Worldwide, cardiovascular disease (CVD) is estimated to be the leading cause of death and loss of disability-adjusted life years. Although age-adjusted cardiovascular death rates have declined in several developed countries in past decades, rates of cardiovascular disease have risen greatly in low-income and middle-income countries [1]. CVD is now the leading cause of death in all developing regions, with the exception of sub-Saharan Africa [1]. It causes twice as many deaths as HIV, malaria, and tuberculosis combined. Furthermore, due to the increasing prevalence of risk factors and lack of appropriate preventive measures, a relatively younger population is affected by CVD in these countries [2]. This leads to the loss of many potential years of productive life and places a huge economic burden on these countries. Hence, efforts to produce even modest reductions in age-specific disease rates could have a very large economic impact.

Epidemiologic research findings from the Framingham Heart Study and many others have established high blood pressure, high blood cholesterol, smoking, obesity, diabetes, and physical inactivity as major risk factors for CVD [3]. These risk factors have been shown in other studies to apply almost universally among racial and ethnic groups [4]. In INTERHEART, a case–control study of 19,470 people from 52 countries, nine modifiable risk factors were found to have a globally consistent association with myocardial infarction (MI) in both sexes and at all ages and in all regions: abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, dietary factors, physical exercise, and alcohol consumption, with the two most important risk factors being smoking and abnormal lipids [5].

The levels of these risk factors have increased in most non-Western countries over the past two decades [1]. Social and economic changes have driven these trends. The epidemiologic transition is a term used to describe the observation that people are living longer, and those who live longer have greater exposure to risk factors. Westernized diets and patterns of physical inactivity result in elevations in blood pressure, body weight, blood sugar levels, and lipid concentrations. Moreover, the global expansion of the tobacco trade has led to large increases in the rate of smoking [6].

While clinical trials have provided us with evidence that treatment of people with elevated risk factors is efficacious in preventing CVD, it is less well known that lowering the levels of or eliminating risk factors in communities is effective in reducing the rate of CVD at the population level. The first line of evidence that CVD can be prevented at the population level comes from studying its trends in several high-income countries. For example, in the United States, the CVD mortality rate peaked during the 1960s then reversed direction and has generally steadily fallen since then. Reduction in the CVD mortality rate started before powerful modern medical treatments entered mainstream medical practice [7]. In addition, modeling studies have demonstrated that almost half of the decline in the rate of coronary heart disease in the US between 1980 and 2000 is attributable to the reductions in major risk factors. These signify that improvements in risk factors, primarily smoking, total cholesterol, and blood pressure, were key elements to initiate the decline [8].

Another line of evidence that population-based interventions can be effective in lowering the burden of CVD in the community comes from several epidemiologic studies, as mentioned bellow.

Primordial prevention is defined as prevention of the development of risk factors in the first place, and primary prevention are defined as interventions designed to modify adverse levels of risk factors once present with the goal of preventing an initial CVD event. Although no multi-decade, population-based, longitudinal studies have been conducted linking absolute levels of risk factors in childhood to incident clinical CVD events in adult life, several lines of evidence support the need for and value of prevention beginning early in life.

Barker et al., have suggested a developmental model for the origin of chronic non-communicable disease and suggested that people who develop cardiovascular disease or type 2 diabetes grew differently than other people in their early life. They tend to grow slowly in utero and in the first 2 years after birth, followed by a rapid compensatory growth later in life. Therefore, variations in fetoplacental and infant development appear to be linked to later chronic non-communicable disease [12]. Moreover, studies have shown that high maternal weight and adiposity are associated with the development of insulin deficiency, type 2 diabetes, and coronary heart disease in the offspring [13, 14]. Therefore, prevention efforts started early in life may have a lasting impact later or even from one generation to the next.

Additional evidence supporting the need for primordial and primary prevention beginning early in life comes from epidemiological studies indicating that major risk factors for CVD in adulthood, including cigarette smoking, dyslipidemia, elevated blood pressure, physical inactivity, and obesity, are prevalent in childhood and adolescence [15, 16], and are potentially modifiable [17, 18]. Furthermore, noninvasive imaging studies demonstrated that adverse levels of major risk factors for CVD measured in childhood and adolescence are associated with a significant subclinical atherosclerosis [19]. Risk factor exposures in 12- to 18-year-old adolescents predict increased carotid intima-media thickness in adulthood independently of the risk factors for CVD present in adulthood [20]. Children with type 2 diabetes mellitus have significantly greater carotid intima-media thickness and stiffer carotid arteries than their healthy counterparts [21]. Moreover, a combined data analysis from 4 cohorts comprising 4380 patients showed that risk factors from 9 years of age were predictive of carotid intima-media thickness in adulthood [22].

The efficacy and safety of modifying major CVD risk factors in early life with therapeutic lifestyle change and pharmacologic interventions have also been demonstrated. Lowering dietary intake of total fat, saturated fat, and cholesterol in prepubertal boys and girls aged 8–10 years resulted in significant reduction in low-density lipoprotein cholesterol levels [23]. Other studies have shown that 2 years of pravastatin therapy induced a significant regression of carotid atherosclerosis in children with familial hypercholesterolemia, with no adverse effects on growth, sexual maturation, hormone levels, or liver or muscle tissue [24]. School-based prevention interventions, including nutrition and physical activity components, led to significant decrease in weight and blood pressures, particularly among girls [25]. Finally, favorable risk factor levels in middle age are associated with a lower lifetime risk for CVD mortality, increased survival, and improved quality of life. Framingham Heart Study participants who were free of CVD at 50 years of age had very low lifetime risk for CVD and markedly longer survival [26]. Collectively, these results should promote efforts aimed at preventing development of risk factors in young individuals.

The economic impact of CVD comes both in direct costs to the health care system and indirectly in losses to the economy through work loss. This is particularly of importance in developing countries where CVD more frequently affects those of working age, and therefore leads to the loss of potential years of healthy life [3]. Hence, efforts to produce even modest reductions in age-specific disease rates could have very large economic impacts. For example, a 2 % annual reduction in cardiovascular death rates, as proposed by the World Health Organization (WHO) in 2005, may avert the loss of $8.1 billion over a decade, including $1.36 billion in China, $1.64 billion in India, and $1.49 billion in Russia [7]. There is no legal standard or regulation for what is cost-effective and this may vary among the countries. The WHO Commission on Macroeconomics and Health recommended choosing interventions that were less than three times a country’s growth national income (GNI) per capita [27]. The strategies reviewed below are generally acceptable in all developing regions, particularly since many are cost- saving interventions.