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Circulation. 2007;116:344-357
Published online before print June 25, 2007, doi: 10.1161/CIRCULATIONAHA.107.184595
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(Circulation. 2007;116:344-357.)
© 2007 American Heart Association, Inc.


AHA Scientific Statements

Primary Prevention of Cardiovascular Disease in Nursing Practice: Focus on Children and Youth

A Scientific Statement From the American Heart Association Committee on Atherosclerosis, Hypertension, and Obesity in Youth of the Council on Cardiovascular Disease in the Young, Council on Cardiovascular Nursing, Council on Epidemiology and Prevention, and Council on Nutrition, Physical Activity, and Metabolism

Laura L. Hayman, PhD, RN, FAAN, FAHA; Janet C. Meininger, PhD, RN, FAAN; Stephen R. Daniels, MD, PhD, FAHA; Brian W. McCrindle, MD, MPH; Liz Helden, MEd, BSN, RN; Joyce Ross, MSN, RN; Barbara A. Dennison, MD, FAHA; Julia Steinberger, MD, MS; Christine L. Williams, MD, MPH, FAHA


Key Words: AHA Scientific Statements • cardiovascular diseases • children • pediatrics • prevention • risk factors


*    Introduction
up arrowTop
*Introduction
down arrowEvidence for CVD Prevention...
down arrowPromoting Cardiovascular Health...
down arrowSummary
down arrowReferences
 
Cardiovascular disease (CVD) is a leading cause of morbidity and premature mortality in women and men in the United States, most of the industrialized world, and many developing countries.1 Data accumulated over the past 3 decades indicate that atherosclerotic-CVD processes begin early in childhood and are influenced over the life course by genetic and potentially modifiable risk factors and environmental exposures. Taken together, these data provide compelling evidence for primary prevention of CVD beginning early in childhood. Within the pediatric healthcare community, this evidence has prompted and informed the development of science-based guidelines with recommendations for individual/high-risk and population-based approaches to primary prevention of CVD in children and youth. The purpose of this statement is to provide an overview of the evidence and current science-based recommendations and to emphasize the role of advanced practice nurses in the implementation of strategies consistent with population-based and individual/high-risk approaches to CVD prevention in children and youth.


*    Evidence for CVD Prevention in Childhood
up arrowTop
up arrowIntroduction
*Evidence for CVD Prevention...
down arrowPromoting Cardiovascular Health...
down arrowSummary
down arrowReferences
 
Evidence-based guidelines for primary and secondary prevention of CVD in adults are informed by the results of randomized controlled trials. The existing evidence (discussed below) argues convincingly for prevention of CVD beginning early in childhood. It is noteworthy that data from randomized controlled trials documenting the effect of risk reduction in childhood on the development of CVD in adulthood are nonexistent. Similarly, no long-term longitudinal studies have been conducted to determine the absolute levels of risk factors measured in childhood that predict CVD in adult life. However, evidence from laboratory, clinical, and epidemiological studies supports the need for primary prevention of CVD beginning early in life and has prompted and informed existing guidelines for children and adolescents.

Laboratory/Pathology and In Vivo/Clinical Studies
Autopsy studies conducted as part of the Bogalusa Heart Study2,3 and the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study4,5 demonstrate significant positive associations between potentially modifiable CVD risk factors and the presence and extent of atherosclerotic lesions in the aorta and coronary arteries.2–5 In the pathology component of the Bogalusa Heart Study, a long-term epidemiological study of risk factors for CVD in a biracial (black-white) population, risk factors were measured in free-living, healthy children and adolescents before death from non-CVD causes.2,3 The PDAY study quantified risk factors by analyses of postmortem blood samples obtained at autopsy from {approx}3000 persons 15 to 34 years of age who died from external causes, including accidents and homicides.4,5 Findings from PDAY4,5 and Bogalusa2,3 confirmed the positive associations between modifiable risk factors, including hypertension, tobacco use, obesity, atherogenic lipids (non–high-density lipoprotein cholesterol [HDL-C]), and the presence and extent of arterial lesions and the negative association of cardioprotective HDL-C with these lesions.2–5 More recently, noninvasive imaging has been used to examine the association of risk factors for CVD and vascular structure and function in childhood and adolescence and atherosclerosis in young adult life. Investigators from the Muscatine Study, a landmark longitudinal, observational study of CVD risk factors in children and youth, used carotid ultrasound in adults 33 to 42 years of age and found that carotid intima-media thickness was positively associated with levels of total serum cholesterol and body mass index (BMI) measured in childhood.6 Similar results were observed in Bogalusa: childhood low-density lipoprotein cholesterol (LDL-C) level and BMI predicted increased carotid intima-media thickness in adulthood.7 Results from the Young Finns Study reaffirm the link between risk factor exposures (including LDL-C, BMI, cigarette smoking, and systolic blood pressure [SBP]) in 12- to 18-year-old adolescents and preclinical atherosclerosis in adulthood.8 Results from this population-based prospective cohort study of 2229 young adults 24 to 39 years of age are noteworthy because risk factors present in adolescence predicted adult common carotid intima-media thickness independently of contemporaneous risk factors.8 Data from other noninvasive studies of adolescents and young adults are consistent with these results indicating that intraindividual clustering of multiple risk factors adversely affects carotid intima-media thickness during these developmental periods.9,10

Taken together, the results of laboratory/pathology studies and more recent noninvasive studies provide convincing evidence of the link between established potentially modifiable risk factors and accelerated atherosclerotic processes in adolescence and adulthood and support the need for primary prevention beginning early in life.

Epidemiological Studies
Several sources, including the National Health and Nutrition Examination Surveys (NHANES),11 the Centers for Disease Control and Prevention–Youth Risk Behavior Surveillance Surveys (CDC-YRBSS),12 the National Heart, Lung, and Blood Institute (NHLBI),13 and the American Heart Association (AHA),1 provide nationally representative data on the distribution, prevalence and trends, and tracking of major risk factors and CVD-related health behaviors in children and youth. Data on potentially modifiable risk factors and behaviors, which are essential for the development of both individual and public health approaches to primary prevention, are presented below.

Lipids and Lipoproteins
Population-based data from the Lipid Research Clinics indicate that serum lipids and lipoproteins increase throughout the first 2 years of life and reach young adult levels by 2 years of age.14 Partly on the basis of these observations of non-Hispanic white and black males and females, the National Cholesterol Education Program15 issued the first guidelines for assessing the lipid profile and recommended selective screening for high-risk children (as defined by family history of premature CHD or parental dyslipidemia) after 2 years of age.

Population-based data from NHANES III (1988–1994) indicate that among children and adolescents (4 to 19 years old), the mean total cholesterol (TC) was 165 mg/dL. The mean age-specific values for TC peaked at 171 mg/dL just before puberty at 9 to 11 years of age and decreased thereafter.11 Females had significantly higher mean TC and LDL-C than males. Children and adolescents classified as non-Hispanic black had higher LDL-C and cardioprotective HDL-C compared with those classified as non-Hispanic white or Mexican American.11 Approximately 10% of adolescents (12 to 19 years old) had TC levels >200 mg/dL. An analysis of time trends for adolescents 12 to 17 years of age revealed a decline in mean TC of 7 mg/dL from 1966–1970 to the 1988–1994 survey.11 A similar but greater decline has been observed in adults, providing evidence of a strong prevention effect in the United States from 1959 to 1994.16 However, data from NHANES 1999–2000 indicate that mean levels of TC for children and adolescents (4 to 17 years old) have remained relatively unchanged since NHANES III.17 The Figure illustrates trends in mean TC observed in adolescents (12 to 17 years old) in the NHANES surveys.


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Figure. Trends in mean total blood cholesterol among adolescents 12 to 17 years of age by sex, race, and survey. NHES indicates National Health Examination Surveys.

Although population-based prevention efforts aim to lower the distribution of TC and LDL-C for all children and adolescents, cut points for acceptable, borderline, and high levels have been established for assessment of individuals between the ages of 2 and 19 years as follows: acceptable (TC <170 mg/dL; LDL-C <110 mg/dL); borderline (TC 170 to 199 mg/dL; LDL-C 110 to 129 mg/dL); and high (TC ≥200 mg/dL; LDL-C ≥130 mg/dL).15 Baseline data (collected in 1991) in the Child and Adolescent Trial for Cardiovascular Health (CATCH) indicated that 13.3% of children in the fourth grade in 4 geographic areas in the United States had TC levels ≥200 mg/dL, with a higher percentage of girls (15.6%) than boys (11.1%) at this high level. A higher prevalence of elevated TC was observed for African American (17.4%) than Anglo-American (12.5%) or Latino (13.2%) subjects.18 A similar overall percentage (12.6%) was observed for 8- to 10-year-old subjects in the Cardiovascular Health in Children (CHIC) baseline study (conducted in the early 1990s) in North Carolina; however, gender differences were not pronounced. The CHIC study confirmed a higher percentage of African American children (18.7%) with high TC compared with Anglo-American children (11%) and others (11.8).19

Examining gender and ethnic/racial group differences in lipids and lipoproteins across broader age ranges is more complex. Longitudinal follow-up of children and adolescents in Project HeartBeat! in Texas demonstrated that development has a profound impact on TC values and that these developmental patterns are different for males and females.20 Recent longitudinal evidence from 2 biracial cohort studies is consistent with these observations indicating that pubertal stage affects estimated prevalence of dyslipidemia as defined by current single cut points.21 Age-gender patterns are further complicated by the fact that African American children have, on average, an earlier onset of sexual maturation than other racial/ethnic groups in the United States.22

Taken together, these observations underscore the need to reexamine current recommendations for assessment and management of the lipid profile in children and adolescents. Attention to the documented influences of gender, race/ethnicity, and sexual maturation on lipids and lipoproteins is likely to increase the sensitivity and specificity of screening and improve management of dyslipidemia as part of CVD risk reduction for children and youth.

Tracking of lipids and lipoproteins, particularly TC and LDL-C from childhood to young adulthood, has been observed in males and females from diverse racial/ethnic groups and is particularly evident in the upper and lower extremes of the distribution. In the Muscatine Study, 75% of children who were 5 to 18 years of age at baseline and had TC levels greater than the 90th percentile had elevated TC (≥200 mg/dL) at 20 to 25 years of age.23,24 Bogalusa data indicate that {approx}70% of children with elevated TC in childhood persisted with elevated levels in young adulthood.25 Tracking, maintenance of percentile rank over time, is relevant to primary prevention because of the potential for identifying children at risk for future CVD.

Blood Pressure
Compared with NHANES III (1988–1994),26 results from the most recent survey (1999–2000) of 5582 black, Hispanic, and white children 8 to 17 years of age indicate substantial increases in SBP and diastolic blood pressure (DBP) for all age, race/ethnic, and gender subgroups examined.27 In NHANES III, children’s mean SBP was 104.6 mm Hg, and mean DBP was 58.4 mm Hg.26 In the most recent survey, children’s mean SBP was 106 mm Hg, and mean DBP was 61.7 mm Hg.27 Adjustment for the BMI distribution in 1988–1994 and 1999–2000 reduced the increases in SBP and DBP by 29% and 12%, respectively.27 These results suggest that increases in BP in US children and youth are partially attributable to the increases in the prevalence of overweight. Other data underscore the clinical significance of these adverse trends indicating that, for each increment of 1 to 2 mm Hg in SBP, children have a 10% greater risk of developing hypertension in adulthood.28 Additionally, modest elevations in BP levels in childhood have an adverse effect on vascular structure and function, with target organ damage (ie, left ventricular hypertrophy) documented in hypertensive children and adolescents.29,30

Although African American adults have significantly higher levels of blood pressure (BP) and higher prevalence and mortality from CVD, ethnic group differences in BP among children and adolescents are not evident in all studies and when present have produced conflicting results.31 Detailed studies with ambulatory BP monitoring indicate that differences between African and European American adolescents in levels and diurnal patterns of BP are evident, but some of these differences are accounted for by other variables such as body size, sexual maturation, and socioeconomic status.32,33 Few studies have included adequate numbers of Hispanic American children and adolescents to allow for subgroup analysis. An exception is a study of 7207 children 5 to 17 years of age that included Mexican American (58.2%), African American (13.2%), and non-Hispanic white children (28.3%).34 There were no consistently significant differences in SBP or DBP across ethnic/racial groups.34 Recent NHANES data, however, indicate slightly higher levels of BP among Mexican American youth (8 to 17 years of age) compared with their non-Hispanic white counterparts.27 Analysis of pooled data from large national studies in the United States revealed an interaction between BMI and ethnic group; these interactions were different for SBP and DBP and not consistent across age and gender groups. In general, at lower levels of BMI, black youth had higher SBP and DBP, whereas at higher levels of BMI, white youths had higher SBP and DBP.31

Tracking of BP during childhood and adolescence and from childhood to adulthood tends to be weaker and more disparate for BP than for other risk factors for CVD, largely because of the inherent variability of BP. Nevertheless, elevated BP in childhood predicted hypertension in young adulthood for participants in the Bogalusa Heart Study.35 Similarly, with the use of data from an East Boston cohort and by averaging BP measurements over several years during childhood, tracking correlations for SBP were 0.55 in boys and 0.66 in girls, and for DBP, were 0.47 for boys and 0.57 for girls.36

Although not common in children, primary hypertension has been observed, is usually characterized by mild or stage 1 hypertension, and is often associated with family history of this risk factor and/or CVD.29,37 As documented in the most recent NHANES,27 overweight and obesity are positively associated with elevated BP levels in childhood and adolescence. Data from school health screening programs indicate a progressive increase in the prevalence of hypertension with increases in BMI.38 Intraindividual clustering of CVD risk factors, including low HDL-C, elevated triglycerides, hyperinsulinemia, and truncal obesity, has been observed in children with elevated BP.39–42

Collectively, these results have informed recent guidelines for clinical practice that place emphasis on comprehensive assessment of the CVD risk factor profile in children and youth with elevated levels of SBP and/or DBP.42 These guidelines, the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents, were published in 2004.42 They also recommend that children ≥3 years of age have their BP measured when seen in a medical setting. Correct methods of measurement are described in this report along with recommended dimensions for BP cuff bladders.42 Assessing whether a BP level of a child is elevated is difficult in that the standards for SBP and DBP are specific for age, gender, and percentile of height. Interpretation is facilitated by free software available from the NHLBI, which can be downloaded to a personal digital device.43 Assessment of BP in children is further complicated by the necessity of confirming an elevated BP on multiple occasions before characterizing a child as having hypertension.42

BMI, Adiposity, and Related Comorbidities
For children in the United States, the CDC age- and genderspecific nomograms are used to monitor patterns of growth and define overweight and obesity.44 On the basis of cross-sectional data from sequential measurements of representative samples of US children, cut points (by age and gender) are defined as follows: normal weight (BMI percentile >5th and <85th); at risk for overweight (BMI percentile between 85th and 95th); and overweight (BMI percentile ≥95th).44,45 It is noteworthy that some recent reports, including a report issued by the Institute of Medicine, classify children with BMI ≥95th percentile as obese.46

Recognized as a major risk factor for CVD in adulthood, overweight and obesity in children and adolescents in the United States (and globally) have become major public health challenges.47–49 With overweight defined as a BMI for age and gender ≥95th percentile, data from the most recent NHANES (2003–2004) indicate that 17.4% of adolescents (12 to 19 years old) and 18.8% of children (6 to 11 years old) are overweight.49 During 1999–2004, significant time trends were also observed for male and female children and adolescents, with increases in overweight prevalence from 13.8% to 16.0% and from 14.0% to 18.2% in female and male children and adolescents, respectively. As illustrated in Table 1, across the past 3 NHANES reports and consistent with other data, higher prevalence of excess BMI has been observed in non-Hispanic black and Mexican American children and adolescents compared with their non-Hispanic white counterparts.49


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TABLE 1. Percentage of Children and Adolescents Who Are Overweight*

Particularly important from a CVD prevention perspective are the documented comorbidities associated with overweight in children, including atherogenic dyslipidemia, hypertension, left ventricular hypertrophy, insulin resistance, and the clustering and tracking of risk factors recognized as metabolic syndrome in adults.50–56 Although controversy exists regarding the specific components, cut points, and clinical utility of defining metabolic syndrome in children and youth, studies have estimated prevalence rates using Adult Treatment Panel III criteria adapted for pediatric populations. Accordingly, a report from NHANES III estimated that 1 million US adolescents meet the criteria for metabolic syndrome, with an estimated population prevalence of 4%.52 In overweight children and youth, prevalence estimates range from 30% to 50%.52,53,55

With the use of the Adult Treatment Panel III criteria, a recent longitudinal assessment of predictors of metabolic syndrome in black and white females (18 to 19 years old) from the NHLBI Growth and Health Study indicated a prevalence of 3.5% and 2.4% in black and white females, respectively, in adolescence.57 Results of multivariate analysis indicated that central adiposity, as measured by waist circumference at baseline (9 to 10 years of age), was a significant predictor of metabolic syndrome. Racial differences in prevalence of components of metabolic syndrome were observed; increases in body size, central adiposity, and SBP and DBP in black females exceeded those observed in white females.57 However, the increase in insulin sensitivity (as defined by homeostasis model assessment–insulin resistance scores), consistent with completion of puberty, reduced the risk of metabolic syndrome. Racial differences in triglyceride levels were observed, with considerable increases from baseline noted in white females only. The contribution of adverse levels of triglycerides as a defining component of metabolic syndrome was less in black females than in their white counterparts. Patterns observed in adiposity-triglyceride associations at follow-up (18 to 19 years of age) suggest racial differences in triglyceride metabolism and warrant further research.57

Paralleling the increases observed in the prevalence of overweight/obesity is the increase in type 2 diabetes mellitus in youth. A recent report that combined results from population-based studies and clinical case series conducted in North America, Europe, and the Asian-Pacific region documents a global spread of type 2 diabetes mellitus.58 Although type 2 diabetes mellitus accounted for {approx}3% of incident cases of diabetes in youth in 1990, combined results from this report indicate that 45% of new cases of diabetes in youth are type 2 diabetes mellitus.58 The patterns and trends observed (by geographic region, ethnicity, and culture) suggest that attention to the epidemiology of this chronic condition in adults may assist in predicting incident type 2 diabetes mellitus in youth. Limitations in differential diagnosis and classification (type 1 versus type 2 diabetes mellitus) notwithstanding,58 results are consistent with obesity–type 2 diabetes mellitus associations documented in other clinical and population-based studies.59,60

Taken together, these results suggest the potential for manifest CVD earlier in adult life for our current generation of children and youth and underscore the critical importance of primary prevention of overweight/obesity as part of a comprehensive profile approach to cardiovascular health and CVD risk reduction in childhood. They also suggest the need for increased attention to ethnic, cultural, and gender-related factors and issues in tailoring individual approaches to preventive interventions.

Health Behaviors
The cornerstone of cardiovascular health promotion and risk reduction in childhood and adolescence is healthy lifestyle behaviors and therapeutic lifestyle change. Recent population-based prevalence and trend data on health behaviors central to current recommendations, however, provide cause for concern. Although some positive trends have been observed in tobacco use, a recent (2006) report from the Office of National Drug Control Policy indicated that 730 000 adolescent girls and 565 000 adolescent boys in the United States initiated cigarette smoking in 2004.61 Early adolescence is recognized as a critical period for smoking initiation; {approx}80% of persons who use tobacco begin before the age of 18 years.61,62

Data from CDC-YRBSS for 2003 indicate that 30.3% of male high school students and 24.6% of female students use tobacco.63 A very recent report from CDC-YRBSS indicates that the prevalence of lifetime, current, and frequent cigarette use among high school students remains basically unchanged from 2003 to 2005.64,65 Several surveys of adolescents in the United States indicate racial/ethnic and gender differences in patterns of tobacco use. A consistent observation across recent CDC and NHANES surveys is higher prevalence of tobacco use for non-Hispanic whites compared with their non-Hispanic black and Hispanic counterparts.63–65 Among high school students, CDC data indicate a higher percentage of current cigarette use among black males (19.3%) than black females (10.8%).63 This survey, based on 2003 data, also indicated high prevalence (26.6%) of current smoking in non-Hispanic white females.63 Data from the most recent survey indicate persistence in gender and ethnic differences in current cigarette use, with no significant changes observed except for black males, whose current use declined from 19.3% to 14.0%.65 Socioeconomic status emerged as an important predictor of tobacco use in the analysis of Winkleby et al66 of NHANES data, with higher prevalence observed among youth of lower socioeconomic status.

Although the determinants of smoking initiation in youth are multifaceted and include individual and familial factors, the role of broader socioecological influences and multilevel policies cannot be overemphasized. For example, statewide tobacco control programs have been instrumental in preventing smoking initiation. In California, where intense tobacco control and prevention programs were implemented in 1990, the proportion of 12- to 17-year-old persons who reported never smoking increased from 60% of males and 66% of females in 1990 to 70% of both males and females in 1999. From 2002 to 2004, however, overall statewide spending on tobacco prevention and control programs declined by 28% in the United States.67 Program cuts exceeded 75% in some states, including Minnesota, where reductions were associated with decreased awareness of the antitobacco campaign and a substantial increase in smoking susceptibility in youth.68

As emphasized in pediatric guidelines for cardiovascular health and CVD risk reduction, patterns of dietary intake and physical activity for a majority of children and adolescents are not meeting current recommendations.65,69–71 Data indicate adverse trends in food consumption, particularly among older school-aged children and adolescents.65,72–74 These trends include reduction of high-fiber fruits and vegetables and dairy products consumed and increased consumption of nutrient-poor foods and sweetened beverages and increased percentage of total calories from snacks.65,72–74 In adolescents, these changes in dietary patterns have resulted in median intakes below the recommended values of several micronutrients, including calcium and potassium, and sodium intakes that are well above recommended levels.63,65,74 Data from the US Department of Agriculture (2005) also document dietary deficiencies (in male and female children and adolescents) in micronutrients necessary for healthy immune and metabolic functions, including magnesium, iron, zinc, and vitamins B6, C, D, and E.71

Similarly, adverse trends in physical education and patterns of leisure-time physical activity have been documented, particularly among adolescent girls. Recent (2005) data from the CDC indicate that only 54.2% of students nationwide are enrolled in physical education classes on 1 or more days of an average school week, and 33.0% are enrolled in daily physical education.65 Nationwide, 35.8% of students reported the recommended levels of moderate to vigorous physical activity of at least 60 minutes per day on at least 5 days per week.65 The prevalence of meeting this recommendation was higher among male (43.8%) than female (27.8%) students and lowest in black females (21.3%).65 Consistent with results from the CDC,65 a population-based study of black and white girls documented substantial declines in leisure-time physical activity throughout adolescence; by age 18 or 19 years, 56% of black girls and 31% of white girls reported no habitual recreational activity.75

Sedentary behaviors such as television viewing are considered risk factors for obesity in children and adolescents. On the basis of data linking these sedentary behaviors with overweight in childhood and adolescence and data indicating that reduction in viewing time can be an effective strategy for improving weight status,76–78 current recommendations limit television viewing (and other sedentary behaviors) to <2 hours per day.79 Current national estimates, however, indicate that 37.2% of students watched television at least 3 hours per day on an average school day.65 The prevalence of this behavior was higher among black (64.1%) than white (29.2%) and Hispanic students (45.8%).65 As discussed below, these health behavior data support the need for population-based as well as individual approaches to cardiovascular health promotion and CVD risk reduction in children and adolescents.


*    Promoting Cardiovascular Health and Reducing Risk for CVD in Children and Youth
up arrowTop
up arrowIntroduction
up arrowEvidence for CVD Prevention...
*Promoting Cardiovascular Health...
down arrowSummary
down arrowReferences
 
Background
Primary prevention of CVD beginning in childhood includes and encompasses both cardiovascular health promotion and reduction of established, modifiable risk factors for CVD.79 Primordial prevention goes beyond prevention of risk factor development in children and refers to "preserving risk-factor free societies from the penetration of risk factor epidemics."80 This level of prevention addresses the societal and environmental conditions that foster risk factor development. Two main strategies are recommended for prevention of CVD across the life course, including children and adolescents. Population-based (or public health) approaches are designed to move the population distribution of risk factors to lower, more desirable levels. The rationale supporting this approach is that the vast majority of cases of CVD arise from the broad middle range of the distribution of risk factors. Thus, concentrating only on those with extreme values may prevent or delay disease in a relatively small segment of those at risk.81 Individually oriented approaches are designed to identify and manage children and youth at highest risk for atherosclerotic disease. These strategies are complementary in CVD prevention and are frequently implemented in tandem in pediatric clinical (and community-based) settings. Central to the population approach and a major cornerstone of CVD risk reduction for children and adolescents with identified risk factors is adoption of healthy lifestyle behaviors. As reflected in guidelines and statements issued by the AHA,79,82,83 the American Academy of Pediatrics,84 and numerous expert panels, emphasis is placed on healthy lifestyle training to promote cardiovascular health in childhood; to normalize levels of identified, modifiable risk factors; and to reduce the risk and burden of CVD in adult life. As discussed below, nurses, including advanced practice nurses and nurse practitioners, equipped with the evidence base in prevention, developmental life course, and behavioral science and the respective skill sets and competencies are well prepared to implement strategies consistent with both individual and population-based approaches to CVD prevention in children and youth.

Population-Based Approaches to CVD Prevention
Population-based or public health approaches normally involve interventions at the community level, such as the CVD prevention trials implemented in the United States and Sweden during the 1970s.85 Schools, preschools, and other community-based settings in which child care is provided are important venues for implementing population-based strategies in children and adolescents. As detailed in integrative reviews,86–89 school-based interventions have been effective in conveying knowledge and improving attitudes and CVD-related health behaviors; however, the influence of multicomponent interventions on physiological risk factors for CVD, including dyslipidemia and obesity, has been less than optimal and variable across studies.86–89 Lessons learned from methodologically rigorous and resource-intensive randomized controlled trials clearly indicate the importance of developmentally appropriate, culturally sensitive individual (student-level) interventions combined with modifications of the school food and physical activity environments.90 Additional research is needed, however, to define the duration, intensity, and specific intervention elements relevant to physical activity and dietary modification necessary to reduce physiological risk factors (ie, overweight) as part of school-based interventions. In addition, as currently emphasized in social-ecological models of health, attention to the multiple levels of environmental influences (including regulatory policies) will be necessary to promote and sustain healthy patterns of behavior across the life course of individuals and diverse populations.46,91 The epidemic of childhood obesity exemplifies the importance of an ecological approach and has called attention to the potential impact of school communities (including the built environment), the food industry, and the media in primordial prevention of overweight in childhood. The AHA, American Academy of Pediatrics, Institute of Medicine, and National Association of Pediatric Nurse Practitioners and Associates advocate prevention approaches that address these levels of influence as well as individual- and family-level factors.45,46,84,92

Numerous opportunities exist for nurses and advanced practice nurses/nurse practitioners in implementing population-based approaches to CVD prevention. The American Heart Association Guide for Improving Cardiovascular Health at the Community Level provides examples and evidence-based recommendations for cardiovascular health promotion at the community level.93 The recommendations included in this guide are consistent with those recently issued by the CDC94 and the Task Force on Community Preventive Services.95 The AHA’s Scientific Statement Cardiovascular Health Promotion in the Schools88 is particularly applicable for population-based primordial and primary prevention focused on children and youth. This statement builds on the community guide and endorses the school environment (including preschools and after-school programs) as an integral part of population-based strategies designed to promote cardiovascular health for all US children and youth.88 Consistent with the population approach outlined in the AHA’s guidelines for primary prevention,79 the goals and recommendations emphasize heart health education and behavioral skill training, school policies, and school and community linkages necessary to optimize the capacity of school environments in shaping health behaviors, including patterns of dietary intake and physical activity.88

School nurses are particularly well positioned to assume leadership roles relevant to several major recommendations issued in this statement and in those offered by the National Association of Pediatric Nurse Practitioners and Associates for nurses and nurse practitioners in school and community-based settings: (1) advocating for and conducting evidence-based, comprehensive, age-appropriate heart health education; (2) implementing age-appropriate and culturally sensitive curricula on changing students’ patterns of dietary intake, physical activity, and smoking behaviors; (3) screening and referral of children identified as at risk for CVD; and (4) establishing links with community resources and infrastructures necessary to support the school environment in promoting the cardiovascular health of children and youth at the district, school, and individual levels.88,92 Consistent with recommendations 1 and 2 (above) are the implications for school nurses resulting from the Child Nutrition and Women, Infants, and Children Reauthorization Act of 2004.96 Specifically, this mandate requires all school districts with federally funded meal programs to develop and implement wellness policies by the start of the 2006–2007 school year. Schools are required to (1) set goals for nutrition education, physical activity, and other school-based initiatives designed to promote wellness; (2) establish nutrition standards for all foods that are available on each school campus during the school day; (3) monitor the implementation of the wellness policy; and (4) involve a broad group of individuals in its development.96 The expertise of the school nurse can be a valuable addition to the educational team in establishing goals relevant to school wellness, including curricular development and revision aimed at improving health behaviors and reducing CVD risk. As recognized experts on children’s health, school nurses are well positioned to advocate (on multiple levels) for policy changes necessary for the actual implementation of age-appropriate heart health education, behavioral skill training, and policy changes necessary for increasing physical education in the school curriculum and increasing nutritious foods as part of meals served, à la carte, and vending machine menus.97 School nurses can also be instrumental in advocating for alternative nonfood rewards and promoting inclusion of nutritious and culturally appropriate foods for holiday parties and school functions.

Not all children receive regular physical examinations or well-child care outside of that provided in the school environment. Assessment and identification of risk factors for CVD are key components of primary prevention; thus, incorporating CVD risk factor screening with school-based (and preschool) health assessments would assist in early identification of children at risk.98 School-based screening for overweight and other risk factors often stretches the limits of time available to school nurses in view of the increasing health needs of school-age children. University–school district partnerships are one approach to expanding opportunities for CVD risk factor screening in schools.99 As experts on resources in their communities, school nurses are well positioned to provide appropriate referrals for children and their families once identification of a risk factor has been established.

It is noteworthy that other pediatric agencies and expert groups have also suggested schools as viable settings for population-based approaches to CVD prevention in children and adolescents and have issued recommendations consistent with those of the AHA.46,92 Thus, with authority and empowerment to implement the strategies suggested herein, school nurses could have a pivotal role in optimizing population-based approaches to cardiovascular health in children and youth.

Individual/High-Risk Approaches to CVD Prevention
Across healthcare settings, individual approaches begin with a comprehensive assessment of the total CVD risk profile. As emphasized in child health guidelines and recommendations.42,45,79,82,83 CVD-related health behaviors, the cornerstone of cardiovascular health promotion and disease prevention (interventions designed to normalize levels of risk factors and deter atherosclerotic disease processes), are assessed and monitored at each well-child visit. The AHA recommends a developmental, profile approach to the assessment and management of tobacco use, physical activity, dietary intake, family history of CVD, and physiological risk factors.79,82 For young children (<2 years old), assessment of parents’/caregivers’ health behaviors is recommended, including patterns of household smoking. An important part of individual/high-risk assessment approaches is a multigenerational family history of CVD (including age of onset) and diagnostic and treatment history of attendant risk factors and comorbidities (ie, hypertension, dyslipidemia, obesity, diabetes). The family health history/portrait should be updated at visits throughout childhood and adolescence. Consistent with recommendations advanced by the National Cholesterol Education Program,15 the AHA emphasizes early identification and follow-up of children with a family history of premature CVD (age of onset ≤55 years in males and ≤65 years in females).79

Levels of concern for CVD risk factors and behaviors (Table 2) and recommendations for follow-up (Table 3) are based on currently available data. Although cut points are provided to assist clinicians in identifying children at risk and in guiding treatment decisions, it is important to emphasize that no long-term longitudinal studies have been conducted to determine the absolute levels in childhood and adolescence that accelerate atherosclerotic processes and predict CVD in adult life. In addition, the relationship between established risk factors (eg, LDL-C, hypertension) and CVD is continuous and graded. Thus, these are important factors for consideration in clinical decision making regarding both identification of risk status and management/treatment of risk factors.


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TABLE 2. Cardiovascular Risk Profile


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TABLE 3. Guidelines for CVD Risk Reduction Intervention for Children and Adolescents With Identified Risk*

As illustrated in Table 3, lifestyle modification (therapeutic lifestyle change) with emphasis on normalization of body weight and healthy patterns of dietary intake and physical activity is essential for treatment of children identified with CVD risk factors. Central to therapeutic lifestyle change are effective strategies for behavioral change.100 Table 4 includes evidence-based strategies that have been effective in modifying CVD-related health behaviors in children and families.100–102


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TABLE 4. Behavioral Change Principles and Strategies for Children, Adolescents, and Families*

Prescriptions for an adequate trial of therapeutic lifestyle change consider the specific risk factor(s) identified, severity of risk (ie, overweight versus morbidly obese), child’s age, developmental level, and presence of comorbidities. For example, the recommended treatment plan for a 10-year-old male who presents with dyslipidemia (LDL-C of 145 mg/dL measured in a fasting state on 2 occasions), BMI at the 85th age- and gender-specific percentile, no other comorbidities, and a negative multigenerational family history would have a diet and physical activity prescription as outlined in Table 3. An adequate trial (ie, 6 to 12 months) of therapeutic lifestyle change is recommended, with dietary modifications initiated in conjunction with a trained dietitian (ie, restriction of dietary intake of saturated fat, trans fat, and cholesterol; increase of total fiber with emphasis on viscous fiber)103 and physical activity/energy expenditure necessary to normalize body weight. Individual modifications are based on caloric (and macronutrient and micronutrient) needs necessary to sustain growth and developmental processes and adjusted on the basis of the child’s response to treatment.

Pharmacological interventions for children with dyslipidemia and/or other CVD risk factors are (currently) prescribed as defined in Table 3 and are normally initiated in collaboration with physicians with expertise and experience in treating the respective risk factor in children. A comprehensive discussion of pharmacological agents approved for use in reducing CVD risk factors and prevention of CVD in children and adolescents is beyond the scope of this statement and is presented elsewhere.104 The AHA guidelines (2007) for drug therapy of lipid abnormalities have recently been revised and updated104 on the basis of available evidence. Revised guidelines for treatment of hypertension in children appear in the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents.42

Across healthcare settings, management of dyslipidemia, hypertension, and other CVD risk factors in children and adolescents is best accomplished with a multidisciplinary collaborative team approach. Advanced practice nurses/nurse practitioners and nurses experienced in assessment and management of CVD risk factors in children and adolescents, including family-focused strategies for behavioral change, are essential for optimizing initiation of and long-term adherence to the treatment plan. The effectiveness of multidisciplinary nurse-directed management as a model for improving outcomes in adults with coronary heart disease risk factors and coronary heart disease has been demonstrated.105–107 This collaborative, multidisciplinary approach is highlighted in a recent statement issued by the AHA105 and emphasized in integrative reviews and analyses of studies that tested such models and demonstrated improved outcomes in persons with coronary heart disease (secondary prevention) and/or with coronary heart disease risk factors (primary prevention).106,107 The essential characteristics are consistent with elements defined in the chronic care model108,109 and include the following: advanced practice nurse with specialized knowledge and skill for collaborative practice; comprehensive, individually tailored lifestyle management programs that incorporate principles of health behavior change; systematic mechanisms for follow-up, adherence monitoring, and tracking; and coordination of services with multiple providers.106,107 Although nurse-managed, multidisciplinary models adapted for CVD prevention with children and families have been suggested and are being implemented in selected clinical settings, process and outcome evaluation data are not available.


*    Summary
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up arrowIntroduction
up arrowEvidence for CVD Prevention...
up arrowPromoting Cardiovascular Health...
*Summary
down arrowReferences
 
Compelling evidence accumulated over the past 3 decades supports a life course approach to primary prevention of CVD with efforts beginning early in childhood. Data from laboratory, clinical, and epidemiological studies also underscore the importance of both population-based/public health and individual/high-risk strategies for CVD prevention beginning early in childhood and extending across the life course. Current science-based recommendations, highlighted in this statement, emphasize the development and maintenance of healthy lifestyle behaviors and therapeutic lifestyle change as the cornerstone of interventions focused on promoting cardiovascular health and reducing the risk and burden of CVD. Additional research is needed, however, to inform, guide, and evaluate optimal life course strategies for CVD prevention, including multidisciplinary models and integrated systems of healthcare that link individual/high-risk and population-based/public health strategies. Equipped with the evidence base in prevention, developmental life course, and behavioral science and the respective skill sets and competencies, nurses will continue to be central and essential in the design and implementation of effective strategies for CVD prevention.


*    Acknowledgments
 
Disclosures


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Writing Group Disclosures


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Reviewer Disclosures


*    Footnotes
 
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.

This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on March 19, 2007. A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0414. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.

Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.americanheart.org/presenter.jhtml?identifier=3023366.

Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.americanheart.org/presenter.jhtml?identifier=4431. A link to the "Permission Request Form" appears on the right side of the page.


*    References
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up arrowIntroduction
up arrowEvidence for CVD Prevention...
up arrowPromoting Cardiovascular Health...
up arrowSummary
*References
 
1. Heart Disease and Stroke Statistics: 2006 Update. Dallas, Tex: American Heart Association; 2006.

2. Newman WP III, Freedman DS, Voors AW, Gard PD, Srinivasan SR, Cresanta JL, Williamson GD, Webber LS, Berenson GS. Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis: the Bogalusa Heart Study. N Engl J Med. 1986; 314: 138–144.[Abstract]

3. Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, Wattigney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: the Bogalusa Heart Study. N Engl J Med. 1998; 338: 1650–1656.[Abstract/Free Full Text]

4. McGill HC Jr, McMahan CA, Zieske AW, Malcolm GT, Tracy RE, Strong JP. Effects of nonlipid risk factors on atherosclerosis in youth with a favorable lipoprotein profile. Circulation. 2001; 103: 1546–1550.[Abstract/Free Full Text]

5. McGill HC Jr, McMahan CA, Malcolm GT, Oalmann MC, Strong JP; the PDAY Research Group: Pathobiological Determinants of Atherosclerosis in Youth. Effects of serum lipoproteins and smoking on atherosclerosis in young men and women. Arterioscler Thromb Vasc Biol. 1997; 17: 95–106.[Abstract/Free Full Text]

6. Davis PH, Dawson JD, Riley WA, Lauer RM. Carotid intimal-medial thickness is related to cardiovascular risk factors measured from childhood through middle age: the Muscatine Study. Circulation. 2001; 104: 2815–2819.[Abstract/Free Full Text]

7. Li S, Chen W, Srinivasan SR, Bond MG, Tang R, Urbina EM, Berenson GS. Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study. JAMA. 2003; 290: 2271–2276.[Abstract/Free Full Text]

8. Raitakari OT, Juonala M, Kahonen M, Taittonen L, Laitnen T, Maki-Torkko N, Jarvisalo MJ, Uhari M, Jokinen E, Ronnemaa T, Akerblom HK, Viikari JS. Cardiovascular risk factors in childhood and carotid intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA. 2003; 290: 2277–2283.[Abstract/Free Full Text]

9. Knoflach M, Kiechl S, Kind M, Said M, Sief R, Gisinger M, van der Zee R, Gaston H, Jarosch E, Willeit J, Wick G. Cardiovascular risk factors and atherosclerosis in young males: ARMY study (Atherosclerosis Risk-Factors in Male Youngsters). Circulation. 2003; 108: 1064–1069.[Abstract/Free Full Text]

10. Sanchez A, Barth JD, Zhang L. The carotid artery wall thickness in teenagers is related to their diet and the typical risk factors of heart disease among adults. Atherosclerosis. 2000; 152: 265–266.[CrossRef][Medline] [Order article via Infotrieve]

11. Hickman TB, Briefel RR, Carroll MD, Rifkind BM, Cleeman JI, Maurer KR, Johnson CL. Distributions and trends of serum lipid levels among United States children and adolescents ages 4–19 years: data from the Third National Health and Nutrition Examination Survey. Prev Med. 1998; 27: 879–890.[CrossRef][Medline] [Order article via Infotrieve]

12. Centers for Disease Control and Prevention. Surveillance summary. MMWR. 2004; 53: 1–96.[Medline] [Order article via Infotrieve]

13. National Heart, Lung, and Blood Institute, National Institutes of Health. Publications for Health Professionals. Available at: http://www.nhlbi.nih.gov/health/pubs/pub_prof.htm. Accessed May 1, 2006.

14. National Heart, Lung, and Blood Institute. The Lipid Research Clinics Population Studies Book, Volume I: The Prevalence Study. Washington, DC: US Department of Health and Human Services, Public Health Service, National Institutes of Health; 1980. NIH publication 80-1527.

15. National Cholesterol Education Program. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Washington, DC: US Department of Health and Human Services, Public Health Service, National Institutes of Health; 1991. NIH publication 91-2732.

16. Goff DC, Labarthe DR, Howard G, Russell GB. Primary prevention of high blood cholesterol concentrations in the United States. Arch Intern Med. 2002; 162: 913–919.[Abstract/Free Full Text]

17. Ford ES, Mokdad AH, Ajani UA. Trends in risk factors for cardiovascular disease among children and adolescents in the United States. Pediatrics. 2004; 114: 1534–1544.[Abstract/Free Full Text]

18. Webber LS, Osganian V, Luepker RV, Feldman HA, Stone EJ, Elder JP, Perry CL, Nader PR, Parcel GS, Broyles SL, McKinlay SM. Cardiovascular risk factors among third grade children in four regions of the United States: the CATCH Study: Child and Adolescent Trial for Cardiovascular Health. Am J Epidemiol. 1995; 141: 428–439.[Abstract/Free Full Text]

19. Bradley CB, Harrell JS, McMurray RG, Bangdiwala SI, Frauman AC, Webb JP. Prevalence of high cholesterol, high blood pressure, and smoking among elementary school children in North Carolina. N C Med J. 1997; 58: 362–367.[Medline] [Order article via Infotrieve]

20. Labarthe DR, Nichaman MZ, Harrist RB, Grunbaum JA, Dai S. Development of cardiovascular risk factors from ages 8 to 18 in Project Heartbeat! Study design and patterns of change in plasma total cholesterol concentration. Circulation. 1997; 95: 2636–2642.[Abstract/Free Full Text]

21. Friedman LA, Morrison JA, Daniels SR, McCarthy WF, Sprecher DL. Sensitivity and specificity of pediatric lipid determinations for adult lipid status: findings from the Princeton Lipid Research Clinics Prevalence Program Follow-Up Study. Pediatrics. 2006; 118: 165–172.[Abstract/Free Full Text]

22. Sun SS, Schubert CM, Chumlea WC, Roche AF, Kulin HE, Lee PA, Himes JH, Ryan AS. National estimates of the timing of sexual maturation and racial differences among US children. Pediatrics. 2002; 110: 911–919.[Abstract/Free Full Text]

23. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine Study. Pediatrics. 1988; 82: 309–318.[Abstract/Free Full Text]

24. Lauer RM, Clarke WR. Use of cholesterol measurements in childhood for the prediction of adult hypercholesterolemia: the Muscatine Study. JAMA. 1990; 264: 3034–3038.[Abstract/Free Full Text]

25. Webber LS, Srinivasan SR, Wattigney WA, Berenson GS. Tracking of serum lipids and lipoproteins from childhood to adulthood: the Bogalusa Heart Study. Am J Epidemiol. 1991; 133: 884–899.[Abstract/Free Full Text]

26. National Center for Health Statistics. Plan and Operation of the Third National Health and Nutrition Examination Survey, 1988–1994. Rockville, Md: US Department of Health and Human Services; 1994. Publication 94-1308.

27. Muntner P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in blood pressure among children and adolescents. JAMA. 2004; 291: 2107–2113.[Abstract/Free Full Text]

28. Ingelfinger JR. Pediatric antecedents of adult cardiovascular disease: awareness and intervention. N Engl J Med. 2004; 350: 2123–2126.[Free Full Text]

29. Daniels SD, Meyer RA, Loggie JM. Determinants of cardiac involvement in children and adolescents with essential hypertension. Circulation. 1990; 82: 1243–1248.[Abstract/Free Full Text]

30. Hanevold C, Waller J, Daniels SR, Portman R, Sorof J; International Pediatric Hypertension Association. The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the International Pediatric Hypertension Association. Pediatrics. 2004; 113: 328–333.[Abstract/Free Full Text]

31. Rosner B, Prineas R, Daniels SR, Loggie J. Blood pressure differences between blacks and whites in relation to body size among US children and adolescents. Am J Epidemiol. 2000; 151: 1007–1019.[Abstract/Free Full Text]

32. Meininger JC, Liehr P, Chan W, Smith G, Mueller WH. Developmental, gender, and ethnic group differences in moods and ambulatory blood pressure in adolescents. Ann Behav Med. 2004; 28: 10–19.[CrossRef][Medline] [Order article via Infotrieve]

33. Meininger JC, Liehr P, Mueller WH, Chan W, Chandler PS. Predictors of ambulatory blood pressure: identification of high-risk adolescents. ANS Adv Nurs Sci. 1998; 20: 50–64.[Medline] [Order article via Infotrieve]

34. Park MK, Menard SW, Yuan C. Comparison of blood pressure in children from three ethnic groups. Am J Cardiol. 2001; 87: 1305–1308.[CrossRef][Medline] [Order article via Infotrieve]

35. Bao W, Threefoot SA, Srinivasan SR, Berenson GS. Essential hypertension predicted by tracking of elevated blood pressure from childhood to adulthood: the Bogalusa Heart Study. Am J Hypertens. 1995; 8: 657–665.[CrossRef][Medline] [Order article via Infotrieve]

36. Cook NR, Gillman MW, Rosner BA, Taylor JO, Hennekens CH. Combining annual blood pressure measurements in childhood to improve prediction of young adult blood pressure. Stat Med. 2000; 19: 2625–2640.[CrossRef][Medline] [Order article via Infotrieve]

37. Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics. 1989; 84: 633–641.[Abstract/Free Full Text]

38. Sorof J, Daniels S. Obesity hypertension in children: a problem of epidemic proportions. Hypertension. 2002; 40: 441–447.[Abstract/Free Full Text]

39. Sorof JM, Poffenbarger T, Franco K, Bernard L, Portman RJ. Isolated systolic hypertension, obesity, and hyperkinetic hemodynamic states in children. J Pediatr. 2002; 140: 660–666.[CrossRef][Medline] [Order article via Infotrieve]

40. Sinaiko AR, Steinberger J, Moran A, Prineas RJ, Jacobs JR Jr. Relation of insulin resistance to blood pressure in childhood. J Hypertens. 2002; 20: 509–517.[CrossRef][Medline] [Order article via Infotrieve]

41. Boyd GS, Koenigsberg J, Falkner B, Gidding S, Hassink S. Effect of obesity and high blood pressure on plasma lipid levels in children and adolescents. Pediatrics. 2005; 116: 442–446.[Abstract/Free Full Text]

42. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004; 114 (suppl): 555–576.[Free Full Text]

43. Department of Health and Human Services, National Heart, Lung, and Blood Institute, National Institutes of Health. Clinical reference tool for the 4th Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents. Available at: http://hp2010.nhlbihin.net/nhlbi_peds/hbppedpda.htm. Accessed July 31, 2006.

44. Centers for Disease Control and Prevention, National Center for Health Statistics. 2000 CDC growth charts: United States. Available at: http://www.cdc.gov/nchc/about/major/nhanes/growthcharts/datafiles.htm. Accessed April 15, 2006.

45. Daniels SR, Arnett DK, Eckel RH, Gidding SS, Hayman LL, Kumanyika S, Robinson TN, Scott BJ, St Jeor S, Williams CL. Overweight in children and adolescents: pathophysiology, consequences, prevention and treatment. Circulation. 2005; 111: 1999–2012.[Abstract/Free Full Text]

46. Koplan JP, Liverman CT, Kraak VI, eds. Preventing Childhood Obesity: Health in the Balance. Washington, DC: Institute of Medicine, National Academies Press; 2004.

47. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986–1998. JAMA. 2001; 286: 2845–2848.[Abstract/Free Full Text]

48. Grunbaum JA, Kann L, Kinchen S, Ross J, Hawkins J, Lowry R, Harris WA, McManus T, Chyen D, Collins J. Youth risk behavior surveillance: United States. MMWR. 2004; 53: 87–90.

49. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM. Prevalence of overweight and obesity in the United States, 1999–2004. JAMA. 2006; 295: 1549–1555.[Abstract/Free Full Text]

50. Chen W, Srinivasan SR, Elkasabany A, Berenson GS. Cardiovascular risk factors clustering features of insulin resistance syndrome (syndrome X) in a biracial (black-white) population of children, adolescents, and young adults: the Bogalusa Heart Study. Am J Epidemiol. 1999; 150: 667–674.[Abstract/Free Full Text]

51. Goodman E, Dolan LM, Morrison JA, Daniels SR. Factor analysis of clustered cardiovascular risks in adolescence: obesity is the predominant correlate of risk among youth. Circulation. 2005; 111: 1970–1977.[Abstract/Free Full Text]

52. Cook S, Weitzman A. Auinger P, Nguyen M, Dietz WH. Prevalence of a metabolic syndrome phenotype in adolescents: findings from the Third National Health and Nutrition Examination Survey, 1988–1994. Arch Pediatr Adolesc Med. 2003; 157: 821–827.[Abstract/Free Full Text]

53. de Ferranti SD, Gauvreau K, Ludwig DS, Newfeld EJ, Newburger JW, Rifai N. Prevalence of the metabolic syndrome in American adolescents: findings from the Third National Health and Nutrition Examination Survey. Circulation. 2004; 110: 2494–2497.[Abstract/Free Full Text]

54. Lambert M, Paradis G, O’Loughlin J, Delvin EE, Hanley JA, Levy E. Insulin resistance syndrome in a representative sample of children and adolescents from Quebec, Canada. Int J Obes Relat Metab Disord. 2004; 28: 833–841.[CrossRef][Medline] [Order article via Infotrieve]

55. Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, Allen K, Lopes M, Savoye M, Morrison J, Sherwin RS, Caprio S. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004; 350: 2362–2374.[Abstract/Free Full Text]

56. Sinaiko AR, Steinberger J, Moran A, Prineas RJ, Vessby B, Basu S, Tracy R, Jacobs DR. Relation of body mass index and insulin resistance to cardiovascular risk factors, inflammatory factors, and oxidative stress during adolescence. Circulation. 2005; 111: 1985–1991.[Abstract/Free Full Text]

57. Morrison JA, Friedman LA, Harlan WR, Harlan LC, Barton BA, Schreiber GB, Klein DJ. Development of the metabolic syndrome in black and white adolescent girls: a longitudinal assessment. Pediatrics. 2005; 116: 1178–1182.[Abstract/Free Full Text]

58. Pinhas-Hamiel O, Zeitler P. The global spread of type 2 diabetes mellitus in children and adolescents. J Pediatr. 2005; 146: 693–700.[CrossRef][Medline] [Order article via Infotrieve]

59. Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr. 1996; 128 (pt 1): 608–615.[CrossRef][Medline] [Order article via Infotrieve]

60. Scott CR, Smith JM, Cradock MM, Pihoker C. Characteristics of youth-onset noninsulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus at diagnosis. Pediatrics. 1997; 100: 84–91.[Abstract/Free Full Text]

61. Office of National Drug Policy Control. Girls and Drugs. Washington, DC: Office of National Drug Policy Control; 2006. Available at: http://www.mediacampaign.org/pdf/girls_and_drugs.pdf. Accessed May 1, 2006.

62. US Department of Health and Human Services. Reducing Tobacco Use: A Report of the Surgeon General. Atlanta, Ga: US Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2000.

63. Grunbaum JA, Kann L, Kinchen S, Ross J, Hawkins J, Lowry R, Harris WA, McManus T, Chyen D, Collins J. Youth Risk Behavior Surveillance: United States, 2003 (abridged). J Sch Health. 2004; 74: 307–324.[Medline] [Order article via Infotrieve]

64. Centers for Disease Control and Prevention (CDC). Cigarette use among high school students: United States, 1991–2005. MMWR Morb Mortal Wkly Rep. 2006; 55: 724–726.[Medline] [Order article via Infotrieve]

65. Eaton DK, Kann L, Kinchen S, Ross J, Hawkins J, Harris WA, Lowry R, McManus T, Chyen D, Shanklin S, Lim C, Grunbaum JA, Wechsler H. Youth Risk Behavior Surveillance: United States, 2005. MMWR Surveill Summ. 2006; 55: 1–108.[Medline] [Order article via Infotrieve]

66. Winkleby MA, Robinson TN, Sundquist J, Kraemer HC. Ethnic variation in cardiovascular disease risk factors among children and young adults: findings from the Third National Nutrition Examination Survey, 1988–1994. JAMA. 1999; 281: 1006–1113.[Abstract/Free Full Text]

67. Centers for Disease Control and Prevention (CDC). Estimated exposure of adolescents to state-funded anti-tobacco television advertisement: 37 states and the District of Columbia, 1999–2003. MMWR Morb Mortal Wkly Rep. 2005; 54: 1077–1080.[Medline] [Order article via Infotrieve]

68. Sly DF, Arheart K, Dietz N, Trapido EJ, Nelson D, Rodriguez R, McKenna J, Lee D. The outcome consequences of defunding the Minnesota youth tobacco-use prevention program. Prev Med. 2005; 41: 503–510.[CrossRef][Medline] [Order article via Infotrieve]

69. US Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health. 2nd ed. Washington, DC: US Government Printing Office; 2000.

70. Strong WB, Malina RM, Blimkie CJ, Daniels SR, Dishman RK, Gutin B, Hergenroeder AC, Must A, Nixon PA, Pivarnik JM, Rowland T, Trost S, Trudeau F. Evidence based physical activity for school-age youth. J Pediatr. 2005; 146: 732–737.[CrossRef][Medline] [Order article via Infotrieve]

71. US Department of Agriculture, Agricultural Research Service. What We Eat in America. 2005. NHANES 2001–2002: usual nutrient intakes from food compared to dietary reference intakes. Available at: http://www.ars.usda.gov/ba/bhnrc/fsrg. Accessed October 15, 2006.

72. Nielsen SJ, Siega-Riz AM, Popkin BM. Trends in energy intake in the U.S. between 1977 and 1996: similar shifts seen across age groups. Obes Res. 2002; 10: 370–378.[Medline] [Order article via Infotrieve]

73. Cavadini C, Siega-Riz AM, Popkin BM. US adolescent food intake trends from 1965 to 1996 [published correction appears in Arch Dis Child. 2002;87:85]. Arch Dis Child. 2000; 83: 18–24.[Abstract/Free Full Text]

74. Wright JD, Wang CY, Kennedy-Stephenson J, Ervin RB. Dietary intake of ten key nutrients for public health, United States: 1999–2000. Adv Data. 2003: 1–4.

75. Kimm SY, Glynn NW, Kriska AM, Barton BA, Kronsberg SS, Daniels SR, Crawford PB, Sabry ZI, Liu K. Decline in physical activity in black girls and white girls during adolescence. N Engl J Med. 2002; 347: 709–715.[Abstract/Free Full Text]

76. Dietz WH Jr, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics. 1985; 75: 807–812.[Abstract/Free Full Text]

77. Robinson TN, Hammer LD, Killen JD, Kraemer HC, Wilson DM, Hayward C, Taylor CB. Does television viewing increase obesity and reduce physical activity? Cross-sectional and longitudinal analyses among adolescent girls. Pediatrics. 1993; 91: 273–280.[Abstract/Free Full Text]

78. Robinson TN. Reducing children’s television viewing to prevent obesity: a randomized controlled trial. JAMA. 1999; 282: 1561–1567.[Abstract/Free Full Text]

79. Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Taubert K; American Heart Association. American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood [duplicate publication in J Pediatr. 2003;142:368–372]. Circulation. 2003; 107: 1562–1566.[Free Full Text]

80. Strausser T. Reflections on cardiovascular diseases. Interdisc Sci Rev. 1978; 3: 225–230.

81. Rose G. Sick individuals and sick populations. Int J Epidemiol. 1985; 14: 32–38.[Medline] [Order article via Infotrieve]

82. Williams CL, Hayman LL, Daniels SR, Robinson TN, Steinberger J, Paridon S, Bazzarre T. Cardiovascular health in childhood: a statement for health professionals from the Committee on Atherosclerosis, Hypertension, and Obesity in the Young (AHOY) of the Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2002; 106: 143–160.[Free Full Text]

83. Gidding SS, Dennison BA, Birch LL, Daniels SR, Gillman MW, Lichtenstein AH, Rattay KT, Steinberger J, Stettler N, Van Horn L; American Heart Association; American Academy of Pediatrics. Dietary recommendations for children and adolescents: a guide for practitioners: consensus statement from the American Heart Association. Circulation. 2005; 112: 2061–2075.[Abstract/Free Full Text]

84. Council on Sports Medicine and Fitness; Council on School Health. Active healthy living: prevention of childhood obesity through increased physical activity. Pediatrics. 2006; 117: 1834–1842.[Abstract/Free Full Text]

85. Stone EJ, Pearson TA, eds. Community trials for cardiopulmonary health: directions for public health practice, policy and research. Ann Epidemiol. 1997; S7: S1–S124.[CrossRef]

86. Resnicow T, Robinson TN. School-based cardiovascular disease prevention studies: review and synthesis. Ann Epidemiol. 1997; S7: S14–S31.[CrossRef]

87. Meininger JC. Primary prevention of cardiovascular disease risk factors: review and implications for population-based practice. Adv Pract Nurs Q. 1997; 3: 70–79.[Medline] [Order article via Infotrieve]

88. Hayman LL, Williams CL, Daniels SR, Steinberger J, Paridon S, Dennison BA, McCrindle BW. Cardiovascular health promotion in the schools: a statement for health and education professionals and child health advocates form the Committee on Atherosclerosis, Hypertension, and Obesity in Youth (AHOY) of the Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004; 110: 2266–2275.[Free Full Text]

89. Meininger JC. School-based interventions for primary prevention of cardiovascular disease: evidence of effects for minority populations. Ann Rev Nurs Res. 2000; 18: 219–244.[Medline] [Order article via Infotrieve]

90. Luepker RV, Perry CL, McKinlay SM, Nader PR, Parcel GS, Stone EJ, Webber LS, Elder JP, Feldman HA, Johnson CC, Kelder SH, Wu M; CATCH Collaborative Group. Outcomes of a field trial to improve children’s dietary patterns and physical activity: the Child and Adolescent Trial for Cardiovascular Health (CATCH). JAMA. 1996; 275: 768–776.[Abstract/Free Full Text]

91. Hayman LL. Behavioral medicine across the life course: challenges and opportunities for interdisciplinary science. Ann Behav Med. 2007; 33: 319–324.

92. The National Academy of Nurse Practitioners (NAPNAP). Healthy Eating and Activity Together (HEAT): Clinical Practice Guideline: Identifying and Preventing Overweight in Childhood. Cherry Hill, NJ: NAPNAP; 2006.

93. Pearson TA, Bazzarre TL, Daniels SR, Fair JM, Fortmann SP, Franklin BA, Goldstein LB, Hong Y, Mensah GA, Sallis JF Jr, Smith S Jr, Stone NJ, Taubert KA. American Heart Association guide for improving cardiovascular health at the community level: a statement for public health practitioners, healthcare providers, and health policy makers from the American Heart Association Expert Panel on Population and Prevention Science. Circulation. 2003; 107: 645–651.[Free Full Text]

94. Centers for Disease Control and Prevention. National Action Plan for Cardiovascular Health: A Comprehensive Public Health Strategy to Prevent Heart Disease and Stroke. Atlanta, Ga: Centers for Disease Control and Prevention; 2002.

95. Task Force on Community Preventive Services. Recommendations to increase physical activity in communities. Am J Prev Med. 2002; 22 (suppl): 67–72.[CrossRef][Medline] [Order article via Infotrieve]

96. Child Nutrition and WIC Reauthorization Act of 2004. Public L No. 108-265, Stat 2507, §204. Local Wellness Policy. Available at: http://www.schoolwellnesspolicies.org/resources/Section204LocalWellnessPolicies.pdf. Accessed July 20, 2006.

97. French SA, Story M, Fulkerson JA, Gerlach AF. Food environment in secondary schools: a la carte, vending machines, and food policies and practices. Am J Public Health. 2003; 93: 1161–1167.[Abstract/Free Full Text]

98. Barton AJ, Gilbert L, Baramee J, Granger T. Cardiovascular risk in Hispanic and non-Hispanic preschoolers. Nurs Res. 2006; 55: 172–179.[CrossRef][Medline] [Order article via Infotrieve]

99. Brosnan CA, Upchurch SL, Meininger JC, Hester LE, Johnson G, Eissa MA. Student nurses participate in public health research and practice through a school-based screening program. Public Health Nurs. 2005; 22: 260–266.[CrossRef][Medline] [Order article via Infotrieve]

100. Burke LE, Fair J. Promoting prevention: skill sets and attributes of health care providers who deliver behavioral interventions. J Cardiovasc Nurs. 2003; 18: 256–266.[Medline] [Order article via Infotrieve]

101. Hayman LL, Reineke PR. Preventing coronary heart disease: the implementation of healthy lifestyle strategies for children and adolescents. J Cardiovasc Nurs. 2003; 18: 294–301.[Medline] [Order article via Infotrieve]

102. Ockene IS, Hayman LL, Pasternak RC, Schron ES, Dunbar-Jacob J. Task force #4: adherence issues and behavior changes: achieving a long-term solution: 33rd Bethesda Conference. J Am Coll Cardiol. 2002; 40: 630–640.[Free Full Text]

103. Williams CL, Bollella M, Wynder E. A new recommendation for dietary fiber in childhood. Pediatrics. 1995; 96 (pt 2): 985–988.[Abstract/Free Full Text]

104. McCrindle BW, Urbina EM, Dennison BA, Jacobson MS, Steinberger J, Rocchini AP, Hayman LL, Daniels SR. Drug therapy of high-risk lipid abnormalities in children and adolescents: a scientific statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee, Council on Cardiovascular Disease in the Young, with the Council on Cardiovascular Nursing. Circulation. 2007; 115: 1948–1967.[Abstract/Free Full Text]

105. Fletcher B, Berra K, Ades P, Braun LT, Burke LE, Durstine JL, Fair JM, Fletcher GF, Goff D, Hayman LL, Hiatt WR, Miller NH, Krauss R, Kris-Etherton P, Stone N, Wilterdink J, Winston M. Managing blood lipids: a collaborative approach. Circulation. 2005; 112: 3184–3209.[Abstract/Free Full Text]

106. Allen JK, Scott LB. Alternative models in the delivery of primary and secondary prevention programs. J Cardiovasc Nurs. 2003; 18: 150–156.[Medline] [Order article via Infotrieve]

107. Berra K, Miller NH, Fair JM. Cardiovascular disease prevention and disease management: a critical role for nursing. J Cardiopulm Rehabil. 2006; 26: 197–206.[CrossRef][Medline] [Order article via Infotrieve]

108. Bodenheimer T, Wagner EH, Grumbach K. Improving primary care for patients with chronic illness. JAMA. 2002; 288: 1775–1779.[Abstract/Free Full Text]

109. Glasgow RE, Orleans CT, Wagner EH. Does the chronic care model serve also as a template for improving prevention? Milbank Q. 2001; 79: 579–612.[CrossRef][Medline] [Order article via Infotrieve]




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