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(Circulation. 2001;104:2855.)
© 2001 American Heart Association, Inc.

Clinical Cardiology: New Frontiers

Global Burden of Cardiovascular Diseases

Part II: Variations in Cardiovascular Disease by Specific Ethnic Groups and Geographic Regions and Prevention Strategies

Salim Yusuf, FRCP, DPhil; Srinath Reddy, MD; Stephanie Ôunpuu, PhD; Sonia Anand, FRCP(C), MSc

From the Population Health Research Institute and Division of Cardiology (S.Y., S.O., S.A.), McMaster University, Hamilton, Ontario, Canada; and the All India Institute of Medical Sciences (S.R.), New Delhi, India.

Correspondence to Salim Yusuf, Population Health Research Institute and Division of Cardiology, 2nd Floor, McMaster Clinic, Hamilton General Hospital, 237 Barton Street East, Hamilton, ON L8L 2X2, Canada. E-mail yusufs{at}mcmaster.ca

	Abstract

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
This two-part article provides an overview of the global burden of atherothrombotic cardiovascular disease. Part I initially discusses the epidemiological transition which has resulted in a decrease in deaths in childhood due to infections, with a concomitant increase in cardiovascular and other chronic diseases; and then provides estimates of the burden of cardiovascular (CV) diseases with specific focus on the developing countries. Next, we summarize key information on risk factors for cardiovascular disease (CVD) and indicate that their importance may have been underestimated. Then, we describe overarching factors influencing variations in CVD by ethnicity and region and the influence of urbanization. Part II of this article describes the burden of CV disease by specific region or ethnic group, the risk factors of importance, and possible strategies for prevention.

Key Words: heart diseases • epidemiology • prevention

	Introduction

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
This second part of our article describes ethnic and regional variations in cardiovascular (CV) risk factors and disease and illustrates some of the changing rates for cardiovascular disease (CVD) in several countries. It also emphasizes the preventive strategies for CVD that have been used most successfully in developed countries and could be of potential value in preventing or reversing the rise in developing countries. We conclude with some recommendations for prevention that are likely to be of relevance globally.

	European Origin

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
People of European origin include those who originate from diverse backgrounds in Northern Europe (Nordic countries), Western Europe (eg, United Kingdom and France), Southern Europe (eg, Spain and Italy), and Eastern Europe (eg, Poland and Ukraine).

Disease Burden
Differences in the Age-Standardized Mortality Rates (ASMR) vary widely between European populations. Data from the World Health Organization (WHO) indicate that the cardiovascular disease mortality rate is 6-fold higher among men and women in the Russian Federation compared with people in France. In 1996, the ASMR for coronary heart disease (CHD) among males in the Russian Federation was 390/100 000 compared with 60/100 000 among males in France.¹ The cerebrovascular disease (CBVD) ASMR was 244/100 000 among males in the Russian Federation compared with 40/100 000 in France.¹ Although the CVD mortality rates are much lower among women compared with men, similar variations among women between countries also exist. Eastern European countries such as the Ukraine, the Russian Federation, Hungary, and the Czech Republic have among the highest and increasing CVD rates in the world, which is in marked contrast to most economically stable European countries where declines in CVD mortality rates have been experienced over the past 30 years.

Risk Factors
CVD among European populations is mainly attributable to classical risk factors, namely diets high in saturated fats, elevated serum cholesterol and blood pressure (BP), diabetes, and smoking. The epidemic of CVD in Eastern European countries is partly related to high levels of smoking and excessive alcohol use (causing strokes) along with diets high in saturated fat² and poor social conditions. Research to explain why the Italian and French populations remain relatively protected from CHD has yielded numerous hypotheses. It is believed that the high consumption of monounsaturated fats such as olive oil and antioxidants may be responsible for the low rates of CHD in Italy. In France, the CHD mortality rate remains very low.³ Although this relative protection from CHD has been attributed to high consumption of alcohol, and in particular wine,⁴ others believe the lower rate of CHD mortality may simply be due to a time-lag between increases in consumption of animal fat and elevations in serum cholesterol concentrations (which have occurred only recently) and the expected increase in mortality.⁵

Prevention
In Finland, which had one of the highest rates of CHD mortality in the 1960s and 1970s, an impressive 55% reduction in CHD mortality and stroke was observed between 1972 to 1992. About three quarters of this decline in CHD mortality can be explained by a lowering of serum cholesterol by 13% (0.88 mmol/L) in men and by 18% (1.18 mmol/L) in women, reductions in diastolic BP by 9% (8.6 mm Hg) in men and by 13% (12.2 mm Hg) in women, and a significant reduction in smoking rates (by 30% in men).⁶ Similar declines have been documented in several Western countries and is partially attributable to improved primary and secondary prevention as well as improved medical and surgical management in patients with established coronary disease.⁷ The declines in CHD have also paralleled changes in human behavior (regarding food, activity, etc.) that accompany changes in the economy from one that is predominantly based on manufacturing and extractive industry to one based on high technology and services.^8,9 In Poland, during the 1990s about a 25% decrease in CHD deaths in early middle age was observed, which has been attributed in a large part to a marked decrease in animal fats and increase in vegetable fats consumption.¹⁰ By contrast, a marked increase in death rates from CVD, accidents, violence, and infectious diseases has been observed in Russia¹¹ over a relatively short period of time and is thought to be due to socioeconomic upheaval. This illustrates the regressive stage (Stage V) of the epidemiological transition. Moreover, the rapidity with which CV diseases rise (as in Russia) or fall (as in Poland) indicate that societal factors can have a substantial and rapid impact on disease rates.

	Japanese

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Disease Burden
In parallel with a rise in economic prosperity, CVD rates in Japan have declined more markedly than those of western countries, and the life expectancy in Japan is among the highest in the world. Mortality rates from CHD have traditionally been much lower in Japan than in western countries.¹ In Japan, the ASMR for CHD in males is 43/100 000 and in females is 22/100 000, which is one-fourth the rate of CHD in North America, and for CBVD is 72/100 000 and 46/100 000 among males and females, respectively.¹ This pattern of higher CBVD compared with CHD among Japanese differs from western populations.¹²

Risk Factors
Hypertension is the most important CVD risk factor among Japanese, more so than cholesterol and cigarette smoking. The Hisayama prospective population–based study showed a decline in BP level from 1961 to 1987,¹³ likely due to improved diagnosis and treatment of hypertension. This has been accompanied by a marked decline in stroke mortality. Low serum cholesterol related to a diet low in saturated fat and cholesterol is also likely responsible for the low rates of CHD mortality observed in the Japanese. The prevalence of non–insulin dependent diabetes mellitus (NIDDM) in Japanese males (13%) and females (9%) is higher than the rates in most western countries.¹⁴ During 1961 to 1987, with westernisation there was a 2- to 3-fold increase in glucose intolerance, NIDDM, obesity, and hypercholesterolemia (the mean cholesterol is only 10% lower than in the US in 1989).^15,16 It is possible that as cholesterol and glucose levels rise, the impact of the high cigarette smoking on increased CVD rates may become manifest.

Prevention
With increasing adoption of western lifestyles in Japan, the rates of CHD risk factors could approach those of Americans. Although the prevalence of smoking among men decreased from 80% in 1961 to 50% in the mid 1980s, it remains high among males.¹⁶ Combined with increasing rates of elevated cholesterol and obesity, Japan may soon experience a significant epidemic of CHD after a lag of a few years. Therefore, maintenance of a low fat diet and avoidance of obesity through both decreased energy intake and regular physical activity will likely prevent the development of glucose intolerance, elevated cholesterol, and hypertension. Furthermore, avoidance of cigarette smoking is also critical in preventing a future increase in CHD in Japan.

	Chinese

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Disease Burden
Death rates from CVD (particularly CHD) have been increasing in China in recent decades.¹⁶ Although the CVD mortality rate in China is approximately the same as that in the US, the CHD mortality rates are approximately 50% lower than the rates observed in most western countries, and the CBVD rate is significantly higher. In 1996, in urban China, the ASMR for CHD for men and women aged 35 to 74 was 100/100 000 in men and was 69/100 000 in women.¹⁷ However, the ASMR for CBVD in men and women aged 35 to 74 was 251/100 00 in men and 170/100 000 in women.¹⁷ Intracerebral hemorrhage occurs between 2 and 3 times more frequently in the Chinese than in white Caucasians. Only 6% to 12% of strokes in European populations are reported as intracerebral hemorrhages compared with 25% to 30% of hemorrhagic strokes in Chinese.¹⁸

Risk Factors
A case-control study from Hong Kong of acute myocardial infarction (AMI) sufferers indicates that conventional risk factors (eg, cigarette smoking, hypertension, or diabetes) are important.¹⁹ Although the mean serum cholesterol among Chinese is low (mean 4.2 mmol/L at baseline) by western standards, serum cholesterol was directly related (continuous relationship) to CHD mortality even at relatively low levels.²⁰ Cigarette smoking is highly prevalent among Chinese males (over 60%) and increasing.²¹

Geographic Variations
The CHD mortality rate is higher in northern China (Beijing) than in southern China (Shanghai and Guangzhou) and higher in urban than rural areas,^22,23 yet surprisingly the stroke rates only differ modestly between urban and rural areas. The prevalence of hypertension, mean levels of serum cholesterol, and body mass index (BMI) were all lower in the south compared with the north and in rural compared with urban areas.

Migrant Patterns
The prevalence of CHD by ECG was 6 times greater among Chinese migrants to Mauritius (24%) than in Beijing, China (4%),²⁴ with higher cholesterol levels among Mauritius Chinese (5.4 mmol/L) than in Beijing (4.3 mmol/L), whereas the prevalence of hypertension and smoking was greater in Beijing.²⁴ Therefore, although the prevalence of hypertension and smoking may decline with migration, the rates of obesity, late onset diabetes, elevated serum cholesterol, and CHD increase. In Canada, Chinese exhibit markedly lower rates of CHD compared with other groups and yet have low and similar rates of CBVD compared with South Asians or Europeans (Figure 1).²⁵ Given that Canada has the second lowest rate of strokes in the world, these data indicate that marked declines in stroke rates can occur among Chinese without a concomitant increase in CHD. The low rates of risk factors among Chinese in Canada are accompanied by low rates of atherosclerosis and CHD.²⁵ These data also suggest that if risk factor levels rise among Chinese to levels that are similar to Europeans, the rates of CHD may become similar.

View larger version (34K): [in this window] [in a new window]   Figure 1. Variations in the rates of cardiovascular disease (CHD) between ethnic groups in Canada.25 Note the high rates of CHD among Canadians of European and South Asian descent compared with the markedly low rates among Chinese. The rates of cerebrovascular disease are low and similar in all 3 ethnic groups. By contrast, cancer death rates are lowest among South Asians and highest among Europeans, with Chinese exhibiting intermediate rates. This apparent dissociation of CHD and cancer rates is surprising because several of the common causes of heart disease and common cancers tend to be the same (eg, tobacco use or obesity).

Prevention
Economic development in China is accompanied by increased prevalence of conventional CVD risk factors,²⁶ which could lead to higher CHD rates in the future. Prevention strategies should target an approach that includes tobacco avoidance/cessation, maintenance of a "traditional Chinese" diet (high consumption of vegetables and low consumption of animal fats) to prevent obesity, diabetes, elevated serum cholesterol, and elevated BP.

	South Asians

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South Asian (SA) refers to people who originate from India, Sri Lanka, Bangladesh, Nepal, and Pakistan.

Disease Burden
There are relatively few mortality studies from India, as there is no uniform completion of death certificates and no centralized death registry for CVD.²⁷ However, the WHO and the World Bank estimate that deaths attributable to CVD have increased in parallel with the expanding population in India, and that CVD now accounts for a large proportion of disability adjusted life years (DALY) lost.²⁸ Of all deaths in 1990, approximately 25% were attributable to CVD, compared with 10% from diarrheal diseases, 13% from respiratory infections, and 8% from tuberculosis.²⁸ SA migrants to the United Kingdom, South Africa, Singapore, and North America experience 1.5 to 4.0 times higher CHD mortality compared with indigenous populations).²⁹

Temporal Trends
In India, the CHD rate 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 CVD prevalence.³⁰ By contrast, in the UK and Canada, although the CHD mortality rate of SAs compared with other populations remains high, a decline in CHD rates has been observed over the past 10 years.^31,25 These data indicate that the high rates of CHD with economic changes are reversible and perhaps even avoidable. Therefore, lessons learnt from migrant SAs may be helpful in developing prevention strategies for the Indian subcontinent.

Risk Factors
Compared with Europeans, SAs (in the UK and Canada) do not display high rates of smoking, hypertension, or elevated cholesterol but still have higher rates of CHD.^25,32,33 However, smoking, hypertension, and diabetes are strongly associated with CHD among SAs.³⁴ SAs in the UK and Canada suffer a high prevalence of impaired glucose tolerance (IGT), central obesity, elevated triglycerides, and low HDL cholesterol,^32,35 and NIDDM at rates 4 to 5 times higher than in Europeans (19% versus 4% by age 55 years).^33,35 High rates of diabetes has been reported among SAs in the UK (10% to 19%), Trinidad (21%), Fiji (25%), South Africa (22%), Mauritius (20%), and Canada (10%).^36,32 By contrast, the prevalence of diabetes in rural India is 2% to 3% and approximately 8% in urban areas.³⁷ In addition, there is increasing evidence that elevations in blood glucose even in the nondiabetic range increases CHD risk among SAs.³⁴ SAs have elevated levels of Lp(a), a lipoprotein which is genetically mediated and associated with increased atherosclerosis, thrombogenesis, and clinical events.^32,38 Recent studies have confirmed that SAs also have higher levels of homocysteine, fibrinogen, and plasminogen activator inhibitor (PAI-1),³² all of which could increase the risk for thrombosis. Although the degree of subclinical atherosclerosis is related to clinical events, it appears that SAs have a higher propensity for clinical events compared with Europeans or Chinese, even after adjusting for all known risk factors and the degree of atherosclerosis³² (Figure 2). This probably suggests the potential for greater plaque rupture and thrombotic events among SAs.

View larger version (15K): [in this window] [in a new window]   Figure 2. Prevalence of CVD for specific degrees of carotid atherosclerosis. Note that the prevalence of CVD increases with increasing carotid atherosclerosis in each ethnic group. However, it appears that South Asians (SA) have more CVD compared with Chinese (CH) and Europeans (EU) for the same degree of atherosclerosis. Reproduced with permission from Reference 32.

Geographic Variations
Marked increases in both CHD prevalence and risk factors is observed in urban India compared with rural settings.³⁹ A recent overview of prevalence surveys conducted over 2 decades in India reported a 9-fold increase of CHD in urban centers, compared with a 2-fold increase in CHD rates among rural populations.³⁹ This increase in CHD rates in urban areas is associated with an increase in the prevalence of lipid and glucose abnormalities as well as hypertension and obesity. By contrast, the rates of tobacco smoking are higher in rural compared with urban populations. (Although these studies used somewhat different methods of sampling and varying definitions for CHD, collectively, they suggest that there is likely a real increase in CHD; however, the magnitude of the increase remains uncertain).

Migration Patterns
SAs in the UK have higher risk factor levels compared with their siblings living in India (BMI, 27 versus 23 kg/m²; systolic BP, 144 versus 137 mm Hg; total cholesterol, 6.3 versus 5.0 mmol/L; lower HDL cholesterol, 1.14 versus 1.27 mmol/L; and higher fasting glucose, 5.4 versus 4.6 mmol/L).⁴⁰ Therefore, adverse changes in CVD risk factors and disease rates are observed when South Asians adopt an urban lifestyle whether they live in India or abroad.

	Hispanics

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The term Hispanic includes Americans of Cuban, Mexican, and Puerto Rican descent. There are approximately 35.3 million Mexican-Americans living in the US, and they comprise approximately 12.5% of the US population.⁴¹ CVD is the leading cause of death among Hispanic males (28%) and females (34%).⁴¹ Although earlier studies suggested that the age-adjusted mortality rates for major CVD among Mexican-Americans (28.8 and 26.6 per 100 000 men and women, respectively) were lower than those of African-Americans (40.5 and 39.6, respectively) and whites (30.0 and 23.8 per 100 000),⁴² recent data from the Corpus Christi Heart Project, reported a greater incidence of myocardial infarction (MI) in Mexican-Americans compared with non-Hispanic whites.⁴³ The age-adjusted MI incidence was higher by 1.25 and 1.52 among Mexican-American men and women compared with non-Hispanic whites,⁴⁴ with greater MI case-fatality rate among Mexican-Americans than non-Hispanic whites.

Under the age of 60 years, Hispanics have a significantly elevated CBVD death rate compared with non-Hispanic whites (32 versus 19 and 23 versus 18 per 100 000 in men and women, respectively). However, in older age categories the CBVD rate in Hispanics is substantially lower than whites (589 versus 765 and 535 versus 847, respectively).⁴⁵ Although declines in CHD and CBVD mortality have occurred in Mexican-Americans over the past 20 years, this decline has been less than that which has occurred among non-Hispanic whites.⁴⁴

Risk Factors
Mexican Americans suffer a high prevalence of conventional CVD risk factors such as smoking (42.5% in men and 23.8% in women), hypertension (17% and 14%, respectively), low HDL cholesterol (<0.90 mmol/L: 15.2% men, 5% women), elevated cholesterol (total cholesterol 6.2 mmol/L: 16.6% men and 16.5% women), diabetes (24%), physical inactivity (39%), and obesity (BMI>85th percentile, 30% men, 39% women).^46,47

Prevention
Programs to decrease obesity and promote physical activity are needed to reduce the rate of glucose intolerance in this group. Furthermore, Mexican-Americans are less likely to receive treatment for diabetes, hypercholesterolemia, and hypertension compared with non-Hispanic whites.⁴⁸

	Aboriginal Populations

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The rates of chronic degenerative diseases such as CVD, diabetes, cancer, and mental illness are increasing among Aboriginal peoples. These trends parallel the epidemiological transition that is occurring in other developing populations throughout the world.

Disease Burden
Mortality rates for CVD among aboriginal populations had been reported to be lower than people of European ancestry; however, CHD is the leading cause of death in North American Indians and Alaskan Natives.⁴¹ The Strong Heart Study,⁴⁹ which was initiated in 1988, studied 4549 American Natives aged 45 to 74 years from 13 tribes in the Southern US. The prevalence estimates of definite MI in those aged 45 to 74 years was 2.8% in men without diabetes and 5.3% in men with diabetes, and 0.4% in women without diabetes and 1.4% in women with diabetes. In the US, the CBVD mortality rates under the age of 65 years is similar in Native Americans and white Americans, and substantially lower than rates in African Americans.⁵⁰

In Canada, CVD is the leading cause of death among Aboriginal peoples.⁵¹ Although the CHD mortality rates among Aboriginal and Canadian males are similar, the CHD mortality among Aboriginal women is 61% higher compared with Canadian women. In addition, the stroke mortality rate is 44% and 93% higher among Aboriginal men and women, respectively, compared with the general Canadian population.⁵² However, all the above data are based on studies conducted 10 or more years ago. A recent prevalence study in Canada indicates a 2.5-fold higher rate of CVD among aboriginal peoples compared with Canadians of European origin.⁵³

Temporal Trends
As more Aboriginal people give up their traditional lifestyles and adopt "urban" lifestyles, the prevalence of CVD and its risk factors will likely increase. Comparing Canadian data from 1979 to 1983 to data from 1984 to 1985 reveals a 25% decline in CHD among Native men, but a 5% increase among Native women.⁵² In the US, the age-adjusted rates of CBVD mortality declined by about 20% between 1980 and 1990 in Native Americans, which is similar to the 26% decline in white Americans.⁵⁰

Risk Factors
The common CHD risk factors among Aboriginal men and women include diabetes, obesity, and low HDL-cholesterol. The prevalence of cigarette smoking is high, with wide variations between reserves.⁵⁴ The prevalence of diabetes in the Strong Heart Study was 48% in the group aged 45 to 64 years compared with approximately 5.5% in the US general population. The prevalence of obesity ranged from 26% to 41%, with an average BMI of 31 and waist-hip ratio of 0.97 in men. By contrast, the prevalence of hypertension and elevated cholesterol among Natives appears to be lower than the general US population.

In a Canadian study, Aboriginal people had a higher prevalence of CVD, atherosclerosis, glucose abnormalities, obesity, and poverty compared with European Canadians. There is a clear inverse relationship between higher incomes and lower rates of risk factors and CVD. However, at each income level, aboriginals had higher risk factors and CVD compared with European Canadians.⁵³

Geographic Variations
There are important regional and intertribal differences in CVD risk factors and disease rates,^49,50,54 but most of the current data on CVD have come from Natives living on reserves, and little is known about the risk factor profiles among city-dwelling Natives. There are only very limited data regarding CVD among Aboriginal populations outside North America. One study in Chile, among the Mapuche Indians indicated substantially lower rates of obesity, diabetes, hypertension, or hyperlipidemia compared with the North American Aboriginal populations.⁵⁵

Prevention
In order to develop strategies for prevention of CVD in Aboriginal populations, more research is required relating psychosocial factors with CVD. There are higher rates of poverty, social isolation, hopelessness, and lack of empowerment, and addressing these issues is key to a culturally sensitive and effective prevention strategy.

	Blacks of African Origin

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CVD rates among blacks in Africa are relatively low when compared with the rates in most western countries. However, among blacks in the US, the rates of CVD are comparable or higher than the rates among whites in the US.

Africa
Disease Burden
CVD mortality data from countries in the Sub-Saharan African region (SSA) are limited, as only 1.1% of all deaths are registered with a central agency.²⁸ Data from other sources such as sample-registries and small-scale population studies indicate that the burden from CHD in 1990 was 4.5 million DALY, and that the CHD mortality was 41/100 000.²⁸ These rates are considerably lower than those of whites who live in Africa, as well as the rates in most western countries, which are on average 4 to 5 times higher.²⁸ Even so, in SSA, the proportional mortality rate from CVD accounts for 10% of all deaths, and CHD accounts for 3% of all deaths.²⁸ Furthermore, the CHD case-fatality rates may be higher in SSA compared with western countries perhaps due to the limited access to health care.

Risk Factors
The prevalence of most conventional risk factors for CHD, with the exception of hypertension (and perhaps smoking among urban areas), is lower among blacks compared with other groups within Africa, and the world.^56,57 Among Tanzanians (35 to 64 years), the prevalence of smoking was 37% among men and 4% among women, the mean BMI was 21 and 22, the mean blood pressure was 126/79 and 125/79 mm Hg, and the mean serum cholesterol was 4.1 and 4.3 mmol/L in men and women, respectively.⁵⁷ When compared with other developing and developed countries, the Tanzanian risk factor profile was more favorable, with the exception of smoking among men. Furthermore, the prevalence of multiple risk factors for CHD was low, as 65% of the population has no identifiable risk factors, 30% had a single risk factor, and only 5% had at least two risk factors, compared with 50%, 40%, and 10%, respectively, in the US.⁵⁷

Geographic Variations
In most urban and virtually all rural regions of SSA, the prevalence of traditional CVD risk factors among blacks is low. However, with urbanization, an increase in conventional cardiovascular risk factors and CHD rates is anticipated.⁵⁸ In South Africa, the rapid migration of blacks to urban centers has led to increased poverty, obesity, hypertension, and elevated cholesterol. This pattern of increasing risk factors with higher rates of urbanization is likely to affect most of SSA.

Prevention
Lessons learned from other regions in the world should be used to develop an aggressive strategy of primordial prevention. This could include control of cigarette smoking by increasing the price of cigarettes and anti-tobacco campaigns, promoting traditional dietary patterns, reducing salt consumption and BP, and promoting regular physical activity, especially among urban populations.

West Indies
Disease Burden
In Trinidad, data from 1989 reveal that the age-adjusted incidence of CHD in people of African origin was 6.8 and 5.4 per 1000 person years among men and women, respectively. The rates among black men approximated those of European descent (6.8 versus 6.5/1000 person years at risk), whereas the rates among black women were higher (5.4 versus 2.9/1000).⁵⁹

Risk Factors
The most prevalent and influential risk factor is hypertension. In Trinidad, the prevalence of hypertension was 33%, diabetes 8.1%, and smoking 39%.⁵⁹ The mean HDL cholesterol was 1.03 and 1.30 mmol/L; the mean LDL cholesterol was 4.04 and 4.11 mmol/L in men and women, respectively.

United States
African-Americans are the largest nonwhite population in the US and represent 12.9% of the population.

Disease Burden
CVD is the leading cause of death among African-Americans. Although the CHD mortality rate in African-American men is similar to that among white men (224 versus 236/100 000), it is higher among African-American women (160 versus 140/100 000).⁴¹ Sudden cardiac death is more common among African-Americans.⁶⁰ In addition, the CBVD mortality rate is substantially higher among African American men (89 versus 62/100 000) and women (76 versus 58/100 000) compared with whites.⁴¹

Temporal Trends
Since the 1960s, CV mortality has been declining among Americans of all races.^61,62 However, since the mid 1970s, the rate of decline has slowed down among African Americans,^58,63 leading to a widening disparity in CVD death rates between blacks and whites.

Geographical Variations
Early investigators noted high stroke mortality rates among black Americans in the southeastern coastal states. By late 1980s, this "stroke belt" had dissipated in the south eastern coastal areas and shifted to the Midwest regions of the Mississippi and Ohio river valleys.⁶⁴ CHD mortality has shown a similar westward shift to the so called coronary valley.⁶⁵ The increased CVD mortality among blacks has been mainly confined to the southern states (Mississippi River valley). Although changes in regional profile of risk factors, local environment, and migration pattern may have played a role, recent economic shifts in these areas may be the principal reason for changes in disease rates.⁶⁴ Whereas southeastern coastal areas have undergone considerable economic development, the more westwardly regions have not kept pace.⁶⁵ In Mississippi, one of the most economically and educationally disadvantaged US states, CVD mortality has risen among African Americans over the past two decades while among whites there has been a decline.⁶⁶ Similar patterns are also observed in the Northeast and the Midwest.⁶⁷

Risk Factors
Compared with whites, African-Americans develop hypertension at an earlier age. The reason for black-white differences in hypertension prevalence likely involves a complex interaction between environmental response to diet, stress, and a potential genetic/physiological difference in sodium/potassium excretion. Serum cholesterol levels are similar among African-Americans compared with white Americans, but the former group has higher HDL cholesterol levels, despite having more diabetes. Cigarette smoking rates are similar among African-Americans compared with whites (eg, 32.3% of men, 22.3% of women versus 27.3% of men and 23.9% of women). Obesity is an emerging problem especially in women, with approximately 21% of African-American men and 38% of women having a BMI >30, compared with 21% and 23% of white American men and women, respectively. Approximately 33% of African-American men and 43% of women report no leisure time physical activity compared with 25% and 28% among white American men and women, respectively. Furthermore, the prevalence of diabetes in African-Americans is higher than in whites (7.6% in African American men and 9.5% in women compared with 5.4% and 4.7% in white men and women).⁴¹ However, even after consideration of differences in conventional risk factors, socioeconomic factors that affect access to health care likely play a role in the slower decline in CVD rates observed among blacks.

Prevention
Special efforts at detection, prevention, and treatment of hypertension (which is the dominant CVD risk factor) through lifestyle changes and appropriate pharmacological therapy are necessary. In the US, the lower socioeconomic status of blacks probably contributes to the higher disease burden because of less awareness and access to prevention and treatment modalities. Therefore, strategies that are culturally sensitive to the African American blacks and targeted at those in the lower socioeconomic subset are required.

	General Prevention Strategies: From Epidemiological Evidence to Prevention Program

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
The previous sections emphasize some general points: first, that atherothrombotic CVD is a global problem that affects every ethnic group; second, that as societies undergo "urbanization," the risk factor levels for CVD increase; third, conscious efforts at the societal level (through changes in legislation or social policies) and at the individual level (through risk factor modification and use of evidence based treatments) can prevent or reverse the adverse consequences of urbanization, as demonstrated by the marked declines in CVD rates in many countries; fourth, even though there may be variations in genetic susceptibility among different ethnic groups, the common environmental and risk factors usually play a dominant role in the development of clinical disease in all ethnic groups. It is therefore likely that lessons learned regarding prevention from one region or a particular ethnic group are likely to be relevant to another region or ethnic group, with appropriate modifications that take into account genetic susceptibility, as well as social, economic, and cultural factors.

Two complementary strategies that are usually advocated for primary prevention are the "population approach" and "high-risk approach." In the former, community wide interventions seek to modify behaviors and thereby influence the distribution of risk factors in the population. Even modest changes in risk factors are expected to contribute to a substantial reduction in the cumulative population risk of CVD because of the large number of people affected. The high risk strategy, on the other hand, seeks to identify the few individuals who are at high risk, either because of marked elevation of single or multiple risk factors; targeted behavioral or pharmacological interventions follow. The population strategy aims to reduce the burden of disease in the whole community while conferring small benefits to each individual. The high-risk strategy, on the other hand, provides large benefits to the few individuals who are most vulnerable but the benefits to the whole community may be relatively limited because the beneficiaries are few.⁶⁸

The promise of the population approach has, however, not been adequately delivered by several community-based randomized intervention trials targeting multiple risk factors.⁶⁹ Therefore, the scientific basis for developing community-based program similar to those undertaken during the 1970s and 1980s has been questioned.⁷⁰ This view contrasts with the reported success of the North Karelia program,⁶ the lifestyle program in Mauritius,⁷¹ and the delayed benefits observed in the MRFIT trial.⁷² Projects evaluating the benefits of the population approach face several methodological problems. First, although the numbers of individuals in these studies are relatively large, because communities and not individuals are the sampling units, the number of communities compared are small, which dramatically reduces statistical power. Second, only a small impact of the intervention on risk factors is possible because of inefficient delivery of the intervention, "contamination" of the control population who tend to partially adopt the intervention package, and declining disease rates overall, all of which reduce statistical power.⁷⁰ Therefore, more research is needed into the determinants of risk factors at societal levels and how they can be modified more effectively through governmental or social policies. Based on the currently available data (chiefly from individual level interventions and observations correlating declines in CHD to declines in risk factors), it would still be prudent to advocate policy changes and community level programs that control tobacco, reduce obesity, increase physical activity, and promote a healthy diet.

By contrast, the high risk approach has yielded clear proof of efficacy, whether for lifestyle interventions⁷³ or for pharmacological interventions (eg, trials of statins,⁷⁴ aspirin,⁷⁵ or ACE inhibitors⁷⁶). However, it must be recognized that the majority of CVD arise from the large segments of the population who exhibit average levels of risk factors and are, therefore, at modest risk. Hence, the high risk approach, which reduces the risk in a limited number of individuals, needs to be complemented by a more embracive risk reduction approach which addresses the larger population attributable risk.

The clinical trials for secondary prevention have also contributed substantially to documenting the importance of modifying risk factors. By demonstrating reductions in major cardiovascular events from interventions aimed at specific risk factors (like cholesterol,⁷⁴ blood pressure,⁷⁷ or mediators of thrombogenesis⁷⁸) or involving dietary regimes (like fish⁷⁹ or the Mediterranean diet⁸⁰), they have reinforced the belief that risk factors and protective factors are critical to the prevention of cardiovascular disease. By progressively lowering the thresholds for such clinical interventions, the clinical norms have come closer to the prevention norms. Thus, it is no longer surprising to see clinical guidelines advocating LDL cholesterol target levels lower than 130 mg/dL (or below 100 mg/dL in those with clinical disease) or identifying the optimal blood pressure as lower than 140/80 mm Hg in otherwise healthy individuals or 120/80 mm Hg in high risk individuals (eg, diabetics). Therefore, there is considerable overlap between a population approach and a high risk approach to prevention.

Because risk factors track from early childhood to adulthood and old age, and subclinical atherosclerosis occurs even in children if they have elevated risk factors, preventive strategies should start as early as possible. Because lifelong pharmacological treatment is not desirable except in a few very high risk children, this would emphasize further the need for community level prevention with special focus on the family as the unit in a high risk strategy. If the Barker hypotheses⁸¹ is true, prevention of CVD may start with ensuring that the maternal risk factors are controlled and intrauterine nutrition is appropriate. This suggests an intergenerational approach to prevention, which requires both a community wide population strategy and a targeted high risk individual strategy that would be applicable across the entire life span of individuals (Figures 3 and 4).

View larger version (33K): [in this window] [in a new window]   Figure 3. Schema for societal level "Pathway" for the development of atherothrombotic cardiovascular diseases. *The contrasting lifestyles between urban and rural settings are typical for countries in early and mid transition. However, in late transition countries, lifestyles in rural settings have been altered due to mechanization and various social influences so that they are similar to urban settings. Consumption of inappropriate diets, higher rates of tobacco use, and decreases in physical activity even in rural settings increase risk factors and lead to higher CVD rates. These changes are already evident in North America. Risk factors probably play a role from the intrauterine period, through childhood to adulthood.

View larger version (30K): [in this window] [in a new window]   Figure 4. An integrated population-based and high risk individualized strategy for the prevention of CVD. The arrows represent the interactive nature of the various strategies. For example, in a community that has a tobacco control policy, it is easier for an individual subject to quit smoking. Conversely, encouraging a patient with clinical coronary artery disease to quit smoking may promote appropriate changes among family members and coworkers. This in turn may encourage children to adopt healthy lifestyles.

	Summary

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
Over the 20th century, most countries in the world have experienced great transitions in social structures, economics, politics, education, and home environments. This has resulted in a shift from agricultural and rural societies to industrial and urban societies in the first 3 quarters of the 20th century, with a further shift in the last quarter to information-based societies. These social and economic transitions have resulted in major changes in population demography, industrial structure, income levels, expenditure patterns, education levels, family structures, eating habits, and physical activity. These changes have markedly increased CV risk factors and disease rates.

CVD is a major global health problem, with the majority of the burden occurring in developing countries. Most of our knowledge about prevention and treatment derives from studies conducted in developed countries and predominantly among white populations. Therefore, there is an urgent need to establish appropriate research studies, increase awareness of the CVD burden, and develop preventive strategies in developing countries. In the meantime, as it is likely that most risk factors will be of some importance in all ethnic populations in the world, prevention and treatment strategies that have been proven to be effective in developed countries should be adapted for developing countries. These strategies should include approaches to prevent the development of risk factors in the population as a whole by changes in social and governmental policy as well as approaches that can be applied to high risk individuals. Some approaches are relatively low cost and readily applicable (eg, promoting physical activity, use of aspirin, or angiotensin-converting enzyme inhibitors in high risk subjects and controlling blood pressure using thiazides or beta-blockers), whereas others may only be applicable to relatively affluent sections of some societies (eg, statins or coronary artery bypass graft surgery). Therefore, both population-level and individual-level strategies should be tailored to each country, community, and socioeconomic stratum (Figure 4). Translating our current knowledge of CVD prevention into effective implementation could be expected to substantially blunt or even reverse the current and future global epidemic of CVD.

	Acknowledgments

 
We acknowledge that this article largely focuses on atherothrombotic cardiovascular diseases. We have not covered the topics of valvular heart disease, Chagas disease, or heart failure, all of which remain significant global health problems.

Salim Yusuf is the recipient of a Canadian Institutes of Health Research Senior Scientist Award and holds a Heart and Stroke Foundation of Ontario Research Chair. Sonia Anand holds a Canadian Institutes of Health Research Clinician Scientist Award. Stephanie Ôunpuu holds a Canadian Institutes of Health Research Senior Research Fellowship. We thank Sandra Nevills for secretarial assistance and several colleagues around the world who provided us with relevant information and references.

	References

Top Abstract Introduction European Origin Japanese Chinese South Asians Hispanics Aboriginal Populations Blacks of African Origin General Prevention Strategies:... Summary References

 
1. 1997–1999 World Health Statistics Annual. Geneva, Switzerland: World Health Organization; 2000. Available at: http://www-nt.who.int/whosis/statistics/menu.cfm?path=statistics,whsa&language=english. Accessed January 9, 2001.

2. Marmot M. Coronary heart disease: rise and fall of a modern epidemic.In: Marmot M, Elliot P, eds. Coronary Heart Disease Epidemiology. Oxford: Oxford University Press, 1995: 3–19.

3. Artaud-Wild SM, Connor SL, Sexton G, et al. Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland: a paradox. Circulation. 1993; 88: 2771–2779.[Abstract/Free Full Text]

4. Criqui MH, Ringel BL. Does diet or alcohol explain the French Paradox? Lancet. 1994; 344: 1719–1723.[Medline] [Order article via Infotrieve]

5. Law MR, Wald N. Why heart disease mortality is low in France: the time-lag explanation. Br Med J. 1999; 318: 1471–1480.[Free Full Text]

6. Vartiainen E, Puska P, Pekkanen J, et al. Changes in risk factors explain changes in mortality from ischemic heart disease in Finland. Br Med J. 1994; 309: 23–27.[Abstract/Free Full Text]

7. McGovern PG, Pankow JS, Shahar E, et al. Recent trends in acute coronary heart disease: mortality, morbidity, medical care, and risk factors: the Minnesota Heart Survey Investigators. N Engl J Med. 1996; 334: 884–890.[Abstract/Free Full Text]

8. Wing S, Hayes C, Heiss G, et al. Geographic variation in the onset of decline of ischemic heart disease mortality in the United States. Am J Public Health. 1986; 76: 1404–1408.[Abstract/Free Full Text]

9. Wing S, Barnett E, Casper M, et al. Geographic and socioeconomic variation in the onset of decline of coronary heart disease mortality in white women. Am J Public Health. 1992; 82: 204–209.[Abstract/Free Full Text]

10. Zatonski WA, McMichael AJ, Powles JW. Ecological study of reasons for sharp decline in mortality from ischemic heart disease in Poland since 1991. Br Med J. 1998; 316: 1047–1051.[Abstract]

11. Leon D, Chenet L, Shkolnikov VM, et al. Huge variation in Russian mortality rates 1984–1994: artefact, alcohol, or what? Lancet. 1997; 350: 383–388.[Medline] [Order article via Infotrieve]

12. Shimamoto T, Komachi Y, Inada H, et al. Trends for coronary heart disease and stroke and their risk factors in Japan. Circulation. 1989; 79: 503–515.[Abstract/Free Full Text]

13. Fujishima M, Kiyohara Y, Ueda K, et al. Smoking as cardiovascular risk factor in low cholesterol population: the Hisayama Study. Clin Exp Hypertens A. 1992; 14: 99–108.[Medline] [Order article via Infotrieve]

14. Fujishima M, Kiyohara Y, Kato I, et al. Diabetes and cardiovascular disease in a prospective population survey in Japan: the Hisayama Study. Diabetes. 1996; 45 (suppl 3): S14–S16.

15. Ohmura T, Ueda K, Kiyohara Y, et al. Prevalence of type 2 (non-insulin-dependent) diabetes mellitus and impaired glucose tolerance in the Japanese general population: the Hisayama Study. Diabetologia. 1993; 36: 1198–1203.[Medline] [Order article via Infotrieve]

16. Woo KS, Donnan SP. Epidemiology of coronary arterial disease in the Chinese. Int J Cardiol. 1989; 24: 83–93.[Medline] [Order article via Infotrieve]

17. World Health Statistics Annual. Geneva, Switzerland: World Health Organization; 1998.

18. Thorvaldsen P, Asplund K, Kuulasmaa K, et al. Stroke incidence, case fatality, and mortality in the WHO MONICA project: World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease (erratum appears in Stroke. 1995;26:1504 and Stroke. 1995;26:2376) Stroke. 1995; 26: 361–367.[Abstract/Free Full Text]

19. Donnan SP, Ho SC, Woo J, et al. Risk factors for acute myocardial infarction in a southern Chinese population. Ann Epidemiol. 1994; 4: 46–58.[Medline] [Order article via Infotrieve]

20. Chen Z, Peto R, Collins R, et al. Serum cholesterol concentration and coronary heart disease in population with low cholesterol concentrations. Br Med J. 1991; 303: 276–282.

21. Yang G, Fan L, Tan J, et al. Smoking in China: findings of the 1996 National Prevalence Survey. JAMA. 1999; 282: 1247–1253.[Abstract/Free Full Text]

22. Tao SC, Huang ZD, Wu XG, et al. CHD and its risk factors in the People’s Republic of China. Int J Epidemiol. 1989; 18 (suppl 1): S159–S163.[Abstract]

23. People’s Republic of China–United States Cardiovascular and Cardiopulmonary Epidemiology Research Group. An epidemiological study of cardiovascular and cardiopulmonary disease risk factors in four populations in the People’s Republic of China. Circulation. 1992; 85: 1083–1096.[Free Full Text]

24. Li N, Tuomilehto J, Dowse G, et al. Electrocardiographic abnormalities and associated factors in Chinese living in Beijing and in Mauritius: the Mauritius Non-Communicable Disease Study Group. Br Med J. 1992; 304: 1596–1601.

25. Sheth T, Nair C, Nargundkar M, et al. Cardiovascular and cancer mortality among Canadians of European, south Asian and Chinese origin from 1979 to 1993: an analysis of 1.2 million deaths. Can Med Assoc J. 1999; 161: 132–138.[Abstract/Free Full Text]

26. Chonhua Y, Zhaosu W, Yingkai W. The changing pattern of cardiovascular diseases in China. World Health Stat Q. 1993; 46: 113–118.[Medline] [Order article via Infotrieve]

27. Reddy KS. Cardiovascular disease in India. World Health Stat Q. 1993; 46: 101–7.[Medline] [Order article via Infotrieve]

28. Murray CJL, Lopez AD, eds. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability From Diseases, Injuries, and Risk Factors in 1990 and Projected to 2020. Cambridge, Mass: Harvard University Press; 1996.

29. Enas EA, Yusuf S, Mehta J. Prevalence of coronary artery disease in Asian Indians. Am J Cardiol. 1992; 70: 945–949.[Medline] [Order article via Infotrieve]

30. Reddy KS, Yusuf S. Emerging epidemic of cardiovascular disease in developing countries. Circulation. 1998; 97: 596–601.[Free Full Text]

31. Balarajan R. Ethnicity and variations in mortality from coronary heart disease. Health Trends. 1996; 28: 45–51.

32. Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups. Lancet. 2000; 356: 279–284.[Medline] [Order article via Infotrieve]

33. McKeigue PM, Ferrie JE, Pierpoint T, et al. Association of early-onset coronary heart disease in south Asian men with glucose intolerance and hyperinsulinemia. Circulation. 1993; 87: 152–161.[Abstract/Free Full Text]

34. 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.[Medline] [Order article via Infotrieve]

35. 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.[Medline] [Order article via Infotrieve]

36. McKeigue PM, Miller GJ, Marmot MG. Coronary heart disease in South Asians overseas: a review. J Clin Epidemiol. 1989; 42: 597–609.[Medline] [Order article via Infotrieve]

37. Ramachandran A, Dharmaraj D, Snehalatha C, et al. Prevalence of glucose intolerance in Asian Indians. Diabetes Care. 1992; 15: 1348–1355.[Abstract]

38. Anand S, Enas E, Pogue J, et al. Elevated Lipoprotein (a) Levels in South Asians in North America. Metabolism. 1998; 47: 182–184.[Medline] [Order article via Infotrieve]

39. Gupta R, Gupta VP. Meta-analysis of coronary heart disease prevalence in India. Indian Heart J. 1996; 48: 241–245.[Medline] [Order article via Infotrieve]

40. 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.[Medline] [Order article via Infotrieve]

41. US Bureau of Census. Profiles of General Demographic Characteristics: 2000 Census of Population and Housing. Washington, DC: US Bureau of the Census; 2000.

42. Becker T, Wiggins C, Key C, et al. Ischemic Heart disease mortality in Hispanic American Indians and non-Hispanic whites in New Mexico, 1958–1982. Circulation. 1988; 78: 302–309.[Abstract/Free Full Text]

43. Goff DC, Nichaman MZ, Chan W, et al. Greater incidence of hospitalized myocardial infarction among Mexican-Americans than non-Hispanic whites: the Corpus Christi Heart Project, 1988–1992. Circulation. 1997; 95: 1433–1440.[Abstract/Free Full Text]

44. Stern M, Gaskill S. Secular decline in death rates due to ischemic heart disease in Mexican Americans and non-Hispanic whites, Texas 1970–1980. Circulation. 1987; 76: 1245–1250.[Abstract/Free Full Text]

45. Gillum RF. Epidemiology of stroke in Hispanic Americans. Stroke. 1995; 26: 1707–1712.[Abstract/Free Full Text]

46. Haffner SM, Valdez RA, Hazuda HP, et al. Prospective analysis of the insulin-resistance syndrome (syndrome X). Diabetes. 1992; 41: 715–722.[Abstract]

47. Mitchell BD, Hazuda HP, Haffner SM, et al. Myocardial infarction in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study. Circulation. 1991; 83: 45–51.[Abstract/Free Full Text]

48. Solis JM, Marks G, Garcia M, et al. Acculturation, access to care, and use of preventive services by Hispanics: findings from the HHANES, 1982–84. Am J Public Health. 1990; 80 (suppl): 11–19.

49. Howard BV, Lee ET, Cowan LD, et al. Coronary heart disease prevalence and its relation to risk factors in American Indians: the Strong Heart Study. Am J Epidemiol. 1995; 142: 254–268.[Abstract/Free Full Text]

50. Gillum RF. The epidemiology of stroke in Native Americans. Stroke. 1995; 26: 514–521.[Abstract/Free Full Text]

51. Royal Commission on Aboriginal People. Report of the Royal Commission on Aboriginal People. Vol. 3. Ottawa, Canada: Gathering Strength; 1996.

52. Mao Y, Moloughney BW, Semenciw RM, et al. Indian reserve and registered Indian mortality in Canada. Can J Public Health. 1992; 83: 350–353.[Medline] [Order article via Infotrieve]

53. Anand S, Yusuf S, Jacobs R, et al, for the SHARE-AP Investigators. Risk factors, atherosclerosis, and cardiovascular disease among Aboriginal people in Canada: the Study of Health Assessment and Risk Evaluation in Aboriginal Peoples. Lancet. 2001; 358: 1147–1153.[Medline] [Order article via Infotrieve]

54. Welty TK, Lee ET, Yeh J, et al. Cardiovascular disease risk factors among American Indians: the Strong Heart Study. Am J Epidemiol. 1995; 142: 269–287.[Abstract/Free Full Text]

55. Stockins B, Larenas G, Charles M, et al. Blood pressure and serum lipid levels in Chilean aboriginal populations (Mapuche) living in the Chilean region of Arauncania. Rev Med Chil. 1998; 126: 1291–1299.[Medline] [Order article via Infotrieve]

56. Seedat YK. Ethnicity, hypertension, coronary heart disease, and renal diseases in South Africa. Ethn Health. 1996; 1: 349–357.[Medline] [Order article via Infotrieve]

57. Berrios X, Koponen T, Huiguang T, et al. Distribution and prevalence of major risk factors of noncommunicable diseases in selected countries: the WHO Inter-Health Program. Bull World Health Organ. 1997; 75: 99–108.[Medline] [Order article via Infotrieve]

58. Akinkugbe OO. World epidemiology of hypertension.In: Hall WD, Saunders E, Shulman NB, eds. Hypertension in Blacks: Epidemiology, Pathophysiology, and Treatment. St Louis, Mo: Year Book Publishers; 1985: 13–16.

59. Miller GJ, Beckles GL, Maude GH, et al. Ethnicity and other characteristics predictive of coronary heart disease in a developing community: principal results of the St James Survey, Trinidad. Int J Epidemiol. 1989; 18: 808–817.[Abstract/Free Full Text]

60. Gillum RF. Sudden coronary death in the United States: 1980–1985. Circulation. 1989; 79: 756–765.[Abstract/Free Full Text]

61. Sempos C, Cooper R, Kovar MG, et al. Divergence of the recent trends in coronary mortality for the four major race-sex groups in the United States. Am J Public Health. 1988; 78: 1422–1427.[Abstract/Free Full Text]

62. Pickle LW, Gillum RF. Geographic variation in cardiovascular disease mortality in US blacks and whites. J Natl Med Assoc. 1999; 91: 545–556.[Medline] [Order article via Infotrieve]

63. Pearson TA, Jamison DT, Trejo-Gutierrez H. Cardiovascular disease.In: Jamison DT, ed. Disease Control Priorities in Developing Countries. New York, NY: Oxford University Press; 1993: 577–599.

64. Casper ML, Wing S, Anda RF, et al. The shifting stroke belt: changes in the geographic pattern of stroke mortality in the United States, 1962 to 1988. Stroke. 1995; 26: 755–760.[Abstract/Free Full Text]

65. Casper M, Wing S, Strogatz D. Variation in the magnitude of black-white differences in stroke mortality by community occupational structure. J Epidemiol Community Health. 1991; 45: 302–306.[Abstract/Free Full Text]

66. Jones DW, Sempos CT, Thom TJ, et al. Rising levels of cardiovascular mortality in Mississippi, 1979–1995. Am J Med Sci. 2000; 319: 131–137.[Medline] [Order article via Infotrieve]

67. Geronimus AT, Bound J, Waidmann TA, et al. Excess mortality among blacks and whites in the United States. N Engl J Med. 1996; 335: 1552–1558.[Abstract/Free Full Text]

68. Rose G. The Strategy of Preventive Medicine. New York, NY: Oxford University Press; 1992.

69. European Collaborative Trial of Multifactorial Prevention of Coronary Heart Disease. Final report on the 6-year results: World Health Organisation European Collaborative Group. Lancet. 1986; 1: 869–872.[Medline] [Order article via Infotrieve]

70. Thelle D. Prevention of cardiovascular diseases: a scientific dilemma. Scand Cardiovasc J. 2000; 34: 103–105.[Medline] [Order article via Infotrieve]

71. Dowsen GK, Gareeboo H, George K, et al. Changes in population cholesterol concentration and other cardiovascular risk factor levels after five years of non-communicable disease intervention programme in Mauritius. Br Med J. 1995; 311: 1255–1259.[Abstract/Free Full Text]

72. The Multiple Risk Factor Intervention Trial Research Group. Mortality after 16 years for participants randomized to the Multiple Risk Factor Intervention Trial. Circulation. 1996; 94: 946–951.[Abstract/Free Full Text]

73. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure: DASH Collaborative Research Group. N Engl J Med. 1997; 336: 1117–1124.[Abstract/Free Full Text]

74. Law M. Lipids and cardiovascular disease.In: Yusuf S, Cairns JA, Camm JA, et al, eds. Evidence Based Cardiology. London, UK: BMJ Books; 1998: 191–205.

75. Antiplatelet Trialists’ Collaboration. Collaborative overview of randomised trials of antiplatelet therapy: I, prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients (erratum appears in Br Med J. 1994;308:1540). Br Med J. 1994; 308: 81–106.[Abstract/Free Full Text]

76. The Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. 2000; 342: 145–153.[Abstract/Free Full Text]

77. Collins R, Peto R, MacMahon S, et al. Blood pressure, stroke, and coronary heart disease: part 2, short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet. 1990; 335: 827–838.[Medline] [Order article via Infotrieve]

78. Anand S, Yusuf S. Oral anticoagulant therapy in patients with coronary artery disease: a meta-analysis. JAMA. 1999; 282: 2058–2067.[Abstract/Free Full Text]

79. Ness AR, Whitley E, Burr ML, et al. The long-term effect of advice to eat more fish on blood pressure in men with coronary disease: results from the diet and reinfarction trial. J Hum Hypertens. 1999; 13: 729–733.[Medline] [Order article via Infotrieve]

80. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999; 99: 779–785.[Abstract/Free Full Text]

81. Barker DJP. Mothers, Babies, and Disease in Later Life. London: BMJ Publishing Group; 1994.

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				Z. Milicevic, I. Raz, S. D. Beattie, B. N. Campaigne, S. Sarwat, E. Gromniak, I. Kowalska, E. Galic, M. Tan, and M. Hanefeld Natural History of Cardiovascular Disease in Patients With Diabetes: Role of hyperglycemia Diabetes Care, February 1, 2008; 31(Supplement_2): S155 - S160. [Abstract] [Full Text] [PDF]

				R. Kelishadi, M. Hashemi, N. Mohammadifard, S. Asgary, and N. Khavarian Association of Changes in Oxidative and Proinflammatory States with Changes in Vascular Function after a Lifestyle Modification Trial Among Obese Children Clin. Chem., January 1, 2008; 54(1): 147 - 153. [Abstract] [Full Text] [PDF]

				K. M. King, P. LeBlanc, W. Carr, and Hude Quan Chinese Immigrants' Management of Their Cardiovascular Disease Risk West J Nurs Res, November 1, 2007; 29(7): 804 - 826. [Abstract] [PDF]

				G. Karthikeyan, D. Xavier, D. Prabhakaran, and P. Pais Perspectives on the management of coronary artery disease in India Heart, November 1, 2007; 93(11): 1334 - 1338. [Abstract] [Full Text] [PDF]

				S. M. Donahoe, G. C. Stewart, C. H. McCabe, S. Mohanavelu, S. A. Murphy, C. P. Cannon, and E. M. Antman Diabetes and Mortality Following Acute Coronary Syndromes JAMA, August 15, 2007; 298(7): 765 - 775. [Abstract] [Full Text] [PDF]

				R. Kelishadi Childhood Overweight, Obesity, and the Metabolic Syndrome in Developing Countries Epidemiol. Rev., May 3, 2007; (2007) mxm003v1. [Abstract] [Full Text] [PDF]

				M. Kivimaki, D. A. Lawlor, G. D. Smith, A. Kouvonen, M. Virtanen, M. Elovainio, and J. Vahtera Socioeconomic Position, Co-Occurrence of Behavior-Related Risk Factors, and Coronary Heart Disease: the Finnish Public Sector Study Am J Public Health, May 1, 2007; 97(5): 874 - 879. [Abstract] [Full Text] [PDF]

				D. Prabhakaran, V. Chaturvedi, P. Shah, A. Manhapra, P. Jeemon, B. Shah, and K. Srinath Reddy Differences in the prevalence of metabolic syndrome in urban and rural India: a problem of urbanization Chronic Illness, March 1, 2007; 3(1): 8 - 19. [PDF]

				P. Joshi, S. Islam, P. Pais, S. Reddy, P. Dorairaj, K. Kazmi, M. R. Pandey, S. Haque, S. Mendis, S. Rangarajan, et al. Risk Factors for Early Myocardial Infarction in South Asians Compared With Individuals in Other Countries JAMA, January 17, 2007; 297(3): 286 - 294. [Abstract] [Full Text] [PDF]

				G. A. Mensah and D. W. Brown An Overview Of Cardiovascular Disease Burden In The United States Health Aff., January 1, 2007; 26(1): 38 - 48. [Abstract] [Full Text] [PDF]

				R. M. Califf, R. A. Harrington, L. K. Madre, E. D. Peterson, D. Roth, and K. A. Schulman Curbing The Cardiovascular Disease Epidemic: Aligning Industry, Government, Payers, And Academics Health Aff., January 1, 2007; 26(1): 62 - 74. [Abstract] [Full Text] [PDF]

				P. Paramsothy and R. Knopp Management of dyslipidaemias. Heart, October 1, 2006; 92(10): 1529 - 1534. [Full Text] [PDF]

				P. A Ratner, R. Tzianetas, A. W Tu, J. L Johnson, M. Mackay, C. E Buller, M. Rowlands, and B. Reime Myocardial infarction symptom recognition by the lay public: the role of gender and ethnicity. J Epidemiol Community Health, July 1, 2006; 60(7): 606 - 615. [Abstract] [Full Text] [PDF]

				B. R. Davis, L. B. Piller, J. A. Cutler, C. Furberg, K. Dunn, S. Franklin, D. Goff, F. Leenen, S. Mohiuddin, V. Papademetriou, et al. Role of Diuretics in the Prevention of Heart Failure: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial Circulation, May 9, 2006; 113(18): 2201 - 2210. [Abstract] [Full Text] [PDF]

				J. Lynch, G. Davey Smith, S. Harper, and K. Bainbridge Explaining the social gradient in coronary heart disease: comparing relative and absolute risk approaches J Epidemiol Community Health, May 1, 2006; 60(5): 436 - 441. [Abstract] [Full Text] [PDF]

				D. L. Bhatt, P. G. Steg, E. M. Ohman, A. T. Hirsch, Y. Ikeda, J.-L. Mas, S. Goto, C.-S. Liau, A. J. Richard, J. Rother, et al. International Prevalence, Recognition, and Treatment of Cardiovascular Risk Factors in Outpatients With Atherothrombosis JAMA, January 11, 2006; 295(2): 180 - 189. [Abstract] [Full Text] [PDF]

				K. Steyn, K. Sliwa, S. Hawken, P. Commerford, C. Onen, A. Damasceno, S. Ounpuu, S. Yusuf, and for the INTERHEART Investigators in Africa Risk Factors Associated With Myocardial Infarction in Africa: The INTERHEART Africa Study Circulation, December 6, 2005; 112(23): 3554 - 3561. [Abstract] [Full Text] [PDF]

				M. Ntsekhe and J. Hakim Impact of Human Immunodeficiency Virus Infection on Cardiovascular Disease in Africa Circulation, December 6, 2005; 112(23): 3602 - 3607. [Abstract] [Full Text] [PDF]

				G. J Miller, J. A Cooper, and G. L. Beckles Cardiorespiratory fitness, all-cause mortality, and risk of cardiovascular disease in Trinidadian men--the St James survey Int. J. Epidemiol., December 1, 2005; 34(6): 1387 - 1394. [Abstract] [Full Text] [PDF]

				Combination Pharmacotherapy and Public Health Rese Combination Pharmacotherapy for Cardiovascular Disease Ann Intern Med, October 18, 2005; 143(8): 593 - 599. [Abstract] [Full Text] [PDF]

				G. D. Smith, R. Harbord, J. Milton, S. Ebrahim, and J. A.C. Sterne Does Elevated Plasma Fibrinogen Increase the Risk of Coronary Heart Disease?: Evidence from a Meta-Analysis of Genetic Association Studies Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2228 - 2233. [Abstract] [Full Text] [PDF]

				A. Repetto, B. D. Bello, M. Pasotti, M. Agozzino, M. Vigano, C. Klersy, L. Tavazzi, and E. Arbustini Coronary atherosclerosis in end-stage idiopathic dilated cardiomyopathy: an innocent bystander? Eur. Heart J., August 1, 2005; 26(15): 1519 - 1527. [Abstract] [Full Text] [PDF]

				A S Wierzbicki, S Nishtar, P J Lumb, M Lambert-Hammill, C N Turner, M A Crook, M S Marber, and J Gill Metabolic syndrome and risk of coronary heart disease in a Pakistani cohort Heart, August 1, 2005; 91(8): 1003 - 1007. [Abstract] [Full Text] [PDF]

				M. Ezzati, S. J. Henley, M. J. Thun, and A. D. Lopez Role of Smoking in Global and Regional Cardiovascular Mortality Circulation, July 26, 2005; 112(4): 489 - 497. [Abstract] [Full Text] [PDF]

				A. V. Doobay and S. S. Anand Sensitivity and Specificity of the Ankle-Brachial Index to Predict Future Cardiovascular Outcomes: A Systematic Review Arterioscler. Thromb. Vasc. Biol., July 1, 2005; 25(7): 1463 - 1469. [Abstract] [Full Text] [PDF]

				N Ahmad and R Bhopal Is coronary heart disease rising in India? A systematic review based on ECG defined coronary heart disease Heart, June 1, 2005; 91(6): 719 - 725. [Abstract] [Full Text] [PDF]

				J. Genest, R. McPherson, J. Frohlich, and G. Fodor The analysis by Manuel and colleagues creates controversy with headlines, not data Can. Med. Assoc. J., April 12, 2005; 172(8): 1033 - 1034. [Full Text] [PDF]

				M. Barton Ageing as a determinant of renal and vascular disease: role of endothelial factors Nephrol. Dial. Transplant., March 1, 2005; 20(3): 485 - 490. [Full Text] [PDF]

				P. Barter Role of nicotinic acid in raising high-density lipoprotein cholesterol (HDL-C) to reduce cardiovascular risk: an Asian/Pacific consensus: The Pan-Asian Consensus Panel On Hdl-C The British Journal of Diabetes & Vascular Disease, March 1, 2005; 5(2_suppl): S1 - S15. [Abstract] [PDF]

				M. Schooling, G. M Leung, E. D Janus, S. Y. Ho, A. J Hedley, and T. H. Lam Childhood migration and cardiovascular risk Int. J. Epidemiol., December 1, 2004; 33(6): 1219 - 1226. [Abstract] [Full Text] [PDF]

				J. Emberson, P. Whincup, R. Morris, and M Walker Reducing social inequalities and the prevention of coronary heart disease Int. J. Epidemiol., October 1, 2004; 33(5): 1152 - 1153. [Full Text] [PDF]

				N. Ahmad and R. Bhopal Burden of non-communicable diseases in South Asia: Evidence for epidemic of coronary heart disease in India is weak BMJ, June 19, 2004; 328(7454): 1499 - 1499. [Full Text]

				R. Pyo, K. K. Jensen, M. T. Wiekowski, D. Manfra, A. Alcami, M. B. Taubman, and S. A. Lira Inhibition of Intimal Hyperplasia in Transgenic Mice Conditionally Expressing the Chemokine-Binding Protein M3 Am. J. Pathol., June 1, 2004; 164(6): 2289 - 2297. [Abstract] [Full Text] [PDF]

				H. V. Kuhnlein, O. Receveur, R. Soueida, and G. M. Egeland Arctic Indigenous Peoples Experience the Nutrition Transition with Changing Dietary Patterns and Obesity J. Nutr., June 1, 2004; 134(6): 1447 - 1453. [Abstract] [Full Text] [PDF]

				D. Prabhakaran and S. S Anand The metabolic syndrome: an emerging risk state for cardiovascular disease Vascular Medicine, February 1, 2004; 9(1): 55 - 68. [Abstract] [PDF]

				R. V. Luepker, F. S. Apple, R. H. Christenson, R. S. Crow, S. P. Fortmann, D. Goff, R. J. Goldberg, M. M. Hand, A. S. Jaffe, D. G. Julian, et al. Case Definitions for Acute Coronary Heart Disease in Epidemiology and Clinical Research Studies: A Statement From the AHA Council on Epidemiology and Prevention; AHA Statistics Committee; World Heart Federation Council on Epidemiology and Prevention; the European Society of Cardiology Working Group on Epidemiology and Prevention; Centers for Disease Control and Prevention; and the National Heart, Lung, and Blood Institute Circulation, November 18, 2003; 108(20): 2543 - 2549. [Full Text] [PDF]

				D. G. Hackam and S. S. Anand Emerging Risk Factors for Atherosclerotic Vascular Disease: A Critical Review of the Evidence JAMA, August 20, 2003; 290(7): 932 - 940. [Abstract] [Full Text] [PDF]

				D. G. Hackam Do hypertensive patients with average cholesterol levels benefit from atorvastatin therapy? Can. Med. Assoc. J., June 24, 2003; 168(13): 1689 - 1689. [Full Text] [PDF]

				P. Sritara, S. Cheepudomwit, N. Chapman, M. Woodward, C. Kositchaiwat, S. Tunlayadechanont, T. Sura, B. Hengprasith, V. Tanphaichitr, S. Lochaya, et al. Twelve-year changes in vascular risk factors and their associations with mortality in a cohort of 3499 Thais: the Electricity Generating Authority of Thailand Study Int. J. Epidemiol., June 1, 2003; 32(3): 461 - 468. [Abstract] [Full Text] [PDF]

				J. Genest and T. R. Pedersen Prevention of Cardiovascular Ischemic Events: High-Risk and Secondary Prevention Circulation, April 22, 2003; 107(15): 2059 - 2065. [Full Text] [PDF]

				R. Bhopal Epidemic of cardiovascular disease in South Asians BMJ, March 16, 2002; 324(7338): 625 - 626. [Full Text] [PDF]

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