Randomized controlled trials documenting the effect of risk reduction in childhood on the development of CVD in adults, are lacking.[12,13] However observations from Bogalusa,[14] pathobiological determinants of atherosclerosis in children and young adults (PDAY)[15,16] and Muscatine[17] studies provide compelling evidence linking potentially modifiable cardiovascular risk factors and CVD in adults, and thus support the need for preventive interventions early in life.[5,6]

Physical inactivity is a major modifiable risk factor for CVD.[32] The health benefits associated with physical activity include weight control, lower blood pressure, improved psychological well being and decreased risk of CVD.[33] However, unfortunately, physical activity levels in children are decreasing mainly from sedentary life-style entertainments. The recommended frequency of 150 minutes of physical activity for elementary schools and 225 minutes for middle/junior and senior high schools per week[34] including a mix of recreational and organized aerobic activities based on child's age, sex, race, sexual maturity, size, skill and social class should be implemented.

Tobacco smoking is an important and modifiable cardiovascular risk factor.[35] Both smoking and smokeless tobacco is equally prevalent amongst the youth of developing countries.[36] A recent Indian study reports more than 25% in 13- to 15-year-olds to be tobacco users, contributing to 17% of current total tobacco users.[37] More than 80% established adult smokers initiate smoking before the age of 18 years.[38–40] Hence, there is an urgent need to intervene early.[40] There are numerous interacting determinants that influence smoking behavior.[41] Environmental factors (sociocultural, economic and political) and personal characteristics like demographics, personality, education, and information are main influences in smoking initiation in children.[42] Prenatal maternal smoking has immediate and long-term adverse birth outcomes, including the onset of adult chronic diseases. Therefore, targeting smoking cessation among pregnant women should contribute to a healthy intergenerational effect.

Obesity in childhood and adolescence is attaining an epidemic proportion at about 15–20% in India.[43] Overweight and obesity in childhood are associated with diverse cardiovascular risk factors and has been shown to be related with premature atherosclerotic lesions.[33,44] Unlike in adults it is not possible to identify a single BMI (body-mass-index) cut off point as a threshold for defining obesity in children, as BMI changes with age across development.[45] Further, there is also a need for age and gender specific percentile based cut off points of anthropometric and metabolic variables in South Asian children and adolescents.[46] South Asia is facing the double burden of over and under-nutrition.[47–49] The South Asian newborns, children and adults have higher body fat compared to the Caucasians of similar body weight, and cardiovascular risk manifests at a lower level of adiposity.[50] Obesity in South Asian children is also reported to be related with adverse lipid profile.[51]

Excess body fat, thick truncal subcutaneous fat, and abdominal adiposity are major predisposing factors for insulin resistance in South Asian children.[50] They manifest adiposity, insulin resistance and metabolic perturbations earlier in life with a higher magnitude than with children of other ethnic groups. Since the metabolic syndrome and obesity track into adulthood, these clinical entities need to be recognized early for effective prevention of diabetes and CVD.[7] Insulin resistance and hyperinsulinemia are early metabolic manifestations and should be incorporated to define insulin resistance and metabolic syndrome in these children.[46]

Childhood hypertension is a recognized predisposing factor of adult hypertension as reported in the Bogalusa Heart Study.[52] Current guidelines suggest that children ≥3years of age have to get their blood pressure measured during their routine health assessment.[53] Hypertension in children is defined as systolic or diastolic blood pressure steadily above 95^th percentile on three different occasions.[33] Furthermore children have a 10% higher risk of developing hypertension in adulthood for each 1 to 2 mmHg increment of systolic BP.[54] These guidelines need to be validated and re-examined in South Asian children for population-specific reference values.[20,55]

Epidemiological studies have established positive relationship between conventional dyslipidemia in patients of CVD and their children.[56,57] Lipid abnormalities in children indeed contribute to adult CVD.[51] However, such traditional lipid risk factors do not explain fully the increased susceptibility of South Asians to CVD.[58] Hence, there is a strong need to identify the nontraditional lipid risk factors in childhood such as alterations in serum levels of Lp(a), Apo A-I, and Apo B-100 in children of premature South Asian CVD patients.[56,59] Consequently, emerging concepts like Lipid Tetrad Index [Total cholesterol x triglycerides x Lp(a)/HDL Cholesterol],[60] Lipid Pentad Index (Total Cholesterol x Triglyceride x Lp(a) x Apo B-100]/Apo A-I[59] and Atherogenic Index [Log(Triglycerides/HDL Cholesterol))[61] are to be validated to explain the risk profile of premature CVD in South Asian children and youth. Cholesterol levels track over time,[33] and it is interesting to note that adult serum lipid and lipoprotein levels are observed in children as young as 2 years of age.[62] Consequently, the United States (US) national cholesterol education programme suggested at-risk children screening based on a family history of premature CHD or parental dyslipidemia after 2 years of birth.[63] Nonetheless, gender and ethnic-specific guidelines of similar nature are important potential tools for certain pediatric populations.[64]

Family history of CVD encompasses genetically transmitted risk along with shared environment and behaviors influencing modifiable risk factors.[12] It is an important step in screening children's risk, as CVD tends to cluster in families and is a proxy for inherited tendency for coronary risk. It is an independent CHD risk predictor.[8] Family history of premature CHD is defined as a documented myocardial infarction, angiographic documentation of CHD, angina pectoris, or sudden cardiac death in first or second degree relatives (parents, siblings, grandparents, or blood-related aunts and uncles) ≤ 55 years of age.[33] However there is paucity of data regarding this from South Asia.