2
Epidemiology of Cardiovascular Disease

In recent years, the dominance of chronic diseases as major contributors to total global mortality has emerged and has been previously described in detail elsewhere (Adeyi et al., 2007; WHO, 2008b). By 2005, the total number of cardiovascular disease (CVD) deaths (mainly coronary heart disease, stroke, and rheumatic heart disease) had increased globally to 17.5 million from 14.4 million in 1990. Of these, 7.6 million were attributed to coronary heart disease and 5.7 million to stroke. More than 80 percent of the deaths occurred in low and middle income countries (WHO, 2009e). The World Health Organization (WHO) estimates there will be about 20 million CVD deaths in 2015, accounting for 30 percent of all deaths worldwide (WHO, 2005). The projected trends in CVD mortality and the expected shifts from infectious to chronic diseases over the next few decades are shown in Figure 2.1. By 2030, researchers project that noncommunicable diseases will account for more than three-quarters of deaths worldwide; CVD alone will be responsible for more deaths in low income countries than infectious diseases (including HIV/AIDS, tuberculosis, and malaria), maternal and perinatal conditions, and nutritional disorders combined (Beaglehole and Bonita, 2008). Thus, CVD is today the largest single contributor to global mortality and will continue to dominate mortality trends in the future (WHO, 2009e).

This chapter describes the incidence and trends over time of CVD globally, as well as in specific regions and nations throughout the world. Moreover, it lays out the major individual risk factors associated with acquisition and augmentation of risk for coronary heart disease and stroke throughout the life course. Furthermore, infectious causes of CVD and



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2 Epidemiology of Cardiovascular Disease I n recent years, the dominance of chronic diseases as major contributors to total global mortality has emerged and has been previously described in detail elsewhere (Adeyi et al., 2007; WHO, 2008b). By 2005, the total number of cardiovascular disease (CVD) deaths (mainly coronary heart disease, stroke, and rheumatic heart disease) had increased globally to 17.5 million from 14.4 million in 1990. Of these, 7.6 million were at- tributed to coronary heart disease and 5.7 million to stroke. More than 80 percent of the deaths occurred in low and middle income countries (WHO, 2009e). The World Health Organization (WHO) estimates there will be about 20 million CVD deaths in 2015, accounting for 30 percent of all deaths worldwide (WHO, 2005). The projected trends in CVD mortality and the expected shifts from infectious to chronic diseases over the next few decades are shown in Figure 2.1. By 2030, researchers project that non- communicable diseases will account for more than three-quarters of deaths worldwide; CVD alone will be responsible for more deaths in low income countries than infectious diseases (including HIV/AIDS, tuberculosis, and malaria), maternal and perinatal conditions, and nutritional disorders com- bined (Beaglehole and Bonita, 2008). Thus, CVD is today the largest single contributor to global mortality and will continue to dominate mortality trends in the future (WHO, 2009e). This chapter describes the incidence and trends over time of CVD globally, as well as in specific regions and nations throughout the world. Moreover, it lays out the major individual risk factors associated with ac- quisition and augmentation of risk for coronary heart disease and stroke throughout the life course. Furthermore, infectious causes of CVD and 

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0 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD FIGURE 2.1 Projected global deaths by cause. SOURCE: Beaglehole and Bonita, 2008. the interface between chronic infectious 2-1 Figure diseases and CVD risk are briefly R01642 discussed later in this chapter. Broad systemic drivers that contribute to the global burden of CVD, such as urbanization and image uneditable bitmapped globalization, are referred to in this chapter where they relate to trends in CVD burden and to the classically defined individual risk factors. These are then discussed in more detail in Chapter 3, which focuses on the relationship between CVD and development. Together, these two chapters describe the drivers and trends in CVD worldwide, providing a compelling rationale for the need to act. The remainder of the report proceeds to discuss approaches to influence these factors in order to reduce the burden of disease.

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 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE GLOBAL TRENDS IN CVD BURDEN Global trends in CVD are based on models that use country-specific data from a diverse range of developed and developing countries including those of the European Union (HEM Project Team, 2008; Kotseva et al., 2009a), Saudi Arabia (Al-Hamdan et al., 2005), Pakistan (Nishtar et al., 2004), South Africa (Steyn, 2006), China (Yang et al., 2008), Indonesia (Ng, 2006; Ng et al., 2006), Mexico (Fernald and Neufeld, 2007), India (Goyal and Yusuf, 2006; Reddy, 2007), and the United States (Danaei et al., 2009; Flegal et al., 2007). Over the past decade, the quality and availability of country-specific data on CVD risks, incidence, and mortal- ity has increased in accordance with one of the major recommendations of the 1998 IOM report. What emerges are nationally derived data on risks and CVD outcomes. Therefore, in many developing countries, the lack of country-specific data on risks and CVD outcomes that was prominently highlighted in the 1998 IOM report is less of an impediment to policy development and action. Nonetheless, before beginning a discussion of CVD trends and risk factor incidence around the world and in specific countries and regions, it is important to note several persistent limitations with the available data. Although many countries have established health surveillance systems with death registration data, the quality of the data collected varies substantially across countries. In many countries—especially in low and middle income countries—health statistics are often based on surveillance that does not cover all areas of the country, is incomplete in the areas it does cover, or is collected by undertrained staff who do not, or cannot, accurately report the pertinent data. These realities limit the reliability of some country health data (Mathers et al., 2005; Rao et al., 2005). Despite these limitations, WHO and country health statistics are often the most complete, compa- rable, or only data available and thus remain a key tool for evaluating the status of a CVD epidemic within and between countries. The importance of country-level epidemiological data and the ongoing need to standardize methodologies, increase data collection capacity, and improve the accuracy of national reporting are discussed further in Chapter 4. This chapter uses the most recent data available in each area discussed below, such as deaths by cause, contributions of risk factors to deaths by cause, the composition by risk factor of deaths by a specific cause, and risk factor levels. This introduces some inconsistencies as not all data cited comes from a single source. However, there is available data that is more re- cent for some of these measures than for others, and this was valued above the consistency of a single data source. Wherever possible, this chapter references burden, incidence, and prevalence data from countries’ national health statistics, WHO country and global statistics (which are based on

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 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD national health statistics provided by Member States), or the latest Global Burden of Disease: 00 Update data (also based on WHO country data) (2008a). Global Cardiovascular Mortality Globally, there is an uneven distribution of age-adjusted CVD mortality that is mapped in Figure 2.2. The lowest age-adjusted mortality rates are in the advanced industrialized countries and parts of Latin America, whereas the highest rates today are found in Eastern Europe and a number of low and middle income countries. For example, age-standardized mortality rates for CVD are in excess of 500 per 100,000 in Russia and Egypt; between 400 and 450 for South Africa, India and Saudi Arabia; and around 300 for Brazil and China. This is in contrast to rates of between 100 and 200 per 100,000 for Australia, Japan, France, and the United States. Overall, age-adjusted CVD death rates are today higher in major low and middle income countries than in developed countries (WHO, 2008b). Examination of coronary heart disease (CHD) mortality trends across countries reveals considerable variability in the shape and magnitude of CHD epidemics since the 1950s. Trends are not consistent even among countries within the same geographic region. In general, three trending patterns of CHD mortality can be observed: a rise-and-fall pattern where mortality rates increased, peaked, and then fell significantly; a rising pat- tern, where rates have steadily increased indicating an ongoing epidemic; and a flat pattern, where CHD mortality rates have remained relatively low and stable. The rise-and-fall pattern is most notable in high income Anglo- Celtic, Nordic, and Northwestern Continental European countries as well as in the United States and Australia. In these countries, CHD mortality rates peaked in the 1960s or early 1970s and have since fallen precipitously, by an average of about 50 percent (Beaglehole, 1999; Hardoon et al., 2008; Mirzaei et al., 2009; Unal et al., 2004). The rising pattern of CHD is most notable in Eastern European and former Soviet countries, where mortality rates have continued to increase at an alarming pace and where the high- est mortality rates ever recorded are currently being observed. By contrast, CHD mortality rates in Japan and several European Mediterranean coun- tries have remained relatively low, following the flat pattern (Beaglehole, 1999; Mirzaei et al., 2009). Mortality rates generally appear to be most closely linked to a country’s stage of epidemiological transition. Epidemiological transition, a concept first proposed by Abdel Omran in the 1970s (Omran, 1971), refers to the changes in the predominant forms of disease and mortality burdening a population that occur as its economy and health system develops. In un- derdeveloped countries at the early stages of epidemiological transition,

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FIGURE 2.2 Age-standardized deaths due to cardiovascular disease (rate per 100,000), 2004. NOTE: Rates are age-standardized to WHO’s world standard population. SOURCES: WHO, 2009e; map created with StatPlanet (van Cappelle, 2009).  Figure 2-2 R01642 uneditable bitmapped image landscape

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 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD infectious diseases predominate, but as the economy, development status, and health systems of these countries improve, the population moves to a later stage of epidemiological transition, and chronic noncommunicable diseases become the predominant causes of death and disease (Gaziano et al., 2006). Although this general pattern connecting trends in causes of mortality and stage of development can be observed, it is difficult to make generalized observations about CHD mortality trends for most low and middle income regions. This is due to limited trending data from many low and middle income countries as well as considerable country-to-country variability within regions. The data are strongest from Latin America, where several countries—specifically Argentina, Brazil, Chile, and Cuba—have experi- enced declines in CHD mortality rates in the past several decades. How- ever, with the exception of Argentina, where rates declined by more than 60 percent between 1970 and 2000, the declines have generally occurred more recently (in the 1980s and 1990s) and have been less dramatic (be- tween 20 and 45 percent) than those in high income countries. By contrast, the epidemic in Mexico appears to be worsening, with CHD mortality rates increasing by more than 90 percent between 1970 and 2000 (Mirzaei et al., 2009; Rodriguez et al., 2006). Mortality rates in Peru have remained rela- tively low, following the flat pattern. In Asia, some high income countries— such as Singapore—have followed the rise-and-fall pattern, while CHD deaths in other countries (such as the Philippines and urban China) appear to be rising (Mirzaei et al., 2009). Although trending data for most of Africa is not available, Mayosi et al. (2009) report that mortality rates for CVD and diabetes are rising in South Africa. Because there can be so much variability in the nature of CVD epidemics within regions, Mirzaei et al. (2009) conclude that the most prudent strategy when grouping countries in similar epidemiological situations is to group according to CVD mortality pattern rather than by geographic region. Conclusion 2.1: Chronic diseases are now the dominant contributors to the global burden of disease, and CVD is the largest contributor to the chronic disease cluster. Although CVD death rates are declining in most high income countries, trends are increasing in most low and middle income countries. Age at Death from CVD Not only do age-adjusted CVD death rates tend to be higher in develop- ing countries, but a significantly higher percentage of cardiovascular deaths also occur in younger people in the developing world than in developed countries. For example, the proportion of CVD deaths reported for 35 to

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 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE 64 years is 41 percent in South Africa, 35 percent in India, and 28 percent in Brazil, compared to only 12 percent in the United States and 9 percent in Portugal (Leeder et al., 2004). The median age of heart attack and first stroke and the median age at death from ischemic heart disease (IHD) and stroke offer a means to compare countries and groups in terms of their population experiences of CVD. The WHO 2004 Global Burden of Disease study estimated these variables for countries across the development spectrum. The results for selected countries are summarized in Figure 2.3. As a general trend, men and women in countries with higher development status (measured in terms of gross domestic product [GDP] per capita) experience CVD events older and die much later than in less developed countries. For example, in Japan, Australia, France, and Sweden, the median age at death from IHD averages 85 years in women and 77 years in men. Men in these countries experi- ence an acute myocardial infarction (AMI) more than a decade before their median age at death (WHO, 2009a). Indeed, the survival of individuals after a cardiovascular event has increased in high income countries. This trend of increased survival with CVD has caused an increased prevalence of CVD in many high income countries despite decreasing incidence over time (Davies et al., 2007). A second set of countries experienced median events at much younger ages despite having among the highest measures of GDP growth in the world. They include many Middle Eastern countries with considerable oil wealth. A third set of countries at intermediate levels of GDP per capita achieved above-average median ages at AMI and first stroke occurrence and death. They include Malaysia, Nicaragua, China, and Jamaica. In contrast, Brazil and South Africa, in the same development group as the preceding countries but with higher degrees of social inequality (United Nations Development Program [UNDP], 2007), achieved worse cardiovas- cular outcomes. Thus, even with countries at similar levels of development, some achieve substantially better CVD outcomes than others. These relative success stories give some indication of how preventable and treatable CVD can be. Comparative studies across countries are needed to build a better understanding of the factors that lead to the relative successes in these countries and to help inform the development of more effective approaches to control CVD. REASONS FOR CVD TRENDS OVER TIME A continuing understanding of how trends in CVD change over time is important, as knowledge evolves about the underlying causes of CVD and their relative impact. The empirical base for understanding the specific reasons for changes in CVD trends over time comes from two different

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 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD (a) 90 85 80 75 70 Males Age Females 65 60 55 50 45 Netherlands United States China Peru Argentina Chile France Finland Cote d'Ivoire South Africa Australia Japan Uganda Ghana Russian Federation Saudi Arabia India Thailand Mexico Italy Republic of Korea Egypt Brazil United Kingdom Low Lower Middle Upper Middle High (b) 90 85 80 75 Figure 2-3a 70 Males Age R01642 Females 65 editable vectors 60 55 50 45 Netherlands United States China Peru Argentina Chile France Finland Cote d'Ivoire South Africa Australia Japan Uganda Ghana India Thailand Russian Federation Saudi Arabia Mexico Italy Republic of Korea Egypt Brazil United Kingdom Low Lower Middle Upper Middle High FIGURE 2.3 Median age (a) at acute myocardial infarction, (b) of ischemic heart disease deaths, (c) at first stroke, and (d) of stroke deaths, by country. SOURCE: Data from WHO, 2009a. Figure 2-3b R01642 editable vectors

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Age Age (c) (d) 45 50 55 60 65 70 75 80 85 90 45 50 55 60 65 70 75 80 85 90 Uganda Uganda Ghana Ghana India India Low Low Cote d'Ivoire Cote d'Ivoire Egypt Egypt China China Peru Peru Thailand Thailand Brazil Brazil Lower Middle Lower Middle Russian Federation Russian Federation Argentina Argentina South Africa South Africa Chile Chile Mexico Mexico Upper Middle Upper Middle R01642 R01642 Saudi Arabia Saudi Arabia Figure 2-3c EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE Figure 2-3d Republic of Korea Republic of Korea editable vectors editable vectors Italy Italy Australia Australia France France High High Netherlands Netherlands Finland Finland United Kingdom United Kingdom Japan Japan United States United States Males Males Female Females 

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 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD sets of observations and studies. First, there are those that investigate the causes for the increases in CVD death and incidence rates being experi- enced in many developing countries. Second, there are others that have analyzed the reasons for the substantive decline experienced in developed countries over the past few decades. As described below, the same set of major risk factors consistently play a large role in explaining trends in CVD incidence and death across the world. Taken together, the data in- dicate that poor diet, tobacco use, physical inactivity, excess alcohol use, and psychosocial factors are the major contributors to CVD increases (Anand et al., 2008; Clarke et al., 2009; Critchley et al., 2004; Lopez- Jaramillo et al., 2008; Mayosi et al., 2009; Rosengren et al., 2004; Stein et al., 2005; Yusuf et al., 2004). However, the reasons for the increase or decrease of these risks in various parts of the world are more complex. This section describes the trends in these risks, and subsequent sections of this chapter describe the nature of the relationship between these factors and risk for CVD in more detail. Causes of the Ascent in CVD Mortality and Incidence Data are limited on the specific causes of the increases in CVD incidence and mortality that occurred in developed countries in the early 20th century and in developing countries more recently. It is clear that by 1920 CVD was already the leading cause of death in the United States. Scientific articles from the 1930s and 1940s suggest hypertension, cholesterol, poor nutri- tion, obesity, smoking, physical inactivity, and psychosocial stress as the leading factors contributing to heart disease, but they do not provide strong evidence to support this assertion (Ellis, 1948; Gager, 1931; Heart disease likely fate, 1937). The original publications outlining the rationale for the Framingham Study also cite these potential risk factors, although, again, they do not provide specific supporting evidence (Dawber and Kannel, 1958; Dawber et al., 1951, 1957). Tobacco use has been the most reliably documented, and historical trends in CVD mortality and tobacco use in the United States from 1900 to 1990 closely mirror each other, with both rates increasing through the 1950s, followed by a precipitous fall beginning in the 1960s (Fox et al., 2004; Mirzaei et al., 2009; Shopland, 1995). In the United Kingdom, a 38-year follow-up of men showed that baseline differ- ences in tobacco use, high blood pressure, and cholesterol were associated with a 10- to 15-year shorter life expectancy from age 50 (Clarke et al., 2009). The study has significance for developing countries since many of the baseline levels of risk common in the late 1960s in the United Kingdom are the norm in many developing countries today. There are a few studies that provide more direct insight into the causes of recent increases in CVD incidence and mortality in low and middle in-

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 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE come countries. For example, in their study on the rise of CHD mortality in Beijing from 1984 to 1990, Critchley et al. found that blood lipid increases were the largest contributor—responsible for 77 percent of increased CHD mortality (Critchley et al., 2004). Another likely contributor is a rise in smoking. There has been a steady rise in global cigarette consumption since the 1970s, which is expected to continue over the next decade if current trends continue. In 2010, researchers estimate that 6.3 trillion cigarettes—or more than 900 cigarettes for every person on the earth—will be consumed. This increase in the total number of smokers around the world is driven predominantly by global population growth and is expected to continue unless smoking rates are drastically re- duced. By 2020, if current smoking and population growth trends continue, the global annual cigarette consumption could rise to between 6.7 and 6.8 trillion cigarettes (ERC, 2007; Guindon and Boisclair, 2003; Shafey et al., 2009). This growing burden of tobacco is increasingly falling on low and middle income countries. In fact, three of the top five cigarette-consuming countries are low or middle income countries (China, the Russian Federa- tion, and Indonesia). China alone consumes approximately 2.163 trillion cigarettes every year—37 percent of the world’s annual consumption (ERC, 2007; Guindon and Boisclair, 2003; Shafey et al., 2009). By 2030, WHO projects that more than 80 percent of tobacco-related deaths will occur in developing countries (Shafey et al., 2009; WHO, 2008c). In addition to increasing consumption trends, the amount of tobacco produced globally has nearly doubled since 1960, with production increasing more than 300 percent in low and middle income countries, where by 2007, approximately 85 percent of tobacco was grown (Shafey et al., 2009). In addition, as to- bacco use has declined in rich countries, transnational tobacco companies have increasingly focused on expanding markets for their products in low and middle income countries (Bump et al., 2009; Chelala, 1998; Connolly, 1992; Holzman, 1997; Mackay, 1992; Mackay and Eriksen, 2002; Martinez and Grise, 1990; Wagner and Romano, 1994). An emerging body of evidence suggests that rapid dietary changes asso- ciated with nutritional transition, along with a decrease in levels of physical activity in many rapidly urbanizing societies, also may play a particularly important role in the rise of CVD observed in developing countries (Stein et al., 2005). The nutritional transition currently occurring in many low and middle income countries has created a new phenomenon in which it is not uncommon to see both undernutrition and obesity coexist in the same populations (Caballero, 2005; Dangour and Uauy, 2006; Reddy et al., 2003). Undernutrition has been the hallmark of the low and middle income countries of Africa, Latin America, and South Asia for decades. This situ- ation is progressively being replaced by a distinct trend at the other end of the spectrum. While the global undernourished population is plateauing,

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 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD Kelly, T. N., L. A. Bazzano, V. A. Fonseca, T. K. Thethi, K. Reynolds, and J. He. 2009. Glu- cose control and cardiovascular disease in type 2 diabetes. Annals of Internal Medicine 151(6):1-10. Kengne, A. P., A. Patel, F. Barzi, K. Jamrozik, T. H. Lam, H. Ueshima, D. F. Gu, I. Suh, and M. Woodward. 2007. Systolic blood pressure, diabetes and the risk of cardiovascular diseases in the Asia-Pacific region. Journal of Hypertension 25(6):1205-1213. Kengne, A. P., K. Nakamura, F. Barzi, T. H. Lam, R. Huxley, D. Gu, A. Patel, H. C. Kim, and M. Woodward. 2009. Smoking, diabetes and cardiovascular diseases in men in the Asia Pacific region. Journal of Diabetes 1(3):173-181. Khan, M., and G. Mensah. 2009. Changing practices to improve dietary outcomes and reduce cardiovascular risk: A food company’s perspective. Purchase, NY: Background Paper Commissioned by the Committee. Kotseva, K., D. Wood, G. De Backer, D. De Bacquer, K. Pyorala, and U. Keil. 2009a. Cardio- vascular prevention guidelines in daily practice: A comparison of EUROASPIRE I, II, and III surveys in eight European countries. Lancet 373(9667):929-940. Kotseva, K., D. Wood, G. De Backer, D. De Bacquer, K. Pyorala, U. Keil, and EUROASPIRE Study Group. 2009b. EUROASPIRE iii: A survey on the lifestyle, risk factors and use of cardioprotective drug therapies in coronary patients from 22 European countries. Euro- pean Journal of Cardiovascular Prevention & Rehabilitation 16(2):121-137. Krishnaswamy, G. M., D. S. P. Chi, J. I. M. L. P. Kelley, F. M. Sarubbi, K. J. M. Smith, and A. M. Peiris. 2000. The cardiovascular and metabolic complications of HIV infection. Cardiology in Review 8(5):260-268. Laatikainen, T., J. Critchley, E. Vartiainen, V. Salomaa, M. Ketonen, and S. Capewell. 2005. Explaining the decline in coronary heart disease mortality in Finland between 1982 and 1997. American Journal of Epidemiology 162(8):764-773. Langrish, J. P., N. L. Mills, and D. E. Newby. 2008. Air pollution: The new cardiovascular risk factor. Internal Medicine Journal 38(12):875-878. Law, M. G., N. Friis-Moller, W. M. El-Sadr, R. Weber, P. Reiss, A. D’Arminio Monforte, R. Thiebaut, L. Morfeldt, S. De Wit, C. Pradier, G. Calvo, O. Kirk, C. A. Sabin, A. N. Phillips, J. D. Lundgren, and D. A. D. Study Group. 2006. The use of the Framingham equation to predict myocardial infarctions in HIV-infected patients: Comparison with observed events in the D:A:D study. HIV Medicine 7(4):218-230. Lawes, C. M. M., S. Vander Hoorn, A. Rodgers, and International Society of Hypertension. 2008. Global burden of blood-pressure-related disease, 2001. Lancet 371(9623):1513-1518. Lawlor, D. A., S. Ebrahim, and G. Davey Smith. 2001. Sex matters: Secular and geographi- cal trends in sex differences in coronary heart disease mortality. British Medical Journal 323(7312):541-545: Erratum 325(7364):580. Leeder, S., S. Raymond, and H. Greenberg. 2004. A race against time: The challenge of car- diovascular disease in developing economics. New York: Columbia University. Legato, M. J. 1998. Cardiovascular disease in women: Gender-specific aspects of hypertension and the consequences of treatment. Journal of Women’s Health 7(2):199-209. Lesperance, F., and N. Frasure-Smith. 2007. Depression and heart disease. Cleveland Clinic Journal of Medicine 74(Suppl 1):S63-S66. Lichtman, J. H., J. T. Bigger Jr., J. A. Blumenthal, N. Frasure-Smith, P. G. Kaufmann, F. Lesperance, D. B. Mark, D. S. Sheps, C. B. Taylor, and E. S. Froelicher. 2008. Depression and coronary heart disease: Recommendations for screening, referral, and treatment—a science advisory from the American Heart Association Prevention Committee of the Council on Cardiovascular Nursing, Council on Clinical Cardiology, Council on Epide- miology and Prevention, and Interdisciplinary Council on Quality of Care and Outcomes Research. Circulation 118(17):1768-1775. Lin, H. H., M. Ezzati, and M. Murray. 2007. Tobacco smoke, indoor air pollution and tuber- culosis: A systematic review and meta-analysis. PLoS Medicine 4(1).

OCR for page 49
 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE Liu, G. G., W. H. Dow, A. Z. Fu, J. Akin, and P. Lance. 2008. Income productivity in China: On the role of health. Journal of Health Economics 27(1):27-44. Lopez, A. D., C. D. Mathers, M. Eszati, D. T. Jamison, and C. J. L. Murray. 2006. Global burden of disease and risk factors. Washington, DC: World Bank. Lopez-Jaramillo, P., S. Y. Silva, N. Rodriguez-Salamanca, A. Duran, W. Mosquera, and V. Castillo. 2008. Are nutrition-induced epigenetic changes the link between socio- economic pathology and cardiovascular diseases? American Journal of Therapeutics 15(4):362-372. Low, P. S., C. K. Heng, N. Saha, and J. S. Tay. 1996. Racial variation of cord plasma lipoprotein(a) levels in relation to coronary risk level: A study in three ethnic groups in Singapore. Pediatric Research 40(5):718-722. Lucas, D. L., R. A. Brown, M. Wassef, and T. D. Giles. 2005. Alcohol and the cardiovascular system research challenges and opportunities. Journal of the American College of Car- diology 45(12):1916-1924. Mackay, J. 1992. US tobacco export to third world: Third world war. Journal of the National Cancer Institute Monographs (12):25-28. Mackay, J., and M. Eriksen. 2002. The tobacco atlas. Geneva: World Health Organization. Mackay, J., G. Mensah, S. Mendis, K. Greenlund, and World Health Organization Depart- ment of Management of Noncommunicable Diseases. 2004. The atlas of heart disease and stroke. Geneva: World Health Organization. Manninen, V., L. Tenkanen, P. Koskinen, J. K. Huttunen, M. Manttari, O. P. Heinonen, and M. H. Frick. 1992. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation 85(1):37-45. Marcovina, S. M., J. J. Albers, E. Wijsman, Z. Zhang, N. H. Chapman, and H. Kennedy. 1996. Differences in Lp[a] concentrations and apo[a] polymorphs between black and white Americans. Journal of Lipid Research 37(12):2569-2585. Marin-Neto, J. A., E. Cunha-Neto, B. C. Maciel, and M. V. Simões. 2007. Pathogenesis of chronic Chagas heart disease. Circulation 115(9):1109-1123. Martinez, D., and V. Grise. 1990. With U.S. sale down, tobacco industry looks abroad. Farm- line US Department of Agriculture Economic Research Service 11(3):18-20. Martinez, E., M. Larrousse, and J. M. Gatell. 2009. Cardiovascular disease and HIV infection: Host, virus, or drugs? Current Opinion in Infectious Diseases 22(1):28-34. Martinez-Gonzalez, M. A., M. Bes-Rastrollo, L. Serra-Majem, D. Lairon, R. Estruch, A. Trichopoulou, M. A. Martinez-Gonzalez, M. Bes-Rastrollo, L. Serra-Majem, D. Lairon, R. Estruch, and A. Trichopoulou. 2009. Mediterranean food pattern and the primary prevention of chronic disease: Recent developments. Nutrition Reviews 67(Suppl 1): S111-S116. Mathers, C. D., and D. Loncar. 2006. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 3(11):e442. Mathers, C. D., C. Bernard, K. M. Iburg, M. Inoue, D. M. Fat, K. Shibuya, N. Timijuma, and H. Xu. 2003. Global burden of disease in 00: Data sources, methods, and results. Global Programme on Evidence for Health Policy Discussion Paper No. 54. Geneva: World Health Organization. Mathers, C. D., D. Ma Fat, M. Inoue, C. Rao, and A. D. Lopez. 2005. Counting the dead and what they died from: An assessment of the global status of cause of death data. Bulletin of the World Health Organization 83:171-177c. Mayosi, B. M., L. J. Burgess, and A. F. Doubell. 2005. Tuberculous pericarditis. Circulation 112(23):3608-3616. Mayosi, B. M., A. J. Flisher, U. G. Lalloo, F. Sitas, S. M. Tollman, and D. Bradshaw. 2009. The burden of non-communicable diseases in South Africa. Lancet 374(9693):934-947.

OCR for page 49
 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD Mbewu, A., and J. Mbanya. 2006. Cardiovascular disease. In Disease and mortality in Sub- Saharan Africa. Edited by D. Jamison, R. G. Feachem, M. W. Makgoba, E. R. Bos, F. K. Baingana, K. J. Hofman and K. O. Rogo. Washington, DC: World Bank Group. Pp. 305-328. Mendis, S., D. Abegunde, S. Yusuf, S. Ebrahim, G. Shaper, H. Ghannem, and B. Shengelia. 2005. WHO study on prevention of recurrences of myocardial infarction and stroke (WHO-PREMISE). Bulletin of the World Health Organization 83(11):820-828. Miguez-Burbano, M. J., X. Burbano, D. Ashkin, A. Pitchenik, R. Allan, L. Pineda, N. Rodriguez, and G. Shor-Posner. 2003. Impact of tobacco use on the development of op- portunistic respiratory infections in HIV seropositive patients on antiretroviral therapy. Addiction Biology 8(1):39-43. Miller, T. L., E. J. Orav, S. E. Lipshultz, K. L. Arheart, C. Duggan, G. A. Weinberg, L. Bechard, L. Furuta, J. Nicchitta, S. L. Gorbach, and A. Shevitz. 2008. Risk factors for cardio- vascular disease in children infected with human immunodeficiency virus-1. Journal of Pediatrics 153(4):491-497. Mirzaei, M., A. S. Truswell, R. Taylor, and S. R. Leeder. 2009. Coronary heart disease epidem- ics: Not all the same. Heart 95(9):740-746. Misra, A., and L. Khurana. 2008. Obesity and the metabolic syndrome in developing coun- tries. Journal of Clinical Endocrinology and Metabolism 93(11 Suppl 1):S9-S30. Moncayo, A., and M. I. O. Yanine. 2006. An update on Chagas disease (human American trypanosomiasis). In Annals of Tropical Medicine and Parasitology: Maney Publishing. 100(8):663-677. Morel, C. M., and J. Lazdins. 2003. Chagas disease. Nature Reviews Microbiology 1(1): 14-15. Mukamal, K. J., and E. B. Rimm. 2001. Alcohol’s effects on the risk for coronary heart disease. Alcohol Research and Health 25(4):255-261. Mukamal, K. J., S. E. Chiuve, E. B. Rimm, K. J. Mukamal, S. E. Chiuve, and E. B. Rimm. 2006. Alcohol consumption and risk for coronary heart disease in men with healthy lifestyles. Archives of Internal Medicine 166(19):2145-2150. Muna, W. F. T. 1993. Cardiovascular disorders in Africa. World Health Statistics Quarterly 46(2):125-133. Myint, P. K., R. N. Luben, N. J. Wareham, S. A. Bingham, and K. T. Khaw. 2009. Combined effect of health behaviours and risk of first ever stroke in 20,040 men and women over 11 years’ follow-up in Norfolk cohort of European prospective investigation of cancer (EPIC Norfolk): Prospective population study. British Medical Journal 338:b349. Narkiewicz, K., S. E. Kjeldsen, and T. Hedner. 2006. Hypertension and cardiovascular disease in women: Progress towards better understanding of gender-specific differences? Blood Pressure 15(2):68-70. Nathan, D. M., P. A. Cleary, J. Y. Backlund, S. M. Genuth, J. M. Lachin, T. J. Orchard, P. Raskin, and B. Zinman. 2005. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. New England Journal of Medicine 353(25):2643-2653. Ng, N. 2006. Chronic disease risk factors in a transitional country: The case of rural Indone- sia, Folkhälsa och klinisk medicin, Umeå. Ng, N., H. Stenlund, R. Bonita, M. Hakimi, S. Wall, and L. Weinehall. 2006. Preventable risk factors for noncommunicable diseases in rural Indonesia: Prevalence study using WHO STEPS approach. Bulletin of the World Health Organization 84(4):305-313. Ng, S. W., E. C. Norton, and B. M. Popkin. 2009. Why have physical activity levels declined among Chinese adults? Findings from the 1991-2006 China health and nutrition surveys. Social Science and Medicine 68(7):1305-1314.

OCR for page 49
 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE Nishtar, S., A. M. A. Faruqui, M. A. Mattu, K. B. Mohamud, and A. Ahmed. 2004. The national action plan for the prevention and control of non-communicable diseases and health promotion in Pakistan—cardiovascular diseases. Journal of the Pakistan Medical Association 54(12 Suppl 3):S14-S25. Ntsekhe, M., and B. M. Mayosi. 2009. Cardiac manifestations of HIV infection: An African perspective. Nature Clinical Practice Cardiovascular Medicine 6(2):120-127. Office of National Statistics, L. Henderson, K. Irving, and J. Gregory. 2003. The national diet & nutrition survey: Adults aged  to  years. London: Office of National Statistics. Olshansky, S. J. 2006. Commentary: Prescient visions of public health from Cornaro to Bres- low. International Journal of Epidemiology 35(1):22-23. Olshansky, S. J., and A. B. Ault. 1986. The fourth stage of the epidemiologic transition: The age of delayed degenerative diseases. Milbank Quarterly 64(3):355-391. Omran, A. R. 1971. The epidemiologic transition. A theory of the epidemiology of population change. The Milbank Memorial Fund Quarterly 49(4):509-538. Palomaki, G. E., S. Melillo, and L. A. Bradley. 2010. Association between 9p21 genomic markers and heart disease: A meta-analysis. Journal of the American Medical Associa- tion 303(7):648-656. Pao, V., G. A. Lee, and C. Grunfeld. 2008. HIV therapy, metabolic syndrome, and cardiovas- cular risk. Current Atherosclerosis Reports 10(1):61-70. Pencina, M. J., R. B. D’Agostino, M. G. Larson, J. M. Massaro, and R. S. Vasan. 2009. Predicting the 30-year risk of cardiovascular disease: The Framingham Heart Study. Circulation 119(24):3078-3084. Peng, R. D., H. H. Chang, M. L. Bell, A. McDermott, S. L. Zeger, J. M. Samet, and F. Dominici. 2008. Coarse particulate matter air pollution and hospital admissions for car- diovascular and respiratory diseases among medicare patients. Journal of the American Medical Association 299(18):2172-2179. Pereira, M., N. Lunet, A. Azevedo, and H. Barros. 2009. Differences in prevalence, aware- ness, treatment and control of hypertension between developing and developed countries. Journal of Hypertension 27(5):963-975. Physical Activity Guidelines Advisory Committee. 2008. Physical activity guidelines advisory committee report, 00. Washington, DC: U.S. Department of Health and Human Services. Pietinen, P., E. Vartiainen, R. Seppanen, A. Aro, and P. Puska. 1996. Changes in diet in Fin- land from 1972 to 1992: Impact on coronary heart disease risk. Preventive Medicine 25(3):243-250. Pilote, L., K. Dasgupta, V. Guru, K. H. Humphries, J. McGrath, C. Norris, D. Rabi, J. Tremblay, A. Alamian, T. Barnett, J. Cox, W. A. Ghali, S. Grace, P. Hamet, T. Ho, S. Kirkland, M. Lambert, D. Libersan, J. O’Loughlin, G. Paradis, M. Petrovich, and V. Tagalakis. 2007. A comprehensive view of sex-specific issues related to cardiovascular disease. Canadian Medical Association Journal 176(6):S1-S44: Erratum 176(9):1310. Polk, D. M., and T. Z. Naqvi. 2005. Cardiovascular disease in women: Sex differences in presentation, risk factors, and evaluation. Current Cardiology Reports 7(3):166-172. Pope, C. A., and D. W. Dockery. 2006. Health effects of fine particulate air pollution: Lines that connect. EM: Air and Waste Management Association’s Magazine for Environmental Managers (JUN). Pope, C. A., R. T. Burnett, G. D. Thurston, M. J. Thun, E. E. Calle, D. Krewski, and J. J. Godleski. 2004. Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 109(1):71-77. Prentice, A. M., and S. E. Moore. 2005. Early programming of adult diseases in resource poor countries. Archives of Disease in Childhood 90(4):429-432.

OCR for page 49
 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD Puska, P., E. Vartiainen, J. Tuomilehto, V. Salomaa, and A. Nissinen. 1998. Changes in pre- mature deaths in Finland: Successful long-term prevention of cardiovascular diseases. Bulletin of the World Health Organization 76(4):419-425. Puska, P., E. Vartiainen, T. Laatinkainen, P. Jousilahti, and M. Paavola, eds. 2009. The North Karelia project: From North Karelia to national action. Helsinki: Helsinki University Printing House. Rao, A. V. 1998. Coronary heart disease risk factors in women: Focus on gender differences. Journal of the Louisiana State Medical Society 150(2):67-72. Rao, C., A. D. Lopez, G. Yang, S. Begg, and J. Ma. 2005. Evaluating national cause-of-death statistics: Principles and application to the case of China. Bulletin of the World Health Organization 83:618-625. Ray, K. K., S. R. K. Seshasai, S. Wijesuriya, R. Sivakumaran, S. Nethercott, D. Preiss, S. Erqou, and N. Sattar. 2009. Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: A meta-analysis of randomised controlled trials. Lancet 373(9677):1765-1772. Reddy, K. S. 2007. India wakes up to the threat of cardiovascular diseases. Journal of the American College of Cardiology 50(14):1370-1372. Reddy, S. P., S. Panday, D. Swart, C. C. Jinabhai, S. L. Amosun, S. James, K. D. Monyeki, G. Stevens, N. Morejele, N. S. Kambaran, R. G. Omardien, and H. W. Van den Borne. 2003. Umthenthe uhlaba usamila: The South African Youth Risk Behavior Survey 00. Cape Town: South African Medical Research Council. Reeves, M. J., C. D. Bushnell, G. Howard, J. W. Gargano, P. W. Duncan, G. Lynch, A. Khatiwoda, and L. Lisabeth. 2008. Sex differences in stroke: Epidemiology, clinical pre- sentation, medical care, and outcomes. Lancet Neurology 7(10):915-926. Regitz-Zagrosek, V. 2006. Therapeutic implications of the gender-specific aspects of cardio- vascular disease. Nature Reviews Drug Discovery 5(5):425-438. Rehm, J., C. Mathers, S. Popova, M. Thavorncharoensap, Y. Teerawattananon, and J. Patra. 2009. Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders. Lancet 373(9682):2223-2233. Reuser, M., L. G. Bonneux, and F. J. Willekens. 2009. Smoking kills, obesity disables: A mul- tistate approach of the US Health and Retirement Survey. Obesity 17(4):783-789. Rich, M. W., and G. A. Mensah. 2009. Fifth pivotal research in cardiology in the elderly (price-v) symposium: Preventive cardiology in the elderly—executive summary. Part I: Morning session. Preventive Cardiology 12(4):198-204. Rich, M. W., and G. A. Mensah. 2010. Fifth pivotal research in cardiology in the elderly (price-v) symposium: Preventive cardiology in the elderly—executive summary. Part II: Afternoon session. Preventive Cardiology 13(1):42-47. Rodriguez, T., M. Malvezzi, L. Chatenoud, C. Bosetti, F. Levi, E. Negri, and C. La Vecchia. 2006. Trends in mortality from coronary heart and cerebrovascular diseases in the Ameri- cas: 1970-2000. Heart 92(4):453-460. Roeters van Lennep, J. E., H. T. Westerveld, D. W. Erkelens, and E. E. van der Wall. 2002. Risk factors for coronary heart disease: Implications of gender. Cardiovascular Research 53(3):538-549. Roglic, G., and N. Unwin. 2009. Mortality attributable to diabetes: Estimates for the year 2010. Diabetes Research and Clinical Practice 87(1):15-19. Rosengren, A., S. Hawken, S. Ounpuu, K. Sliwa, M. Zubaid, W. A. Almahmeed, K. N. Blackett, C. Sitthi-amorn, H. Sato, and S. Yusuf. 2004. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): Case-control study. Lancet 364(9438):953-962.

OCR for page 49
 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE Rossouw, J. E., G. L. Anderson, R. L. Prentice, A. Z. LaCroix, C. Kooperberg, M. L. Stefanick, R. D. Jackson, S. A. Beresford, B. V. Howard, K. C. Johnson, J. M. Kotchen, J. Ockene, and Writing Group for the Women’s Health Initiative. 2002. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: Principal results from the Women’s Health Initiative randomized controlled trial. Journal of the American Medical Association 288(3):321-333. Rugulies, R. 2002. Depression as a predictor for coronary heart disease: A review and meta- analysis. American Journal of Preventive Medicine 23(1):51-61. Sabaté, E., WHO Adherence to Long Term Therapies Project, Global Adherence Interdisci- plinary Network, and World Health Organization Deptartment of Management of Non- communicable Diseases. 2003. Adherence to long-term therapies: Evidence for action. Geneva: World Health Organization. Sacks, F. M., M. A. Pfeffer, L. A. Moye, J. L. Rouleau, J. D. Rutherford, T. G. Cole, L. Brown, J. W. Warnica, J. M. Arnold, C. C. Wun, B. R. Davis, and E. Braunwald. 1996. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and recurrent events trial investigators. New England Journal of Medicine 335(14):1001-1009. Sarkar, S., and B. Mukhopadhyay. 2008. Perceived psychosocial stress and cardiovascular risk: Observations among the Bhutias of Sikkim, India. Stress and Health 24(1):23-34. Sassi, F., M. Cecchini, J. Lauer, and D. Chisholm. 2009. Improving lifestyles, tackling obesity: The health and economic impact of prevention strategies. Paris: OECD. Sattelmair, J. R., J. H. Pertman, and D. E. Forman. 2009. Effects of physical activity on cardiovascular and noncardiovascular outcomes in older adults. Clinics in Geriatric Medicine 25(4):677-702. Schaefer, B. M., V. Caracciolo, W. H. Frishman, and P. Charney. 2003. Gender, ethnicity, and genes in cardiovascular disease. Part 2: Implications for pharmacotherapy. Heart Disease 5(3):202-214. Schneidera, N. K., and T. E. Novotnya. 2007. Addressing smoking cessation in tuberculosis control. Bulletin of the World Health Organization 85(10):820. Schulze, M. B., F. B. Hu. 2005. Primary prevention of diabetes: What can be done and how much can be prevented? Annual Review of Public Health 26:445-467. Shafey, O., M. Eriksen, H. Ross, and J. Mackay. 2009. The tobacco atlas. 3rd ed. Atlanta: American Cancer Society. Shen, B. J., Y. E. Avivi, J. F. Todaro, A. Spiro III, J. P. Laurenceau, K. D. Ward, and R. Niaura. 2008. Anxiety characteristics independently and prospectively predict myocardial infarc- tion in men. The unique contribution of anxiety among psychologic factors. Journal of the American College of Cardiology 51(2):113-119. Shepherd, J., S. M. Cobbe, I. Ford, C. G. Isles, A. R. Lorimer, P. W. MacFarlane, J. H. McKillop, and C. J. Packard. 1995. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland coronary prevention study group. New England Journal of Medicine 333(20):1301-1307. Shopland, D. R. 1995. Tobacco use and its contribution to early cancer mortality with a special emphasis on cigarette smoking. Environmental Health Perspectives 103(Suppl 8):131-142. Shuter, J., and S. Bernstein. 2008. Cigarette smoking is an independent predictor of nonadher- ence in HIV-infected individuals receiving highly active antiretroviral therapy. Nicotine and Tobacco Research 10(4):731-736. Slama, K., C. Y. Chiang, D. A. Enarson, K. Hassmiller, A. Fanning, P. Gupta, and C. Ray. 2007. Tobacco and tuberculosis: A qualitative systematic review and meta-analysis. In- ternational Journal of Tuberculosis and Lung Disease 11(10):1049-1061.

OCR for page 49
0 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD Slattery, M. L., and D. E. Randall. 1988. Trends in coronary heart disease mortality and food consumption in the united states between 1909 and 1980. American Journal of Clinical Nutrition 47(6):1060-1067. Sliwa, K., D. Wilkinson, C. Hansen, L. Ntyintyane, K. Tibazarwa, A. Becker, and S. Stewart. 2008. Spectrum of heart disease and risk factors in a black urban population in South Africa (the Heart of Soweto study): A cohort study. Lancet 371(9616):915-922. South African Department of Health and Medical Research Council. 2007. South Africa De- mographic and Health Survey 00. Pretoria, South Africa: South African Department of Health. Srinivasan, S. R., G. H. Dahlen, R. A. Jarpa, L. S. Webber, and G. S. Berenson. 1991. Racial (black-white) differences in serum lipoprotein (a) distribution and its relation to parental myocardial infarction in children. Bogalusa Heart Study. Circulation 84(1):160-167. Stamler, J., R. Stamler, and J. D. Neaton. 1993. Blood pressure, systolic and diastolic, and car- diovascular risks: US population data. Archives of Internal Medicine 153(5):598-615. Steer, A. C., and J. R. Carapetis. 2009. Prevention and treatment of rheumatic heart disease in the developing world. Nature Reviews Cardiology 6(11):689-698. Steer, A. C., J. R. Carapetis, T. M. Nolan, and F. Shann. 2002. Systematic review of rheumatic heart disease prevalence in children in developing countries: The role of environmental factors. Journal of Paediatrics and Child Health 38(3):229-234. Stein, A. D., A. M. Thompson, and A. Waters. 2005. Childhood growth and chronic disease: Evidence from countries undergoing the nutrition transition. Maternal & Child Nutri- tion 1(3):177-184. Stettler, C., S. Allemann, P. Juni, C. A. Cull, R. R. Holman, M. Egger, S. Krahenbuhl, and P. Diem. 2006. Glycemic control and macrovascular disease in types 1 and 2 diabetes mel- litus: Meta-analysis of randomized trials. American Heart Journal 152(1):27-38. Steyn, N. P., D. Bradshaw, R. Norman, J. Joubert, M. Schneider, and K. Steyn. 2006. Dietary changes and the health transition in South Africa: Implications for health policy. Cape Town: South African Medical Research Council. Strong, J. P., G. T. Malcom, C. A. McMahan, R. E. Tracy, W. P. Newman, 3rd, E. E. Herderick, and J. F. Cornhill. 1999. Prevalence and extent of atherosclerosis in adolescents and young adults: Implications for prevention from the pathobiological determinants of atherosclero- sis in youth study. Journal of the American Medical Association 281(8):727-735. Thomas, R. J., P. J. Palumbo, L. J. Melton Iii, V. L. Roger, J. Ransom, P. C. O’Brien, and C. L. Leibson. 2003. Trends in the mortality burden associated with diabetes mellitus: A population-based study in Rochester, Minn, 1970-1994. Archives of Internal Medicine 163(4):445-451. Turnbull, F. M., C. Abraira, R. J. Anderson, R. P. Byington, J. P. Chalmers, W. C. Duckworth, G. W. Evans, H. C. Gerstein, R. R. Holman, T. E. Moritz, B. C. Neal, T. Ninomiya, A. A. Patel, S. K. Paul, F. Travert, and M. Woodward. 2009. Intensive glucose control and macrovascular outcomes in type 2 diabetes. Diabetologia. DOI 10.1007/s00125-00009-01470-00120. Turtzo, L. C., and L. D. McCullough. 2008. Sex differences in stroke. Cerebrovascular Dis- eases 26(5):462-474. Unal, B., J. A. Critchley, and S. Capewell. 2004. Explaining the decline in coronary heart disease mortality in England and Wales between 1981 and 2000. Circulation 109(9): 1101-1107. United Nations Development Program. 2007. Human development report 00/00: Fight- ing climate change: Human solidarity in a divided world. New York: United Nations Development Program. van Cappelle, F. 2009. StatPlanet: Interactive Data Visualization and Mapping Software, Southern and Eastern Africa Consortium for Monitoring Educational Quality, Paris. http://www.sacmeq.org/statplanet (accessed January 21, 2010).

OCR for page 49
 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE van Dam, R. M., T. Li, D. Spiegelman, O. H. Franco, F. B. Hu, R. M. van Dam, T. Li, D. Spiegelman, O. H. Franco, and F. B. Hu. 2008. Combined impact of lifestyle factors on mortality: Prospective cohort study in US women. British Medical Journal 337:a1440. Vartiainen, E., P. Puska, P. Jousilahti, H. J. Korhonen, J. Tuomilehto, and A. Nissinen. 1994a. Twenty-year trends in coronary risk factors in North Karelia and in other areas of Fin- land. International Journal of Epidemiology 23(3):495-504. Vartiainen, E., P. Puska, J. Pekkanen, J. Tuomilehto, and P. Jousilahti. 1994b. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. British Medical Journal 309(6946):23-27. Victora, C. G., L. Adair, C. Fall, P. C. Hallal, R. Martorell, L. Richter, and H. S. Sachdev. 2008. Maternal and child undernutrition: Consequences for adult health and human capital. Lancet 371(9609):340-357. Wagner, S., and R. M. Romano. 1994. Tobacco and the developing world: An old threat poses even bigger problems. Journal of the National Cancer Institute 86(23):1752. Walker, S., and S. George. 2007. Young@heart. USA: Fox Searchlight Pictures. Wang, L., X. Qi, C. Chen, J. Ma, L. Li, K. Rao, L. Kong, G. Ma, H. Xiang, J. Pu, J. Chen, Y. Chen, C. Chen, Y. He, J. Zhang, S. Jin, Y. Wu, X. Yang, J. Hu, C. Yao, W. Zhao, K. Ge, and F. Zai, eds. 2005. Survey and report on the status of nutrition and health of the Chinese people: A comprehensive report for 00. Beijing: People’s Medical Publishing House. Wang, Y., J. Mi, X. Y. Shan, Q. J. Wang, and K. Y. Ge. 2007. Is China facing an obesity epidemic and the consequences? The trends in obesity and chronic disease in China. International Journal of Obesity 31(1):177-188. Warren, C. W. 2003. Differences in worldwide tobacco use by gender: Findings from the global youth tobacco survey global. Journal of School Health 73(6):207-215. Warren, C. W., N. R. Jones, A. Peruga, J. Chauvin, J. P. Baptiste, V. Costa de Silva, F. el Awa, A. Tsouros, K. Rahman, B. Fishburn, D. W. Bettcher, and S. Asma. 2008. Global youth tobacco surveillance, 2000-2007. MMWR Surveillance Summaries 57(1):1-28. Wassertheil-Smoller, S., S. L. Hendrix, M. Limacher, G. Heiss, C. Kooperberg, A. Baird, T. Kotchen, J. D. Curb, H. Black, J. E. Rossouw, A. Aragaki, M. Safford, E. Stein, S. Laowattana, and W. J. Mysiw. 2003. Effect of estrogen plus progestin on stroke in post- menopausal women: The Women’s Health Initiative: A randomized trial. Journal of the American Medical Association 289(20):2673-2684. Watkins, D. A., L. J. Zuhlke, M. E. Engel, and B. M. Mayosi. 2009. Rheumatic fever: Ne- glected again. Science 324(5923):37. Watkins, R. E., and A. J. Plant. 2006. Does smoking explain sex differences in the global tuberculosis epidemic? Epidemiology and Infection 134(2):333-339. WHO (World Health Organization). 1999. The world health report: : Making a differ- ence. Geneva: World Health Organization. WHO. 2002. The world health report 00—reducing risks, promoting healthy life. Geneva: World Health Organization. WHO. 2003. The world health report: 00: Shaping the future. Geneva: World Health Organization. WHO. 2005. Preventing chronic diseases: A vital investment. http://www.who.int/chp/chronic_ disease_report/full_report.pdf (accessed April 23, 2009). WHO. 2007. WHO model list of essential medicines: th edition, revised March 00. Geneva: World Health Organization. WHO. 2008a. Childhood overweight and obesity. http://www.who.int/dietphysicalactivity/ childhood/en/ (accessed December 12, 2008). WHO. 2008b. The global burden of disease: 00 update. Geneva: World Health Organization.

OCR for page 49
 PROMOTING CARDIOVASCULAR HEALTH IN THE DEVELOPING WORLD WHO. 2008c. WHO report on the global tobacco epidemic, 00: The MPOWER package. Geneva: World Health Organization. WHO. 2009a. Global burden of disease 2004 data. Geneva, provided by Colin Mathers. WHO. 2009b. Global health risks: Mortality and burden of disease attributable to selected major risks. Geneva: World Health Organization. WHO. 2009c. WHO model list of essential medicines: th edition, revised March 00. Geneva: World Health Organization. WHO. 2009d. Working document for developing a draft global strategy to reduce harmful use of alcohol. Geneva: World Health Organization. WHO. 2009e. World health statistics 00. Geneva: World Health Organization. WHO Department of Child and Adolescent Health and Development. 2005. The current evidence for the burden of group a streptococcal diseases, Discussion papers on child health. Geneva: World Health Organization. WHO Expert Committee on Problems Related to Alcohol Consumption and WHO. 2007. Second report, World Health Organization technical report series. Geneva: World Health Organization. WHO Expert Committee on the Control of Chagas Disease and WHO. 2002. Control of Chagas disease: Second report of the WHO Expert Committee, WHO technical report series. Geneva: World Health Organization. WHO Regional Office for the Western Pacific. 2007. Mongolian STEPS survey on the preva- lence of noncommunicable disease risk factors 00. Manila, Philippines: WHO Regional Office for the Western Pacific. WHO Study Group on Rheumatic Fever and Rheumatic Heart Disease and WHO. 2004. Rheumatic fever and rheumatic heart disease: Report of a WHO expert consultation, Geneva, 0 October– November 00, World Health Organization technical report series. Geneva: World Health Organization. WHOSIS (World Health Organization Statistical Information System). 2009. World Health Organization. Witt, B. J., and V. L. Roger. 2003. Sex differences in heart disease incidence and prevalence: Implications for intervention. Expert Opinion on Pharmacotherapy 4(5):675-683. The Writing Committee. 2004. Cardio- and cerebrovascular events in HIV-infected persons. AIDS 18(13):1811-1817. Yach, D., C. Hawkes, C. L. Gould, and K. J. Hofman. 2004. The global burden of chronic diseases: Overcoming impediments to prevention and control. Journal of the American Medical Association 291(21):2616-2622. Yach, D., S. R. Leeder, J. Bell, and B. Kistnasamy. 2005. Global chronic diseases. Science 307(5708):317. Yang, G., L. Kong, W. Zhao, X. Wan, Y. Zhai, L. C. Chen, and J. P. Koplan. 2008. Emergence of chronic non-communicable diseases in China. Lancet 372(9650):1697-1705. Young, F., J. Critchley, and N. Unwin. 2009a. Diabetes & tuberculosis: A dangerous liaison & no white tiger. Indian Journal of Medical Research 130(1):1-4. Young, F., J. A. Critchley, L. K. Johnstone, and N. C. Unwin. 2009b. A review of co-morbidity between infectious and chronic disease in Sub Saharan Africa: TB and diabetes mellitus, HIV and metabolic syndrome, and the impact of globalization. Global Health 5:9. Yusuf, P. S., S. Hawken, S. Ounpuu, T. Dans, A. Avezum, F. Lanas, M. McQueen, A. Budaj, P. Pais, J. Varigos, and L. Lisheng. 2004. Effect of potentially modifiable risk factors associ- ated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 364(9438):937-952.

OCR for page 49
 EPIDEMIOLOGY OF CARDIOVASCULAR DISEASE Ziegelstein, R. C., J. A. Fauerbach, S. S. Stevens, J. Romanelli, D. P. Richter, and D. E. Bush. 2000. Patients with depression are less likely to follow recommendations to reduce car- diac risk during recovery from a myocardial infarction. Archives of Internal Medicine 160(12):1818-1823.

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