:684-689
22. Padmavati S. Epidemiology of cardiovascular disease in India. II. Ischaemic heart disease. Circulation 1962; 25:711-717
23. Rose G, Blackburn H. Cardiovascular survey methods. Geneva. WHO 1962
24. Sarvotham SG, Berry JN. Prevalence of coronary heart disease in an urban population in northern India. Circulation 1968; 37:939-952
25. Chadha SL, Radhakrishnan S, Ramachandran K, Kaul U, Gopinath N. Epidemiological study of coronary heart disease in an urban population of Delhi. Indian J Med Res 1990; 92:424-430
26. Gupta R, Prakash H, Majumdar S, Sharma SC, Gupta VP. Prevalence of coronary heart disease and coronary risk factors in an urban population of Rajasthan. Indian Heart J 1995; 47:331-338
27. Mohan V, Deepa R, Rani SS, Premalatha G. Prevalence of coronary artery disease and its relationship to lipids in a selected population in South India. J Am Coll Cardiol 2001; 38:682-687
28. Gupta R, Gupta VP, Sarna M, et al. Prevalence of coronary heart disease and risk factors in an urban Indian population: Jaipur Heart Watch-2. Indian Heart J 2002: 54:59-66
29. Gupta SP, Malhotra KC. Urban-rural trends in epidemiology of coronary heart disease. J Assoc Phys India 1975; 23:885-892
30. Kutty VR, Balakrishnan KG, Jayasree AK, Thomas J. Prevalence of coronary heart disease in the rural population of Thiruvananthapuram district, Kerala, India. Int J Cardiol 1993; 39:59-70
31. Dewan BD, Malhotra KC, Gupta SP. Epidemiological study of coronary heart disease in rural commuity of Haryana. Indian Heart J 1974; 26:68-78
32. Jajoo UN, Kalalntri SP, Gupta OP, Jain AP, Gupta K. The prevalence of coronary heart disease in the rural population from central India. J Assoc Phys Ind 1988; 36:689-693
33. Chadha SL, Gopinath N, Radhakrishnan S, Ramachandran K, Kaul U, Tandon R. Prevalence of coronary heart disease and its risk factors in a rural community in Haryana. Indian J Comm Med 1989; 14:141-147
34. Wander GS, Khurana SB, Gulati R, et al. Epidemiology of coronary heart disease in a rural Punjab population: prevalence and correlation with various risk factors. Indian Heart J 1994; 46:319-323
35. Gupta R, Gupta VP, Ahluwalia NS. Educational status, coronary heart disease and coronary risk factor prevalence in a rural population of India. BMJ 1994; 309:1332-1336
36. Gupta R, Singhal S. Coronary heart disease in India. Circulation. 1997; 96:3785-3786
37. Rose G. Ancel Keys' Lecture. Circulation 1991; 84:1405-1409
38. WHO Expert Group. Primary prevention of coronary heart disease. EURO Reports 98. WHO Regional Office for Europe. 1984
39. Government of India. Economic Survey 1994-95. Ministry of Finance. New Delhi 1995
40. Technical notes. In: Human Development Report 1993: United Nations Development Report. New York, Oxford University Press. 1993; 100-114;
41. WHO Study Group. Diet, nutrition and prevention of chronic diseases. Technical Report Series 797. Geneva. World Health Organisation 1990; 49-50
42. Gulati VP, Phansalkar SJ. Oilseeds and edible oil economy of India. Delhi. Vikas Publishing House. 1994; 251-284
43. Rastogi P, Mathur B, Rastogi S, Gupta VP, Gupta R. Influence of traditional Indian cooking habits on fatty acid composition of commonly used fats. Indian Heart J 2002; 54:510
44. Pakhale SS, Jayant KM, Bhide SV. Chemical analysis of smoke of Indian cigarettes, bidis and other indigenous forms of smoking: level of volatile phenol, hydrogen cyanide and benzo(a)pyrene. Indian J Chest Dis All Sci 1990; 32:75-81
45. He Y, Lam TH, Li LS, et al. Passive smoking at work as a risk factor for coronary heart disease in Chinese women who have never smoked. BMJ 1994; 308:380-384
46. Gupta PC. Survey of socio-demographic characteristics of tobacco use among 99598 individuals in Bombay, India using handheld computers. Tobacco Control 1996; 5:114-120
47. Gupta R, Prakash H, Gupta VP, Gupta KD. Prevalence and determinants of coronary heart disease in a rural population of India. J Clinical Epidemiology. 1997; 50:203-209
48. Pais P, Fay MP, Yusuf S. Increased risk of acute myocardial infarction associated with beedi and cigarette smoking in Indians: final report on tobacco risks from a case-control study. Indian Heart J 2001; 53:731-735
49. Gupta R, Agarwal VS, Gupta VP, Soangra MR. Correlation of smoking, blood pressure levels and hypertension prevalence in urban and rural subjects. J Assoc Phys India 1997; 45:919-922
50. Gupta R, Al-Odat NA, Gupta VP. Hypertension epidemiology in India. Meta-analysis of fifty-year prevalence rates and blood pressure trends. J Hum Hypertens 1996; 10:465-472
51. Gupta R. Trends in hypertension epidemiology in India. J Indian Med Assoc 2003; 101: in press
52. WHO Expert Group. Hypertension and coronary heart disease. Technical Report Series 168. Geneva. World Health Organisation. 1959
53. Dotto BB. Studies onblood pressure, height, weight, cheat and abdominal measurements of 2500 members of the Calcutta police with short notes on their medical impediments. Indian Med Gazette 1949; 84:238-243
54. Dubey VD. A study of blood pressure amongst industrial workers of Kanpur. J Indian Med Assoc 1954; 23:495-498
55. Sathe RV. Incidence and aetiology of hypertension. J Assoc Phys India 1959; 7:395-400
56. Sharma BK, Arora OP, Bansal BL, Sagar S, Khurana SB. Hypertension among the industrial workers and professional classes in Ludhiana, Punjab. Indian Heart J 1985; 37:380-385
57. Gupta R, Guptha S, Gupta VP, Prakash H. The prevalence and determinants of hypertension in the urban population of Jaipur in western India. J Hypertension. 1995; 13:1193-1200
58. Dalal PM. Hypertension. A report on community survey of casual hypertension in Old Bombay. Sir HN Hospital Research Society, Bombay. 1980
59. Gupta PC, Gupta R. Hypertension prevalence and blood pressure trends among 99,589 subjects in Mumbai, India. Abstract. Indian Heart J 1999; 51:691
60. Shah VV, Kunjannam PV. The incidence of hypertension in liquor permit holders and teetotallers. J Assoc Phys India 1959; 7:243-267
61. Gupta R, Sharma AK. Prevalence of hypertension and sub-types in an Indian rural population. Clinical and electrocardiographic correlates. J Human Hypertens 1994; 8:823-829
62. Gilbert EC, Arnold MJ, Grobbee DE. Hypertension and determinants of blood pressure with special reference to socioeconomic status in a rural south Indian community. J Epidemiol Comm Health 1994; 48:258-261
63. Expert Group. The fifth report of the Joint National Committee on detection, evaluation and treatment of high blood pressure. Arch Intern Med 1993; 153:154-186
64. Joseph A, Kutty VR, Soman CR. High risk for coronary heart disease in Thiruvananthapuram City: a study of serum lipids and other risk factors. Indian Heart J 2000; 52:29-35
65. Anand MP. Prevalence of hypertension amongst Mumbai executives. J Assoc Phys Ind 2000; 48:1200-1201
66. Malhotra P, Kumari S, Kumar R, Sharma BK. Prevalence and determinants of hypertension in an unindustrialised rural population of North India. J Human Hypertens 1999; 13:467-472
67. Gupta R, Sharma AK, Gupta VP, Bhatnagar S, Rastogi S, Deedwania PC. Increased variance in blood pressure and changing hypertension prevalence in an urban Indian population. J Human Hypertens 2003; In press
68. Gupta R. Dyslipidaemia and coronary artery disease in the Indian context. In: Dutta AL. Editor. Cardiology Update-2001. Cardiological Society of India. 2001; 127-139
69. Barrington H, Abraham KA, Hill PG, Kanagasabhapathy AS, Cherian G. Serum lipids and lipoproteins in control subjects and patients with ischaemic heart disease. J Assoc Phys India 1980; 28:217-222
70. Gandhi BM. Lipoprotein composition of normal healthy subjects in northern India. Indian J Med Res 1982; 75:393-401
71. Vashisth S, Narula J, Awtade A, et al. Lipids and lipoproteins in normal controls and clinically documented coronary heart disease. Ann Natl Acad Med Sci 1990; 26:57-66
72. Reddy KS, Shah P, Srivastava U, et al. Coronary heart disease risk factors in an industrial population of north India. Can J Cardiol 1997; 13:26B
73. Gopinath N, Chadha SL, Sehgal A, Shekhawat S, Tandon R. What is desirable lipid profile? Indian Heart J 1994; 46:325-327
74. Gupta R, Gupta KD, Jain BK, Nag AK. Influence of alcohol intake on high density lipoprotein cholesterol in middle aged men. Indian Heart J 1994; 46:145-150
75. Gupta R, Prakash H, Kaul V. Cholesterol lipoproteins, triglycerides, rural-urban difference and prevalence of dyslipidaemia among males in Rajasthan. J Assoc Phys India 1997; 45:275-279
76. Goldberg RJ. Temporal trends and declining mortality rates from coronary heart disease in the United States. In: Ockene IS, Ockene JK. Editors. Prevention of coronary heart disease. Boston. Little Brown 1992; 41-68
77. Toshima H, Koga Y, Blackburn H, Keys A. Lessons for Science from the Seven Countries Study. Tokyo. Springer-Verlag.1994
78. Deedwania P, Gupta R. Prevention of coronary heart disease in Asian populations. In: Wong ND, Black HR, Gardin JM. Preventive Cardiology. New York. McGraw Hill. 2000; 503-516
79. Ramachandran A, Snehalatha C, Viswanathan V. Burden of type-2 diabetes and its complications- the Indian scenario. Curr Science 2002; 83:1471-1476
80. Nishtar S. Prevention of coronary heart disease in South Asia. Lancet 2002; 360:1015-1018
81. Gupta R, Gupta VP. Urban-rural differences in coronary risk factors do not fully explain greater urban coronary heart disease prevalence. J Assoc Phys India 1997; 45:683-686
82. Ramachandran A, Snehalatha C, Latha E, Vijay V, Vishwanathan M. Rising prevalence of NIDDM in urban population in India. Diabetologia 1997; 40:232-237
83. Ramachandran A, Snehalatha C, Kapoor A, et al. High prevalence of diabetes and impaired glucose tolerance in India. National Urban Diabetes Survey. Diabetologia 2001; 44:1094-1101
84. 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
85. Enas EA, Garg A, Davidson MA, et al. Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the USA. Indian Heart J 1996; 48:343-354
86. Misra A, Vikram NK. Insulin resistance syndrome (metabolic syndrome) and Asian Indians. Curr Science 2002; 83:1483-1496
87. Gupta R, Mehrishi S. Blood pressure and waist-hip ratio correlation in an urban Indian population. J Indian Med Assoc 1997; 95:412-415
88. Pais P, Pogue J, Gerstein H, et al. Risk factors for acute myocardial infarction in Indians: a case-control study. Lancet 1996; 348:358-363
89. Deepa R, Shantirani CS, Premalatha G, Sastry NG, Mohan V. Prevalence of insulin resistance syndrome in a selected south Indian population. Indian J Med Res 2002; 115:118-127
90. National Cholesterol Education Program. Executive summary of the third report of the Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel-III). JAMA 2001; 285:2486-2497
91. Gupta R, Deedwania PC, Gupta A, Rastogi S, Panwar RB, Kothari K. Prevalence of metabolic syndrome in an urban Indian population. Int J Cardiol 2003: In press
92. Ford ES, Giles WH, Dietz WH. Prevalence of metabolic syndrome among US adults: findings from the Third National Health and Nutrition Examination Survey. JAMA 2002; 287:356-359
93. Hughes K, Aw TC, Kuperan P, Choo M. Central obesity, insulin resistance, syndrome X, lipoprotein(a) and cardiovascular risk in Indians, Malays and Chinese in Singapore. J Epidemiol Comm Health 1997; 51:394-399
94. Enas EA, Dhawan J, Petkar S. Coronary artery disease in Asian Indians: lessons learnt so far and the role of Lp(a). Indian Heart J 1997; 49:25-34
95. Bhatnagar D, Anand IS, Durrington PN, et al. Coronary risk factors in people from the Indian subcontinent living in West London and their siblings in India. Lancet 1995; 345:405-409
96. Gupta R, Kastia S, Rastogi S, Kaul V, Nagar R, Enas EA. Lipoprotein (a) in coronary heart disease: a case-control study. Indian Heart J 2000; 52: 407-410
97. Yamada Y, izawa H, Ichihara S, et al. Prediction of the risk of myocardial infarction from polymorphisms in candidate genes. N Engl J Med 2002; 347:1916-1923
98. Jomini V, Oppliger-Pasquali S, Wietlisbach V, et al. Contribution of major cardiovascular risk factors to familial premature coronary artery disease: the GENECARD project. J Am Coll Cardiol 2002; 40:676-684
99. Joseph A, Nair KG, Ashavaid TF. Angiotensin converting enzyme gene polymorphism in coronary artery disease: the Indian scenario. Clin Chem Lab Med 1998; 36:621-624
100. Mukherjee M, Joshi S, Bagadi S, Dalvi M, Rao A, Shetty KR. A low prevalence of the C677T mutation in the methylene tetrahydrofolate reductase gene in Asian Indians. Clin Genet 2002; 61:155-159
101. Misra A, Nishanth S, Pasha ST, Pandey RM, Sethi P, Rawat DS. Relationship of Xba1 and EcoR1 polymorphisms of apolipoprotein-B gene to dyslipidemia and obesity in Asian Indians in north India. Indian Heart J 2001; 53:177-183
102. Roychoudhury S, Roy S, Dey B, et al. Fundamental genomic unity of ethnic India is revealed by analysis of mitochondrial DNA. Curr Science 2000; 79:1182-1192
103. Khoury MJ, McCabe LL, McCabe ERB. Population screening in the age of genomic medicine. N Engl J Med 2003; 348:50-58
104. Yusuf S, Reddy KS, Ounpuu S, Anand S. Global burden of cardiovascular diseases: Part II: Variations in cardiovascular disease by specific ethnic groups and geographic regions and prevention strategies. Circulation 2001; 104:2855-2864
105. Bordia A, Arora SK. A comparative study of predisposing factors of coronary artery disease in rural and urban population. Indian J Med Res; 1974; 62:565-572
106. Chadha SL, Gopinath N, Shekhawat S. Urban-rural differences in prevalence of coronary heart disease and its risk factors in Delhi. Bulletin WHO; 1997; 75:31-38
107. Bonita R, de Courten M, Dwyer T, et al. The WHO stepwise approach to surveillance (STEPS) of NCD risk factors. Geneva. World Health Organisation, 2001
108. Pearson TA, Blair SN, Daniels SR, et al. AHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 update. Circulation 2002; 106:388-391
109. Cooper R, Cutler J, Desvigne-Nickens P, et al. Trends and disparities in coronary heart disesae, stroke, and other cardiovascular diseases in the Unites States. Findings of the national conference on cardiovascular disease prevention. Circulation 2000; 102:3137-3147
110. Dare L. WHO and the challenges of the next decade. Lancet 2003; 361:170-171