Recent Advances in Preventive Cardiology and

Lifestyle Medicine

Reduction of Risk for Cardiovascular Disease in Children

and Adolescents
Stephen R. Daniels, MD, PhD; Charlotte A. Pratt, PhD, RD; Laura L. Hayman, RN, PhD

A therosclerotic cardiovascular disease (CVD) is the num-

ber 1 cause of death in the United States and other
developed nations.1 After decades of study, risk factors for
the development of atherosclerotic CVD have been identified.
These risk factors include older age, male sex, a positive
family history, hypertension, dyslipidemia, diabetes mellitus,
cigarette smoking, and obesity.2 As these risk factors have
been studied, it has become clear that both genetics and
lifestyle are important contributors to increased risk. The
primary lifestyle components are diet, physical activity, and
smoking.
A fundamental issue has been the timing of the develop-
ment of atherosclerosis. Timing is critical because it deter-
mines, at least in part, when interventions should occur. Both
the prevention of risk factor development (primordial preven-
tion) and modification of risk factors once they are estab-
lished (primary prevention) are important. An impediment to
understanding the development of atherosclerosis has been
the lack of simple, noninvasive methods to follow the
atherosclerotic process longitudinally. This problem led to the
Bogalusa Heart Study and the Pathobiological Determinants
of Atherosclerosis in Youth (PDAY).3– 6 These pathology
studies investigated the aorta and coronary arteries in autop-
sies of young individuals who died of accidental causes. The
investigators were able to evaluate the extent of atheroscle-
rosis and the presence of risk factors. They found that even
relatively advanced levels of atherosclerosis, including fi-
brous plaques, can be present in adolescents and young
adults. They also found that increased body mass index
(BMI), systolic and diastolic blood pressures, and low-
density lipoprotein cholesterol (LDL-C); low levels of high-
density lipoprotein cholesterol (HDL-C); diabetes mellitus;
and the presence of cigarette smoking were all associated
with greater atherosclerotic plaque coverage and more ad-
vanced atherosclerotic lesions.3– 6
Subsequent studies using noninvasive measures of athero-
sclerosis, including carotid intima-medial thickness (CIMT)
and arterial distensibility, have resulted in similar find-
ings.7–10 Therefore, evidence is mounting that atherosclerosis
begins in childhood and is directly associated with the same
CVD risk factors that are well established in adults.
When these results are taken together, they emphasize the
need for appropriate CVD prevention strategies in children
and adolescents. Through these preventive efforts, it should
be possible to maintain low-risk status into adulthood. Low-
CVD-risk status maintained to 50 years of age is associated
with a very low future risk of CVD.11 This is a fundamental
principle behind the American Heart Association’s 2020
goals, which are focused on achieving and monitoring car-
diovascular health.12
In this report, we summarize the evidence and the current
published recommendations regarding the epidemiology of
risk factors for atherosclerotic CVD in childhood. We outline
the recommended clinical approaches to prevent risk factor
development and review cut points for identifying risk factors
and approaches for ameliorating high-risk status once it has
developed. The National Heart, Lung and Blood Institute
(NHLBI) has formed an advisory group to review evidence
and to make recommendations regarding the prevention of
CVD in children and adolescents. This work is in progress
and has not been published. This report is an overview and a
synthesis of previously published recommendations.
Diet
Healthful dietary patterns develop in childhood and are
important for primordial and primary prevention of risk
factors related to CVD from childhood and adolescence
through adulthood. Evidence of the effectiveness of long-
term dietary intervention for the reduction of risk factors for
CVD in children is limited, but ample data suggest that
changes in specific dietary macronutrients (eg, dietary fat and
carbohydrates) and micronutrients (eg, sodium and calcium)
have an impact on the risk of CVD.13
How much energy a child or adolescent should consume
depends on age, sex, stage of growth, body weight and size, and
level of physical activity.14,15 Table 1 presents an estimate of
caloric needs by age, sex, and activity level. Children who are
sedentary need less energy compared with those who are active.

From the Department of Pediatrics, University of Colorado School of Medicine, Aurora (S.R.D.); National Heart, Lung and Blood Institute, National
Institutes of Health, Bethesda, MD (C.A.P.); and College of Nursing and Health Sciences, University of Massachusetts Boston, Boston (L.L.H.).
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.
110.016170/-/DC1.
Correspondence to Stephen R. Daniels, MD, PhD, Professor and Chairman, Department of Pediatrics, University of Colorado School of Medicine, The
Children’s Hospital, 13123 E 16th Ave, B065, Aurora, CO 80045. E-mail Daniels.stephen@tchden.org
(Circulation. 2011;124:1673-1686.)
© 2011 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.110.016170

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1674 Circulation October 11, 2011

Table 1. Suggested Caloric Intake by Sex, Age, and maintenance of a healthy weight throughout childhood and
Activity Level adolescence are likely to prevent the development of CVD in
Activity Level children and adolescents and subsequently in adults. Primary
care providers should counsel their pediatric patients and
Moderately their families to adhere to prudent dietary patterns of low total
Sex Age, y Sedentary* Active† Active‡
and saturated fat and cholesterol; to provide youth with more
Female 2–3 1000 –1200 1000 –1200 1000 –1400 fruits, vegetables, fiber, and fat-free or low-fat dairy; to
4–8 1200–1400 1400–1600 1400–1800 encourage the consumption of less dietary salt and sodium
9–13 1400–1600 1600–2000 1800–2200 and limited or no intake of sugar-sweetened beverages; and to
14–18 1800 2000–2200 2400 control portion sizes in early childhood and throughout
Male 2–3 1000–1200 1000–1200 1000–1400 adolescence.
4–8 1200–1400 1400–1600 1600–2000
9–13 1600–2000 1800–2200 2000–2600
Physical Activity
Evidence accumulated over the past several decades supports
14–18 1800–2400 2400–2800 2800–3200
a multitude of benefits associated with a physically active
Source: Britten P, Marcoe K, Yamini S, Davis C. Development of food intake lifestyle in children and youth.22 Health-related benefits of
patterns for the MyPyramid food guidance system. J Nutr Educ Behav.
regular physical activity documented in clinical and epidemi-
2006;38:S78-S92.15 http://www.cnpp.usda.gov/Publications/MyPyramid/
DevelopmentMaterials/JNEBsupplement/JNEBDevelPatterns.pdf. Based on In- ological studies and summarized in recent comprehensive
stitute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, reviews include improved cardiovascular fitness, increased
Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: bone mass, improved psychological well-being, and lower
National Academies Press; 2002.14 risk of obesity and elevated blood pressure.22,23 In contrast,
*Sedentary means a lifestyle that includes only the physical activity of results of several observational studies of children and ado-
independent living.
lescents (4 –18 years of age) and young adults (19 –21 years
†Moderately active means a lifestyle that includes physical activity equiva-
lent to walking about 1.5 to 3 miles/d at 3 to 4 mph, in addition to the activities of age) demonstrate associations between increased time
of independent living. spent in sedentary activities and decreased levels of physical
‡Active means a lifestyle that includes physical activity equivalent to walking activity, adverse lipid profiles, increased levels of obesity,
⬎3 miles/d at 3 to 4 mph, in addition to the activities of independent living. and related cardiovascular risk factors, including hyperten-
sion and insulin resistance.24,25 Longitudinal data from the
Thus, the types and amount of food groups needed to meet Cardiovascular Risk in Young Finns Study and the Muscatine
caloric needs also vary15 (http://www.mypyramid.gov). Study, similar to observations of adults, indicate that optimal
There is evidence linking diet to cardiovascular health.13,14 cardiovascular risk profiles are seen in individuals who are
Table I in the online-only Data Supplement presents strong consistently physically active.24,25
and moderately strong evidence relating macronutrients, mi- Tracking of levels of physical activity from childhood to
cronutrients, foods, and food environment to health. There is young adulthood has also been documented, with the most
strong and/or moderately strong evidence of a positive consistent tracking observed for high levels of physical
association between adiposity and macronutrients: dietary fat, activity at 9 to 18 years of age predicting higher levels of
total energy intake, and energy density of foods, as well as physical activity in adulthood.26 Physically active children
sugar-sweetened beverages16 and portion sizes (Table I in the and youth are more likely to engage in other health-
online-only Data Supplement). Children and adolescents who promoting behaviors and less likely to engage in health-
consume large portion sizes, more calories than they expend, compromising behaviors than their less active counterparts.27
and high-energy-dense foods gain excess weight and body fat Finally, results of studies that include interventions designed
and increase their CVD risks. Those who eat breakfast have to increase physical activity and to decrease sedentary time
been reported to be at lower risk of being overweight or obese have demonstrated reductions in systolic and diastolic blood
and more likely to consume adequate intakes of essential pressures,28 decreased measures of body fat,29 decreased
nutrients such as calcium and iron.13,17–19 Based on 21 years BMI,30 improved cardiorespiratory fitness,31 and improved
of follow-up data from youth 3 to 18 years of age, the cardiometabolic risk profiles.32 However, the results are not
Cardiovascular Risk in Young Finns Study20 demonstrated consistent across studies, and the dose (duration and inten-
that healthful dietary patterns developed in childhood and the sity) of physical activity required to modify cardiovascular
cardiovascular health benefits accrued from such patterns risk factors in children and youth remains to be clarified.
track into adulthood. Clinical trials have demonstrated that Current recommendations for healthy children and youth (ⱖ6
diets low in total fat (⬍30% of energy), saturated fat years of age) include at least 1 hour of moderate to vigorous
(8%–10% of energy), and cholesterol (200 –300 mg/d) sig- physical activity (MVPA) daily with vigorous-intensity phys-
nificantly reduced total cholesterol (TC), LDL-C, and ical activity and muscle- and bone-strengthening activities on
C-reactive protein.21 at least 3 days of the week.22,33 Moderate intensity is defined
Because dietary habits and preferences are established in as 3.0 to 6.0 metabolic equivalents (METs), and ⬎6.0 METs
early childhood, it is important to intervene early to improve is considered vigorous, expending 3.5 to 7.0 and ⬎7.0
dietary patterns of children and adolescents. Clearly, im- kcal/min, respectively. The reduction of sedentary time (lei-
provements in dietary patterns and physical activity and sure screen time) to ⬍2 h/d is also recommended.33
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 Daniels et al
Although current guidelines recommend 60 min/d of
MVPA, nationally representative data indicate that the ma-
jority of youth (56.3%) are not achieving this goal.34 Data
from the Study of Early Child Care and Youth Development,
designed to examine the patterns and determinants of MVPA
of children from ethnically and economically diverse back-
grounds followed up from 9 to 15 years of age, indicate that
levels of physical activity decrease significantly over that
time period.35 By 15 years of age, adolescents were engaging
in MVPA for 49 minutes per weekday and 35 minutes per
weekend day. Boys were more active than girls, spending 18
and 13 more min/d in MVPA on weekdays and weekends,
respectively. Clearly, both individual/clinical- and population-
based strategies, including advocacy and support for daily
physical education in schools, are needed to improve levels of
physical activity in US children and youth.36
Healthcare providers should assess physical activity and
sedentary behaviors at every well-child visit.37–39 Although
no valid and reliable instruments are currently available for
assessment of physical activity in pediatric primary care
settings, general topics for questions include the amount of
time regularly spent walking, bicycling, and in outdoor play;
use of playgrounds, parks, and gymnasiums; and interactive
play/games with other children and adolescents. Time spent
participating in age-appropriate organized sports should also
be addressed, along with time spent in school or day-care
physical education that includes a minimum of 30 minutes of
coordinated large-muscle exercise (for children ⬎2 years of
age). Sedentary behaviors, including the number of hours per
day spent in leisure screen time such as television viewing
and computer gaming, should also be assessed.
Primary healthcare providers should provide age-
appropriate suggestions (that consider the child and family’s
resources and preferences) for increasing physical activity
and limiting sedentary behaviors in children and youth. For
example, for families with children ⬍5 years of age, recom-
mendations would include unlimited active play time in a safe
supportive environment, family activity at least once a week,
and limitation of screen time to ⬍2 h/d. Screen time should
be zero from birth to 2 years of age. In addition, television
should not be permitted in the child’s bedroom. Beginning
early in life and extending through adolescence, parental role
modeling of physical activity behaviors is important in
promoting physical activity behaviors in offspring. Encour-
agement of parent engagement in physical activities, opti-
mally with the children, is advised. During childhood and
adolescence, 1 h/d of MVPA and vigorous-intensity activity on
at least 3 d/wk and ⬍2 h/d of sedentary activity are recom-
mended, along with matching physical activity recommenda-
tions with the child’s energy intake. Theory-based age-
appropriate behavioral change strategies should be included as
part of individual and family counseling designed to increase
levels of physical activity and to decrease sedentary behaviors.
Although additional research is needed to determine the most
efficient and effective methods for implementation in pediatric
primary care settings, available evidence points to the promise
and potential of multicomponent, tailored interventions that
incorporate principles of behavior change and are delivered by
multidisciplinary teams.36,40
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Reduction of Risk for CVD in Childhood 1675
Obesity
Childhood obesity has reached epidemic proportions in the
United States, with an estimated 17% of children and adoles-
cents being obese.41 Obesity prevalence is estimated at 10.4%
among preschool children, 19.6% among 6 to 11 year olds, and
18.1% among adolescents 12 to 19 years of age.41 Among
infants and toddlers, ⬇10% were above the 95th percentile of the
weight-for-recumbent-length growth charts.41 Mexican American
male boys and non-Hispanic black girls have a higher preva-
lence of obesity compared with non-Hispanic whites (29.2%,
26.8%, and 14.5%, respectively). Higher obesity prevalence was
reported in the National Health and Nutrition Examination
Survey (NHANES) in children of low socioeconomic status
(⬍130% of poverty level; boys, 21.1%; girls, 19.3%) compared
with those of high socioeconomic status (⬎350% of poverty
level; boys, 11.9%; girls, 12%).42
Obesity in children and adolescents is determined from
BMI (weight in kilograms divided by height in meters
squared) and the corresponding BMI-for-age percentile on a
Centers for Disease Control BMI-for-age growth chart (http://
apps.nccd.cdc.gov/dnpabmi/Calculator.aspx); obesity is de-
fined as BMI ⱖ95th percentile and overweight as BMI ⱖ85th
to ⬍95th percentile.43 Obesity in childhood and adolescence
is associated with numerous adverse health outcomes. Car-
diovascular risk factors such as hypertension, type 2 diabetes
mellitus, metabolic syndrome, sleep apnea, left ventricular
hypertrophy,44,45 and abnormal lipid profiles (eg, high triglyc-
erides, low HDL) are higher in obese than in normal-weight
youth.36,46 For example, obese girls had a 6-fold higher
prevalence and a 2- to 3-fold higher incidence of hyperten-
sion compared with their normal-weight counterparts.47 Obe-
sity in childhood and adolescence substantially increases the
risk of adult obesity.48,49 Obese 2- to 5-year-olds had ⬎4
times the likelihood of becoming obese adults compared with
normal-weight children.49 Eighty percent of children who
were overweight at 10 to 15 years of age were obese adults at
25 years of age.48 Twenty five percent of obese adults were
overweight as children.48 Obesity in childhood has been
associated with increased arterial stiffness and CIMT and
increased risk of coronary heart disease in adult life.7–9,50,51
Prevention of obesity in childhood and adolescence is the
mainstay for CVD risk reduction. An improvement in weight
status and a decrease in adiposity are associated with a
decline in blood pressure and an improvement of blood lipids
(ie, TC, HDL-C, and triglycerides), insulin resistance, and
inflammatory markers (see Table II in the online-only Data
Supplement).36
A suggested approach to overweight and obesity manage-
ment in children and adolescents has been published.40 All
children, regardless of their weight status, should have their
weight and height measured and BMI calculated at every visit
with the healthcare provider. The BMI percentile and, for
infants and children, percentile for weight for recumbent
height can then be determined. Parental obesity, family
medical history, BMI trajectory, and CVD risk factors (eg,
diabetes mellitus) are considered in the management of
weight and in CVD risk reduction. For healthy-weight chil-
dren and adolescents (BMI, 5th– 84th percentile), the goal is
to prevent excess weight gain through lifestyle modifications
1676 Circulation October 11, 2011

Table 2. Components of a Staged Approach to Weight (caloric) intake is strongly associated with reduced adiposity
Management for Children and Adolescents in children,13 and caloric expenditure must exceed intake to
Stage Components achieve weight loss. Referral of severely obese children and
those with obesity-related comorbidities to a pediatric weight
1. Prevention plus (“plus” ⱖ5 servings of fruits and vegetable
means providers must spend daily; ⱕ2 h of screen time daily; no
management program is highly recommended. The 4-stage
more time and increase television in child’s bedroom; no intervention and treatment modality for overweight and obese
intensity of the sugar-sweetened beverages; ⱖ60 min youth has been endorsed by many organizations, including
recommendation and of physical activity daily; (graded) the American Academy of Family Physicians and the Amer-
follow-up 3– 6 mo beyond family-based approach to lifestyle ican Academy of Pediatrics (AAP).
usual care) changes; acknowledge cultural Table II in the online-only Data Supplement presents
differences
examples of obesity prevention and nutrition interventions
2. Structured weight Prevention plus; family-based and that were reported in the literature from 2000 to 2010.
management (SWM) balanced macronutrient diet
Interventions that improved BMI were multicomponent (in-
emphasizing small amounts of
energy-dense foods; high-quality, cluded dietary and physical activity improvements)52 and
nutrient-rich diet to prevent muscle multidisciplinary (included pediatricians or primary care physi-
loss; controlled portion sizes; reduced cians and registered dietitians or nurses).53 Interventions that
television and screen time; resulted in weight loss or reduction in excess weight gain were
self-monitoring of diet and physical often family based and included behavioral therapy. Intervention
activity; medical screening
duration varied from 4 weeks to 4 years. The NHLBI Working
3. Comprehensive Prevention plus and structured weight Group on Childhood Obesity Prevention and Treatment recently
multidisciplinary intervention management but more frequent
provided research recommendations to prevent and treat obesity
patient-provider contact, more active
use of behavioral strategies, more
in children to reduce future CVD risk.54
formal monitoring, and feedback to
improve adherence; multidisciplinary Blood Pressure
teams; strong parental involvement for Elevated blood pressure is determined for children when
children ⬍12 y of age; assessment of measured blood pressure exceeds certain percentile values
diet, physical activity, and body fat at based on studies in normal populations. To determine the
specified intervals; food monitoring;
blood pressure percentile, it is important to take into account
structured dietary and physical activity
intervention to improve diet quality and age, sex, and height, variables that are normally associated
result in weight loss with blood pressure level. The Fourth Report on Blood
4. Tertiary care center Continue diet and activity counseling in Pressure in Children from the NHLBI has established levels
stages 2 and 3 plus meal replacement, of blood pressure that should trigger clinical action.55 Prehy-
very low-energy diet, medication, pertension is defined as blood pressure between the 90th and
and/or surgery 95th percentiles for age, sex, and height or 120/80 mm Hg
Source: Barlow SE; Expert Committee. Expert committee recommendations (the level for prehypertension in adults), whichever is lower.
regarding the prevention, assessment and treatment of child and adolescent When prehypertension is identified, the recommended clini-
overweight and obesity: summary report. Pediatrics. 2007;120:S164 –S192.40 cal approach is lifestyle intervention to improve BMI when
obesity is present, to lower dietary sodium, and to increase
that include eliminating the intake of sugar-sweetened bev-
the level of physical activity. Blood pressure elevation or
erages,13 increasing the intake of fruits and vegetables to ⱖ5
hypertension is defined by systolic or diastolic blood pressure
servings daily, limiting television and electronic media use to
above the 95th percentile on a persistent basis. Persistence is
ⱕ2 h/d, and participating in at least 60 minutes of MPVA
defined by elevation on 3 consecutive occasions. Stage 1
daily40 (prevention stage).
Table 2 describes the components of the staged approach to hypertension is present when blood pressure is above the 95th
weight management, and Table 3 presents a suggested staged percentile but below the 99th percentile plus 5 mm Hg
approach to weight management and healthy weight goals for (⬇12 mm Hg above the 95th percentile). Stage 2 hyperten-
children and adolescents by age and BMI percentiles. For sion is present when blood pressure is above the 99th
children and adolescents who are overweight (85th–94th percentile plus 5 mm Hg.55
percentile) or obese (ⱖ95th percentile), a staged lifestyle The management approach to hypertension is presented in
behavioral approach of increasing intensity plus a structured the Figure. For stage 1 hypertension, it is important to
weight management protocol and/or a comprehensive and evaluate left ventricular mass to determine whether left
multidisciplinary weight management protocol consisting of ventricular hypertrophy is present. Left ventricular hypertro-
supervised counseling by a trained physician, nurse practitio- phy is the most useful marker of hypertensive target organ
ner, or a registered trained dietitian are recommended.40 The abnormality and, when present, is an indication that more
management plan includes a low-energy-dense and balanced aggressive treatment is indicated. The initial treatment for
diet, supervised physical activity of at least 60 min/d, ⱕ1 h/d stage 1 hypertension is management of lifestyle and improve-
of screen time, and increased self-monitoring of dietary and ment of BMI as for prehypertension. However, if blood
physical activity behaviors.40 pressure elevation persists despite lifestyle change or if target
For overweight and obese youth, the goal is to improve organ damage is present, then pharmacological intervention
BMI to less than the 85th percentile (Table 3). Lower energy may be indicated. When stage 2 hypertension is present, this
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 Daniels et al Reduction of Risk for CVD in Childhood 1677

Table 3. Suggested Staged Approach to Weight Management and Healthy Weight Goals for Children and Adolescents
BMI Range (Percentile
Age Range, y or Absolute Value) Staged Approach Healthy Weight Goals
2–5 5th– 84th Prevention stage; foster healthful lifestyle in all Normal weight; continue to maintain weight
children; follow national recommendations for
food consumption and physical activity
85th–94th PP; SWM after 3–6 mo of no weight change Weight maintenance until BMI ⬍85th percentile or
or parental obesity slowing of weight gain as indicated by downward
deflection in BMI curve
ⱖ95th PP; SWM after 3–6 mo of no improvement Weight maintenance until BMI ⬍85th percentile or
on PP slowing of rate of weight gain
ⱖ99th or ⬎21 kg/m2 PP; SWM after 3–6 mo of no improvement on Gradual, carefully monitored weight loss of no more
PP; comprehensive, multidisciplinary than 1 lb/mo until BMI is ⬍85th percentile
intervention after 3–6 mo of no improvement
on SWM, comorbidity, or family history of
obesity
6–11 5th–84th Prevention stage; prevention; foster healthful Normal weight; continue to maintain normal weight
lifestyle in all children; follow national
recommendations for food consumption and
physical activity
85th–94th PP; SWM after 3–6 mo if increasing BMI Weight maintenance until BMI is ⬍85th percentile
percentile or medical condition persists or slowing of weight gain as indicated by
downward deflection in BMI curve
95th–98th PP; SWM depending on responses, age, health Weight maintenance until BMI is ⬍85th percentile
risks, and motivation; comprehensive or carefully monitored weight loss of no more than
multidisciplinary intervention if no 1 lb/mo until ⬍85th percentile
improvement on SWM
ⱖ99th PP; SWM depending on age, response to Weight loss not to exceed an average of 2
treatment, health risks, and motivation; lb/wk (0.9 kg/wk) until ⬍85th percentile
advance to comprehensive multidisciplinary
intervention after 3–6 mo on SWM if
comorbidity persists; refer for tertiary care
center for evaluation
12–18 5th–84th Prevention stage; foster healthful lifestyle in all Normal weight; continue to maintain normal weight
children; follow national recommendations for
food consumption and physical activity
85th–94th PP; SWM after 3–6 mo of PP if BMI percentile Weight maintenance until BMI is ⬍85th percentile
or medical condition persists or slowing of weight gain as indicated by
downward deflection in BMI curve
95th–98th PP or SWM depending on age, degree of Weight loss until BMI is ⬍85th percentile; no more
obesity, health risks, and motivation; advance than 2 lb/wk; if greater weight loss is noted,
to intensive intervention depending on monitor patient for causes of weight loss ⬎2 lb/wk
response to treatment, age, health risks, and
motivation
ⱖ99th PP; SWM depending on age, response for Weight loss not to exceed an average of 2 lb/wk
treatment, degree of obesity, health risks, and until ⬍85th percentile
motivation; advance from SWM to
comprehensive multidisciplinary intervention
stage after 3–6 mo with comorbidity and no
improvement; refer to tertiary care center for
evaluation
BMI indicates body mass index; PP, prevention plus; and SWM, structured weight management. Source: Barlow SE; Expert Committee. Expert committee recommendations
regarding the prevention, assessment and treatment of child and adolescent overweight and obesity: summary report. Pediatrics. 2007;120:S164 –S192.40

may signal the presence of a secondary form of hypertension. logical and clinical research on children and adults. First,
A workup for underlying causes of hypertension should be hypertension has been established as a very potent risk factor
instituted on the basis of the presence of suspicious history or for cerebrovascular disease and coronary artery disease in
abnormal physical examination. Stage 2 hypertension may adults.2,56 Treatment of high blood pressure has also been
also require earlier intervention with pharmacological shown to directly lower the risk of CVD in adults.56,57 This
therapy.55 has led to major initiatives to ensure that hypertension is
The recommended approach to blood pressure elevation in recognized and treated and that appropriate blood pressure is
children and adolescents comes from decades of epidemio- achieved in adults.58 Although levels of awareness and
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1678 Circulation October 11, 2011

Measure BP and Height and Calculate BMI

Determine BP category for sex, age, and height

Stage 2 Hypertension Stage 1 Hypertension Prehypertensive Normotensive

Therapeutic Educate on
Repeat BP Lifestyle Heart Healthy
Over 3 visits
Changes* Lifestyle*
For the family
Diagnostic Workup Include Diagnostic Workup Include
Repeat BP
Evaluation for Target-Organ Evaluation for Target-Organ
In 6 months
Damage † Damage †

Consider Diagnostic Workup

Consider Referral Rx Specific Therapeutic and Evaluation for Target-
To provider with expertise for Cause Lifestyle Organ Damage †
in pediatric hypertension Changes* If overweight or comorbidity exists

Drug Rx Weight Weight Monitor Weight

Drug Rx †
Reduction Reduction Q 6 Mo Reduction
and Drug Rxx
Figure. Management algorithm for hypertension. BP indicates blood pressure; BMI, body mass index; Rx, prescription; and Q, every.
*Diet modification and physical activity; †especially if younger, very high BP, little or no family history, diabetic, or other risk factors.
Source: National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, Ameri-
can Academy of Pediatrics. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and ado-
lescents. Pediatrics. 2004;114:555–576.55

effective treatment for adults are not optimum, they have
improved steadily over time.58
Elevated blood pressure levels are known to track over
time. Thus, an adolescent with elevated blood pressure is
much more likely to become an adult with high blood
pressure than an adolescent with normal blood pressure.59,60
Factors that increase the likelihood of blood pressure remain-
ing high are excess weight gain over time and initiation of
cigarette smoking.60 Other factors that may increase the
persistence of high blood pressure but have been less well
studied are low levels of physical activity and dietary patterns
that result in elevated sodium. The use of oral contraceptives
in adolescent girls and young women may also contribute.60
Unfortunately, the prevalence of high blood pressure has
been increasing in children and adolescents.61,62 This is due in
part to the epidemic of obesity in this population, but it
appears that there are likely to be other, yet-to-be-discovered
factors responsible for this increase.63 Din-Dzietham et al61
used national survey data from 1963 to 2002 to evaluate
trends in hypertension for 8- to 17-year-old children and
adolescents. They found that both prehypertension and hy-
pertension are increasing in children and adolescents. They
reported that an increase in abdominal obesity over time may
be more important than overall obesity in relation to blood
pressure elevation. There were also differences by ethnic
group. Blacks and Mexican Americans had a greater preva-
lence of prehypertension and hypertension than whites. Male
subjects had a higher prevalence of hypertension than female
subjects.
McNiece et al62 also evaluated the prevalence of hyperten-
sion in adolescents. After 3 screenings, they found that 15.7%
of adolescents had prehypertension and 3.2% had hyperten-
sion, including 2.6% with stage 1 hypertension and 0.6% with
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stage 2 hypertension. The only correlate of hypertension was
obesity, whereas greater BMI, male sex, and black race were
associated with prehypertension.
These results are quite important from a clinical perspec-
tive in that they demonstrate that primary care providers can
expect to see prehypertension and even hypertension rela-
tively commonly in children and adolescents. Providers
should be ready to identify and treat hypertension in this age
group. Unfortunately, studies have shown that appropriate
identification and treatment of hypertension is not occurring
at an optimum level for pediatric patients. Hansen et al64
examined data on ⬎14 000 children via medical records with
at least 3 blood pressure measurements. Of those, 3.6% met
the criteria for hypertension. However, only 26% of those
were actually diagnosed with hypertension. Of all of the
children with at least 1 blood pressure measurement docu-
menting elevated blood pressure, only 9% had a subsequent
blood pressure recorded to determine whether the elevation
was persistent. This means that measurement of blood pres-
sure, appropriate interpretation, and clinical intervention must
be applied more systematically in pediatric primary care.
Blood pressure elevation in children and adolescents has
been demonstrated to be associated with early atherosclerosis
in autopsy studies3,5 and has been shown to be related to
increased left ventricular mass. For example, Daniels et al65
showed that 8% of children and adolescents with hyperten-
sion already had left ventricular mass index elevated to a level
associated with a 4-fold increased risk of CVD in adults with
hypertension. Lande et al66 have also described problems with
neurocognitive function in children with hypertension. These
results underscore the clinical importance of blood pressure
elevation in children and adolescents. It is clear that hyper-
tension is already having an impact on the heart and vascu-
 Daniels et al
lature even at an early age. Initial treatment should focus on
weight loss if obesity is present and other nonpharmacologi-
cal approaches. Couch et al67 have shown that a Dietary
Approaches to Stop Hypertension–type diet can be successful
in reducing blood pressure even without a reduction in BMI
in adolescents. For those patients in whom lifestyle change is
not effective, pharmacological intervention may be needed.
There is now substantial clinical trial evidence that pharma-
cological agents from a variety of classes can be safe and
effective in lowering elevated blood pressure in children and
adolescents.55 Unfortunately, no studies have documented the
comparative effectiveness of 1 agent or 1 class of agents over
another. This means that several classes, including diuretics,
angiotensin-converting enzyme inhibitors, angiotensin recep-
tor blockers, calcium channel blockers, and ␤-adrenergic
blockers, could be chosen as first-line agents. Preliminary
data demonstrate that pharmacological treatment can be
effective in lowering left ventricular mass and blood pressure
in children.68
It is important to include blood pressure measurement as
part of a cardiovascular risk assessment for children. Blood
pressure should be a routine part of health-maintenance visits
starting at 3 years of age. This should allow better lifetime
control of blood pressure and lower risk for the development
of CVD.
Lipids/Lipoproteins
Over the past 40 years, data have accumulated linking
adverse levels and patterns of lipids and lipoproteins to the
initiation and progression of the atherosclerotic process in
children and adolescents. However, no multidecade, longitu-
dinal population-based studies have been conducted linking
absolute levels of lipids and lipoproteins in childhood to
incident CVD in adult life, and no randomized, controlled
trials have demonstrated that reducing atherogenic lipids and
lipoproteins in early life prevents CVD in adulthood. Several
lines of evidence, however, clearly support the need for
primary prevention, including reduction of adverse levels of
lipids and lipoproteins beginning early in life. This evidence
includes the natural history observed for individuals with
genetic dyslipidemias, such as homozygous familial hyper-
cholesterolemia, in whom LDL-C levels are quite high and
there is substantial increased risk of evolving atherosclerotic
CVD.
Postmortem studies conducted as part of the Bogalusa
Heart Study and the PDAY Study have demonstrated that
early atherosclerotic lesions (fatty streaks) and advanced
lesions (fibrous plaques) are significantly related to eleva-
tions in TC, LDL-C, and non–HDL-C and low levels of
HDL-C, as well as to the presence and intensity of other
potentially modifiable risk factors, including obesity, hyper-
tension, and cigarette smoking.4,5,69 In subsequent analyses
using a risk score derived from these results, non–HDL-C
was found to be the major correlate of coronary atheroscle-
rosis, with a 30 mg/dL increase in non-HDL-C equivalent to
2 years of vascular aging.70 Noninvasive imaging studies
have also 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. In the
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Reduction of Risk for CVD in Childhood 1679
Muscatine Study, a longitudinal, observational study of CVD
risk factors in children and youth, carotid ultrasound in adults
(33– 42 years of age) indicated that CIMT was positively
associated with levels of TC and BMI measured in child-
hood.7 Similar results were observed in the Bogalusa Heart
Study, in which childhood LDL-C and BMI were found to
predict increased CIMT in adulthood.71 In the Young Finns
Study, a population-based prospective cohort study, associa-
tions between risk factor exposures in adolescence, including
LDL-C, BMI, cigarette smoking, and systolic blood pressure,
predicted CIMT in adulthood independently of adult risk
factor levels.8 Results of other imaging studies designed to
assess subclinical atherosclerosis reaffirm these observations,
indicating that abnormal levels of atherogenic lipids and
lipoproteins in childhood and adolescence are associated with
endothelial dysfunction, coronary artery calcium, and in-
creased CIMT.72–74
Taken together, the results of pathology and imaging
studies indicate that adverse levels of lipids and lipoproteins
(and other potentially modifiable established risk factors) are
associated with accelerated atherosclerotic processes in child-
hood and adulthood and point to the importance of primordial
and primary prevention beginning in early life.
Data from the NHANES for 1999 to 2006 indicate that the
prevalence of abnormal lipid levels among all youths 12 to 19
years of age was 20.3%.75 Abnormal serum lipid levels were
classified on the basis of cutoff points suggested in AAP and
AHA guidelines39,76: high LDL-C, ⱖ130 mg/dL; low
HDL-C, ⱕ35 mg/dL; and high triglycerides, ⱖ150 mg/dL. Of
note, the prevalence varied by BMI: 14.2% of normal-weight,
22.3% of overweight, and 42.9% of obese youths had at least
1 abnormal lipid level.75
Tracking of lipids and lipoproteins, particularly TC and
LDL-C, has also been documented in children from diverse
racial/ethnic groups and is particularly evident in the upper
and lower extremes of the distribution. In the Muscatine
Study, for example, 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 (ⱖ200 mg/dL) at 20 to 25 years of
age.77,78 The Bogalusa Heart Study reported that ⬇70% of
children with elevated TC in childhood persisted with ele-
vated levels in adulthood.79 Tracking is relevant to primary
prevention because of the potential for identifying children at
risk for CVD early in life.
Data from the Lipid Research Clinics indicate that serum
lipids and lipoproteins increase throughout the first 2 years of
life and approximate levels in young adults by 2 years of
age.80 These observations of primarily non-Hispanic whites
and blacks contributed to the first guidelines issued by the
NHLBI National Cholesterol Education Panel (NCEP) rec-
ommending selective screening for high-risk children after 2
years of age when lipids and lipoproteins begin to track.81
Data from the Lipid Research Clinics82 and NHANES83
indicate that puberty/maturation has an important impact on
levels of lipids and lipoproteins. In addition, patterns of
change during this developmental period vary by sex and
race/ethnicity.83 For example, in the 1988 to 1994 NHANES,
at 4 to 19 years of age, the mean cholesterol was 165 mg/dL;
at 9 to 11 years of age, however, age-specific values for mean
1680 Circulation October 11, 2011
Table 4. Cut Points for Total Cholesterol and Low-Density
Lipoprotein Concentrations in Children and Adolescents
Total Cholesterol,
Category Percentile mg/dL
Acceptable ⬍75th ⬍170
Borderline 75th–95th 170–199
Elevated ⱖ95th ⱖ200
LDL indicates low-density lipoprotein. From American Academy of Pediatrics and
National Cholesterol Education Panel guidelines for children and adolescents.76,82
cholesterol peaked at 171 mg/dL.83 Female subjects had
higher TC and LDL-C than male subjects and, after pubertal
development, had higher HDL-C than male subjects. Black
children had higher HDL-C and lower triglyceride concen-
trations than their non-Hispanic white and Hispanic
counterparts.83
Current recommendations for management of dyslipidemia
in children and youth issued the by AAP76 and AHA84 reflect
accumulating evidence. There is currently a lack of consensus
within the pediatric healthcare and research communities on
targeted versus universal screening. The AAP recommends a
targeted approach to screening. Specifically, this approach
recommends screening children (⬎2 years of age) who have
a family history of premature CVD or who have parents with
dyslipidemia. Screening is also recommended for children for
whom family history is unknown or children who present
with other CVD risk factors, including hypertension, obesity,
and diabetes mellitus. Since the NCEP recommended targeted
screening, research has shown that the approach has limita-
tions for capturing at-risk children.85–90 Studies of the effec-
tiveness of the targeted approach found that 35% to 46% of
children and youth had cholesterol levels measured on the
basis of positive family history or elevated cholesterol lev-
els.85,89,91 Other research has shown that 30% to 60% of
children and adolescents with elevated cholesterol levels will
be missed by this approach.84,90,92 Clearly, with the increase
in prevalence of childhood obesity and its comorbidities, the
number of children who qualify for screening has increased.76
Cut points recommended by NCEP82 and AAP76 used to
identify children and adolescents with abnormal lipid and
lipoprotein levels are presented in Table 4. These cut points
are recommended for children 2 to 18 years of age. The AHA
has recommended that triglyceride levels of ⱖ150 mg/dL and
HDL-C levels of ⱕ35 mg/dL be considered abnormal for
children and adolescents.39 A single cut point for all children
and youth may be limited by differences in age, sexual
maturation, and race/ethnicity.93 Table III in the online-only
Data Supplement presents lipid and lipoprotein distributions
in children and youth 4 to 19 years of age.83 These data were
collected in 1981 before the increase in prevalence of obesity
with standardized protocols and the use of plasma specimens.
As suggested by the AAP, these tables and percentiles,
stratified by age, are applicable in clinical practice.
Optimizing cholesterol levels and managing dyslipidemia
in children and youth includes both a population approach
and an individual/high-risk approach.76,84 The population
approach focuses on promoting optimal lipid levels in all
children and youth and emphasizes health behaviors, a
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cornerstone of cardiovascular health promotion and risk
reduction in childhood.36,94 Although dietary restrictions are
generally not recommended for children during the first 2
LDL, mg/dL years of life, research has demonstrated the safety and
⬍110
efficacy of a diet consisting of total fat of ⬍30% of the caloric
intake, saturated fat of ⬍10% of the intake, and cholesterol
110–129
intake of ⬍200 mg/dL per day, with 1.5% cow’s milk after 12
ⱖ130
months of age.95 More recent data from this study (Special
Turku Risk Intervention Program) indicate beneficial effects
in boys (lowering of LDL-C) and decreased prevalence of
obesity in girls compared with age-matched control sub-
jects.95 The updated AHA dietary recommendations for
children and youth (ⱖ2 years of age) emphasize a balanced
caloric intake with sufficient physical activity (60 min/d) to
achieve a normal weight and increased consumption of fruits,
vegetables, whole grains, fish, and low-fat dairy products.96
In addition, a reduction of daily intake of trans fatty acids,
which are known to increase LDL-C levels, to ⬍1% of total
intake is recommended.96 Recently, the AHA published
strategies designed to assist healthcare providers in imple-
menting these guidelines with children and families.97
The individual approach focuses on children and adoles-
cents identified as being at risk because of family history of
CVD or because they present with elevated levels of LDL-C
or other major risk factors. Management for these patients
initially involves therapeutic lifestyle change, with an empha-
sis on an adequate trial of dietary therapy (and increased
physical activity). Research has shown that with good adher-
ence to a saturated fat- and cholesterol-restricted diet (⬍7%
and ⬍200 mg/d, respectively), LDL-C levels can be de-
creased 10% to 15% from baseline.81 Children with genetic
dyslipidemias may present with baseline levels that cannot be
reduced to suggested goals. Interindividual differences in
LDL-C levels in response to reduced intakes of saturated fat
and cholesterol are well documented and attributable to a
number of factors. Thus, after an adequate trial of therapeutic-
dietary lifestyle change, some children and adolescents will
be candidates for pharmacological intervention. Other non-
pharmacological approaches to reducing adverse LDL-C
have also been recommended for children and adolescents,
including additional fiber (calculated as the child’s age plus 5
g/d up to a dose of 20 g/d at 15 years of age).84 Results have
not been consistent across studies, but some show modest
(⬇7%) reductions of LDL-C.84 Plant stanols and sterols,
currently added to several food products such as margarines,
orange juice, and cereal bars, have been shown to reduce
cholesterol concentrations by ⬇5% to 10% with minimal
adverse effects.84
The AAP currently recommends that pharmacological
interventions be considered in children ⱖ8 years of age if
LDL-C levels persist at ⱖ190 mg/dL (with no other risk
factors present) and for children with levels that persist at
ⱖ160 mg/dL and have other risk factors such as obesity,
hypertension, positive family history of CVD, and/or ciga-
rette smoking. For children with diabetes mellitus, the AAP
recommends pharmacological intervention for children
whose LDL-C levels are ⱖ130 mg/dL (approximately the
95th percentile).76 Medications such as statins, bile acid–
binding resins,98 and cholesterol absorption inhibitors are
 Daniels et al
currently available for treatment of dyslipidemia in children
and adolescents.84 Therapeutic lifestyle change remains a
cornerstone of CVD risk reduction in childhood and should
continue along with pharmacological intervention in children
and adolescents.
Smoking/Tobacco Exposure
Tobacco use continues to be the single leading preventable
cause of death in the United States and is responsible for ⬇4
million annual deaths worldwide.99,100 Because ⬎80% of
established adult smokers begin smoking before 18 years of
age101 and in view of the unequivocal evidence linking
tobacco use, particularly cigarette use, and adverse health and
developmental outcomes,99,102 prevention of smoking initia-
tion and cessation interventions are essential components of
cardiovascular health promotion and risk reduction for chil-
dren and adolescents.37,39,103
Recent population-based data on tobacco use among mid-
dle and high school students in the United States prompted a
call to action for pediatric healthcare providers and public
health advocates.104 Specifically, data from the Centers for
Disease Control and Prevention National Youth Tobacco
Survey indicated that from 2000 to 2009 the prevalence of
tobacco use among middle school students declined (15.1%–
8.2%), as did cigarette use (11.0%–5.2%) and cigarette
smoking experimentation (29.8%–15.0%). Similar trends
were observed for high school students (tobacco use, 34.5%–
23.9%; cigarette use, 28.0%–17.2%; smoking experimenta-
tion, 39.4%–30.1%). No change was observed, however, in
susceptibility to initiate cigarette smoking as measured by
self-report of openness to trying cigarette smoking.104,105 In
view of 2006 to 2009 prevalence and susceptibility data, both
individual /clinical and public health strategies must continue
unabated to reduce tobacco use. Restrictions on advertising,
promotion, and availability of tobacco products to children
and adolescents should be combined with implementation of
evidence-based, community-wide, comprehensive tobacco
control policies.106,107
The AAP Committee on Environmental Health called
attention to the health hazards of environmental tobacco
smoke in 1997 with evidence-based recommendations for
pediatricians and child health care providers.108 Environmen-
tal tobacco smoke in childhood has been linked with acute
and chronic respiratory conditions, middle ear effusions, risk
factors for and CVD processes (ie, dyslipidemia, impaired
endothelial function), and increased risk for selected cancers
in adulthood.102 The adverse effects of intrauterine exposure
to tobacco smoke on fetal and childhood development and
overall health have also been well documented and include
low birth weight for gestational age and associations with
selected behavioral and cognitive-information processing
problems.102
Smoking prevention and cessation interventions are effec-
tive in adults.103,109,110 Theory-based behavioral interventions
are central to the prevention of initiation and smoking
cessation and are generally applicable to children and youth,
although the evidence base is not as substantial. Office-based
counseling directed at children and youth for the prevention
or cessation of tobacco use has been a cornerstone of
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Reduction of Risk for CVD in Childhood 1681
cardiovascular health promotion, risk reduction, and general
pediatric preventive care.37,39
Christakis and colleagues110 conducted a systematic review
of smoking prevention interventions delivered by healthcare
providers; 1 study showed a significant positive effect on the
prevention of smoking initiation. A more recent systematic
review of family-based smoking prevention interventions that
included 14 randomized, controlled trials111 showed that 4 of
the 9 randomized controlled trials that tested a multicompo-
nent family intervention and included a control group dem-
onstrated significant positive effects, whereas 1 of the 5 that
tested a family intervention versus a school-based interven-
tion had a significant positive outcome. Overall, a signifi-
cantly lower rate of smoking initiation was achieved in
⬇40% of interventions. The quality of the implementation of
the intervention and the amount of training of the imple-
menter were related to positive outcomes; however, the
number of intervention sessions was not. More recently, Pbert
and colleagues112 completed a randomized, controlled trial
designed to examine the effect of a pediatric practice-based
smoking prevention and cessation intervention for adoles-
cents. The provider- and peer-delivered intervention was
based on the 5A model (ask, advise, assess, assist, arrange)
and consisted of brief counseling by the pediatric provider,
followed by 1 visit and 4 telephone calls by older peer
counselors. Results indicated that compared with usual care,
nonsmokers who received the provider- and peer-delivered
intervention were significantly more likely to self-report
having remained abstinent at 6- and 12- month follow-ups.
Smokers who received the intervention, however, were more
likely to self-report having quit at the 6-month but not the
12-month follow-up. Methodological limitations notwith-
standing, including self-report of abstinence, the results
support the feasibility and short-term efficacy of theory-based
multicomponent interventions for the prevention of smoking
initiation and smoking cessation in primary care pediatric
office settings. The results also underscore the need for
prevention of initiation of smoking.112 Adding to the need for
emphasis on the prevention of smoking initiation in pediatric
primary care settings are the conflicting results reported in
recent systematic reviews of the benefits of office-based
counseling on smoking cessation.113 This Cochrane review
found that interventions that used pharmacological aids were
not effective; however, those that incorporated behavioral
change strategies, including motivational interviewing and
stages of change, achieved significant positive results at the
6-month follow-up. Additional research on the efficacy and
effectiveness of combing behavioral change strategies and
pharmacotherapy for long-term abstinence in adolescent
smokers is warranted.
Evidence supports the need for both individual/clinical-
and population-based approaches to the prevention of smok-
ing initiation and interventions for smoking cessation for
children and youth. Current recommendations for pediatric
healthcare providers emphasize a developmental approach
with assessment of smoking status at every well-child
visit.37,39 Parents and guardians are advised to maintain a
smoke-free home environment and to avoid exposure to
secondhand smoke in other environments. For infants and
1682 Circulation October 11, 2011

Table 5. Schedule for Integrated Cardiovascular Promotion in Children

Family History Cholesterol Obesity Blood Pressure Diet Physical Activity Smoking
Age, 0 –2 y
Early heart disease Parent cholesterol Plot height and Family history of Diet history Parent physical activity Parental/household
before 55 y of age screening weight on growth hypertension smoking
charts
Parent total Parent obesity Early foods influence No television viewing If yes, counsel to
cholesterol ⱖ240 future food for infant quit; referral to
mg/dL preferences smoking cessation
Age, 2–5 y
Update family Fasting lipids Plot height, weight, Start routine BP Diet history Encourage active Parental/household
history screening and BMI (kg/m2) on measures at 3 y child-parent play smoking
growth charts of age
(determine if
⬎90th or 95th
percentile for
sex, age, and
height)
Early heart disease Based on family BMI percentiles Low saturated-fat diet, Limit sedentary If yes, counsel to
before 55 y of age history including 1% or nonfat behaviors, including quit; referral to
milk television viewing, to smoking cessation
⬍2 h/d
Parent total Moderate salt intake
cholesterol ⱖ240
mg/dL
Age, 6–10 y
Update family Fasting lipids Plot height, weight, BP measures Diet history Physical activity history Parental/household
history screening and BMI (kg/m2) on smoking
growth charts
Early heart disease Based on family BMI percentiles BP percentiles Low saturated-fat diet, Lifestyle and family If yes, counsel to
before 55 y of age history including 1% or nonfat activities quit; referral to
milk smoking cessation
Parent total Moderate salt intake Reduce sedentary
cholesterol ⱖ240 behaviors such as
mg/dL television viewing
Age, ⬎10 y
Update family Fasting lipids Plot height, weight, BP measures Diet history Physical activity history Parental/
history screening BMI (kg/m2) on household
growth charts smoking
Early heart disease Based on family BMI percentiles BP percentiles Low saturated-fat diet, Lifestyle and family If yes, counsel to
before 55 y of age history including 1% or nonfat activities quit; referral to
milk smoking cessation
Parent total Moderate salt intake Daily moderate to Antismoking
cholesterol ⱖ240 vigorous activity (60 counseling for the
mg/dL min/d), reduce child
sedentary behaviors
BMI indicates body mass index; BP, blood pressure. Adapted from Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Taubert K. American Heart Association
guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood 关published simultaneously in J Pediatr. 2003;142:368 –372兴.
Circulation. 2003;107:1562–1566.39

young children, intervention is directed at parents/guardians
and others in the child’s household who smoke. Parents/
guardians who smoke should be advised of the immediate
health risks to their children; motivated to quit through the
use of behavioral prescriptions such as motivational inter-
viewing, stages of change, and/or the 5A model; and referred
to smoking cessation programs if appropriate. During the
school-age years, assessment of smoking status with clear,
firm and consistent messages about the importance of remain-
ing smoke-free is advised. Five strategies for discussing
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smoking with children are suggested for pediatric healthcare
providers, who are powerful role models for children and
youth. First, encourage young children to actively avoid
environmental smoke whenever possible. Second, emphasize
the importance of not experimenting with smoking, “not even
a puff.” Third, point out the harmful health consequences of
smoking and the addictive habit-forming qualities of nicotine.
Fourth, present information to counter the myths of media
influences (ie, smoking is enjoyable). Fifth, deliver nonsmok-
ing messages in clinical encounters through educational
 Daniels et al
materials in the clinical/office-based setting and advocate for
efforts designed to reduce smoking initiation in community-
based settings.37
In counseling adolescents, a group most at risk for smoking
initiation, pediatric healthcare providers are advised to assess
personal smoking history at every nonurgent encounter and to
provide clear, consistent messages about nonsmoking. For
adolescent smokers, ongoing support and counseling either
personally or through community-based smoking cessation
programs will most likely yield positive outcomes. Resources
such as quit-line numbers and community-based cessation
programs and information on pharmacotherapy for cessation
should be made readily available.37
Conclusion
It is clear that risk factors for atherosclerotic CVD can
develop during childhood and adolescence. This results from
both genetic and environmental factors. When risk factors
develop at an early age, they are likely to track over time,
maintaining a high-risk status. This tracking is reinforced by
ongoing and new adverse health behaviors.
This means that the development of CVD has its origins in
families and that approaches to prevention must be directed at
the developing child and adolescent and the family environ-
ment. Pediatricians and family physicians should view the
prevention of risk factor development (primordial prevention)
and the development of atherosclerotic lesions (primary
prevention) as an important responsibility. This article has
outlined the main risk factors of concern. Healthcare provid-
ers should view this from an integrated perspective, meaning
that each risk factor and the behaviors underlying it should be
addressed through the use of a developmental approach at
every health-maintenance visit.
Kavey et al39 have presented a blueprint for an integrated
approach to pediatric primordial and primary prevention of
atherosclerotic CVD. This approach is presented in Table 5.
Using this approach should maximize opportunities for
prevention. This improves the likelihood that children
and adolescents will maintain low-risk status into young
adulthood.
Prevention of atherosclerotic CVD is best achieved by
maintaining cardiovascular health. Although this is challeng-
ing, it can be achieved by instituting and maintaining opti-
mum health behaviors early in life and stressing improvement
of the family environment as the most important strategy to
achieve these goals.
Disclosures
Dr Daniels has served as a consultant/advisory board member for
Merck, Shering-Plough. Dr Hayman has received research grants for
Health Behaviors of African-American and European-American
Lung Cancer Patients and Family Members (UMB-DF/HCC Com-
prehensive Cancer Partnership Program, NIH/NCI, 1U56CA118635-
03, 11/01/2008-12/31/2010) and Improving Fitness in Children at
Increased Cardiometabolic Risk: Piloting an Interactive Fitness
Program (Harvard Catalyst/The Harvard Clinical and Translational
Science Center, NIH #1 UL1RR 025758-02, 11/01/2009-6/30/2011).
Dr Pratt reports no conflicts. The views expressed and positions
taken in this document are not necessarily those of the National
Heart, Lung, and Blood Institute.
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Reduction of Risk for CVD in Childhood 1683
References
1. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB,
Flegal K, Ford E, Furie K, Go A, Greenlund K, Haase N, Hailpern S, Ho
M, Howard V, Kissela B, Kittner S, Lackland D, Lisabeth L, Marelli A,
McDermott M, Meigs J, Mozaffarian D, Nichol G, O’Donnell C, Roger
V, Rosamond W, Sacco R, Sorlie P, Stafford R, Steinberger J, Thom T,
Wasserthiel-Smoller S, Wong N, Wylie-Rosett J, Hong Y. American
Heart Association Statistics Committee and Stroke Statistics Subcom-
mittee. Circulation. 2009;119:e182.
2. Ezzati M, Hoorn SV, Lopez AD, Danaei G, Rodgers A, Mathers CD,
Murray CJL. Comparative quantification of mortality and burden of
disease attributable to selected risk factors. In: Global Burden of Disease
and Risk Factors. 2nd ed. New York, NY: Oxford University Press;
2007:241–268.
3. Newman WP 3rd, Freedman DS, Voors AW, Gard PD, Srinivasan SR,
Cresant JL, Williamson GD, Webber LS, Berenson GS. Relation of
serum lipoprotein levels and systolic blood pressure to early atheroscle-
rosis: the Bogalusa Heart Study. N Engl J Med. 1986;314:138 –144.
4. 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.
5. 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.
6. McGill HC Jr, McMahan CA, Malcolm GT, Oalmann MC, Stong JP.
Effects of serum lipoproteins and smoking on atherosclerosis in young
men and women: the PDAY Research Group: Pathobiological Deter-
minants of Atherosclerosis in Youth. Arterioscler Thromb Vasc Biol.
1997;17:95–106.
7. 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.
8. Raitakari OT, Juonala M, Kahonen M, Taittonen L, Laitnen T, Maki-
Torkko N, Jarvisalo MJ, Uhari M, Jokinen E, Ronnemaa T, Akerblom
HK, Vikari 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.
9. Urbina EM, Kieltkya L, Tsai J, Srinivasan SR, Berenson GS. Impact of
multiple cardiovascular risk factors on brachial artery distensibility in
young adults: the Bogalusa Heart Study. Am J Hypertens. 2005;18:
767–771.
10. Juonala M, Magnussen CG, Venn A, Dwyer T, Burns TL, Davis PH,
Chen W, Srinivasan SR, Daniels SR, Kähönen M, Laitinen T, Taittonen
L, Berenson GS, Viikari JSA, Raitakari OT. Influence of age on asso-
ciations between childhood risk factors and carotid intima-media
thickness in adulthood. Circulation. 2010;122:2514 –2520.
11. Lloyd-Jones DM, Leip EP, Larson MG, D’Agostino RB, Beiser A,
Wilson PW, Wolf PA, Levy D. Prediction of lifetime risk for cardio-
vascular disease by risk factor burden at 50 years of age. Circulation.
2006;113:791–798.
12. Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van
Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK,
Fonarow GC, Ho PM, Lauer MS, Masoudi FA, Robertson RM, Roger V,
Schwamm LH, Sorlie P, Yancy CW, Rosamond WD. Defining and
setting national goals for cardiovascular health promotion and disease
reduction: the American Heart Association’s strategic Impact Goal
through 2020 and beyond. Circulation. 2010;121:586 – 613.
13. Report of the Dietary Guidelines Advisory Committee, 2010 Dietary
Guidelines for Americans. Evidence based guidelines: http://
www.cnpp.usda.gov/DGAs2010-DGACReport.htm. Accessed May 6,
2011.
14. Institute of Medicine. Dietary Reference Intakes for Energy, Carbo-
hydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids.
Washington, DC: National Academies Press; 2002.
15. Britten P, Marcoe K, Yamini S, Davis C. Development of food intake
patterns for the MyPyramid food guidance system. J Nutr Educ Behav.
2006;38:S78 –S92.
16. Kavey R. How sweet it is: sugar-sweetened beverage consumption,
obesity, and cardiovascular risk in childhood. J Am Diet Assoc. 2010;
110:1456 –1459.
17. Mikkilä V, Räsänen L, Raitakari OT, Pietinen P, Viikari J. Longitudinal
changes in diet from childhood into adulthood with respect to risk of
1684 Circulation October 11, 2011
cardiovascular diseases: the Cardiovascular Risk in Young Finns Study.
Eur J Clin Nutr. 2004;58:1038 –1045.
18. Barton BA, Eldridge AL, Thompson D, Affenito SG, Striegel-Moore
RH, Franko DL, Albertson AM, Crockett SJ. The relation of breakfast
and cereal consumption to nutrient intake and body mass index: the
National Heart, Lung and Blood Institute Growth and Health Study.
J Am Diet Assoc. 2005;105:1383–1389.
19. Affenito SG, Thompson DR, Frank DL, Daniels SR, Obarzanek E,
Schreiber GB, Streiegel-Moore RH. Breakfast consumption by African-
American and white adolescent girls correlates positively with calcium
and fiber intake and negatively with body mass index. J Am Diet Assoc.
2005;105:938 –945.
20. Mikkilä V, Räsänen L, Laaksonen MM, Juonala M, Viikari J, Pietinen
P, Raitakari OT. Long-term dietary patterns and carotid artery intima
media thickness: the Cardiovascular Risk in Young Finns Study. Br J
Nutr. 2009;102:1507–1512.
21. Van Horn L, Obarzanek E, Barton BA, Stevens VJ, Kwiterovich PO Jr,
Lasser NL, Robson AM, Franklin FA Jr, Lauer RM, Kimm SY, Dorgan
JF, Greenlick MR. A summary of results of the Dietary Intervention
Study in Children (DISC): lessons learned. Prog Cardiovasc Nurs.
2003;18:28 – 41.
22. Strong WB, Malina RM, Blimkie CJ, Daniels SR, Dishman RK, Gutin
B. Hergenroeder AC, Must A, Nixon PA, Pivarnik JM, Rowland T,
Trost T, Trudeau F. Evidence based physical activity for school-age
youth. J Pediatr. 2005;146:732–737.
23. Trost SG, Loprinzi PD. Exercise-promoting healthy lifestyles in children
and adolescents. J Clin Lipid. 2008;2:162–168.
24. Raitakari OT, Taimela S. Porkka KV, Telama R, Valimaki I, Akerblom
HK, Vikari JS. Associations between physical activity and risk factors
for coronary heart disease: the Cardiovascular Risk in Young Finns
Study. Med Sci Sport Exerc. 1997;29:1055–1061.
25. Janz KF, Dawson JD, Mahoney LT. Increases in physical fitness during
childhood improves cardiovascular health during adolescence: the Mus-
catine Study. Int J Sports Med. 2002;23(suppl 1):S15–S21.
26. Telama R, Yang X, Viikari J, Valimaki I, Wanne O, Raitakari O.
Physical activity from childhood to adulthood: a 21-year tracking study.
Am J Prev Med. 2005;28:267–273.
27. Suitor CW, Kraak VI. Adequacy of Evidence for Physical Activity
Guidelines Development: Workshop Summary. Institute of Medicine.
Washington, DC: National Academies Press; 2007.
28. Gidding SS, Barton BA, Dorgan JA, Kimm SY, Kwiterovich PO, Lasser
NL, Robson AM, Stevens VJ, Van Horn L, Simon-Morton DG. Higher
self-reported physical activity is associated with lower systolic blood pres-
sure: the Dietary Intervention Study in Childhood (DISC). Pediatrics. 2006;
118:2388–2393.
29. Meyer AA, Kundt G, Lesnschow U, Schuff-Werner P, Kienast W.
Improvement of early vascular changes and cardiovascular risk factors
in obese children after a six-month exercise program. J Am Coll Cardiol.
2006;48:1865–1870.
30. Nemet D, Barkan S, Epstein Y, Friedlan O, Kowen G, Eliakim A.
Short-and long-term beneficial effects of a combined dietary-behavioral-
physical activity intervention for the treatment of childhood obesity.
Pediatrics. 2005;115:e443– e449.
31. Stone EJ, McKenzie TL, Welk GJ, Booth ML. Effects of physical
activity interventions in youth: review and synthesis. Am J Prev Med.
1998;15:298 –315.
32. Shaibi GQ, Cruz ML, Ball GD, Weigensberg MJ, Salem GJ, Crespo NC,
Goran MI. Effects of resistance training on insulin sensitivity in over-
weight Latino adolescent males. Med Sci Sports Exerc. 2006;38:
1208 –1215.
33. US Department of Health and Human Services. 2008 Physical Activity
Guidelines for Americans. www.health.gov/paguidelines. Accessed
October 10, 2010.
34. Eaton DK, Kann L, Kinchen S, Shanklin S, Ross J, Hawkins J, Harris
WA, Lowry R, McManus T, Chyen D, Lim C, Brener ND, Wechsler H.
Youth risk behavior surveillance: United States, 2007. MMWR Surveill
Summ. 2008;57:1–131.
35. Nader PR, Bradley RH, Renate M, Houts RM, McRitchie SL, O’Brien
M. Moderate-to-vigorous physical activity from ages 9 to 15 years.
JAMA. 2008;300:295–305.
36. Hayman LL, Meininger JC, Daniels SR, McCrindle BW, Helden L, Ross
J, Dennison BA, Steinberger J, Williams CL. Primary prevention of
cardiovascular disease in nursing practice: focus on children and youth:
a scientific statement from the American Heart Association Committee
on Cardiovascular Disease in the Young, Council on Cardiovascular
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on March 11, 2015
Nursing, Council on Epidemiology and Prevention, and Council on
Nutrition, Physical Activity, and Metabolism. Circulation. 2007;116:
344 –357.
37. 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, Hyper-
tension and Obesity in the Young (AHOY) of the Council on Cardio-
vascular Disease in the Young, American Heart Association. Circulation.
2002;106:143–160.
38. Davis MM, Gance-Cleveland B, Hassink S, Johnson R, Paradis G,
Resnicow K. Recommendations for prevention of childhood obesity.
Pediatrics. 2007;120(suppl 4):S229 –S253.
39. Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Taubert K.
American Heart Association guidelines for primary prevention of ath-
erosclerotic cardiovascular disease beginning in childhood [published
simultaneously in J Pediatr. 2003;142:368 –372]. Circulation. 2003;
107:1562–1566.
40. Barlow SE; Expert Committee. Expert Committee recommendations
regarding the prevention, assessment and treatment of child and ado-
lescent overweight and obesity: summary report. Pediatrics. 2007;120:
S164 –S192.
41. Ogden CL, Carroll MD, Curtin LR, Lamb MM, Flegal KM. Prevalence
of high body mass index in US children and adolescents, 2007–2008.
JAMA. 2010;303:242–249.
42. Ogden CL, Lamb MM, Carroll MD, Flegal KM. Obesity and socio-
economic status in children and adolescents: United States, 2005–2008.
NCHS Data Brief. 2010;51:1– 8.
43. Ogden CL, Flegal KM. Changes in terminology for childhood over-
weight and obesity. Natl Health Stat Report. 2010;25:1–5.
44. Shah AS, Khoury PR, Dolan LM, Ippisch HM, Urbina EM, Daniels SR,
Kimball TR. The effects of obesity and type 2 diabetes mellitus on cardiac
structure and function in adolescents and young adults. Diabetologia. 2011;
54:722–730.
45. Urbina EM, Kimball TR, Khoury PR, Daniels SR, Dolan LM. Increased
arterial stiffness is found in adolescents with obesity or obesity-related
type 2 diabetes mellitus. J Hypertens. 2010;28:1692–1698.
46. Freedman DS, Mei Z, Srinivasan SR, Berenson GS, Dietz WH. Cardio-
vascular risk factors and excess adiposity among overweight children
and adolescents: the Bogalusa Heart Study. J Pediat. 2007;150:12–17.
47. Obarzanek E, Wu CO, Cutler JA, Kavey RW, Pearson GD, Daniels SR.
Prevalence and incidence of hypertension in adolescent girls. J Pediatr.
2010;157:461– 467.
48. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting
obesity in young adulthood from childhood and parental obesity. N Engl
J Med. 1997;337:869 – 873.
49. Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS.
Relationship of childhood BMI overweight to coronary heart disease
risk factors in adulthood: the Bogalusa Heart Study. Pediatrics. 2005;
115:22–27.
50. Urbina EM, Kimball TR, McCoy CE, Khoury PR, Daniels SR, Dolan
LM. Youth with obesity and obesity-related type 2 diabetes mellitus
demonstrate abnormalities in carotid structure and function. Circulation.
2009;119:2913–2919.
51. Tirosh A, Shai I, Afek A, Dubnov-Raz G, Ayalon N, Gordon B, Derazne
E, Tzur D, Shamis A, Vinker S, Rudich A. Adolescent BMI trajectory
and risk of diabetes versus coronary disease. N Engl J Med. 2011;364:
1315–1325.
52. Marcus C, Nyberg G, Nordenfelt A, Karpmyr M, Kowalski J, Ekelund
U. A 4-year, cluster-randomized, controlled childhood obesity pre-
vention study: STOPP. Int J Obes (Lond). 2009;33:408 – 417.
53. Díaz RG, Esparza-Romero J, Moya-Camarena SY, Robles-Sardı́n AE,
Valencia ME. Lifestyle intervention in primary care settings improves
obesity parameters in Mexican youth. J Am Diet Assoc. 2010;110:
285–290.
54. Pratt CA, Stevens J, Daniels SR. Childhood obesity prevention and
treatment: recommendations for future research. Am J Prev Med. 2008;
35:249 –252.
55. National High Blood Pressure Education Program Working Group on
High Blood Pressure in Children and Adolescents, American Academy
of Pediatrics. The fourth report on the diagnosis, evaluation, and
treatment of high blood pressure in children and adolescents. Pediatrics.
2004;114:555–576.
56. Fields LE, Burt VL, Cutler JA, Hughes J, Roccella EJ, Sorlie P. The
burden of adult hypertension in the United States 1999 to 2000: a rising
tide. Hypertension. 2004;44:398 – 404.
 Daniels et al
57. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo
JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ; Joint
National Committee on Prevention, Detection, Evaluation and
Treatment of High Blood Pressure National, Heart, Lung, and Blood
Institute; National High Blood Pressure Education Program Coordi-
nating Committee. Seventh report of the Joint National Committee on
Prevention, Detection, Evaluation and Treatment of High Blood
Pressure. Hypertension. 2003;42:1206 –1252.
58. Lackland DT. Population strategies to treat hypertension. Curr Treat
Options Cardiovasc Med. 2005;7:253–258.
59. Chen X, Wang Y. Tracking of blood pressure from childhood to adult-
hood: a systematic review and meta-regression analysis. Circulation.
2008;117:3171–3180.
60. Lauer RM, Clarke WR. Childhood risk factors for high adult blood
pressure: the Muscatine study. Pediatrics. 1989;84:633– 641.
61. Din-Dzietham R, Liu Y, Bielo MV, Shamsa F. High blood pressure
trends in children and adolescents in national surveys, 1963 to 2002.
Circulation. 2007;116:1488 –1496.
62. McNiece KL, Poffenbarger TS, Turner JL, Franco KD, Sorof JM,
Portman RJ. Prevalence of hypertension and pre-hypertension among
adults. J Pediatr. 2007;150:640 – 644.
63. Muntner P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in blood
pressure among children and adolescents. JAMA. 2004;291:2107–2113.
64. Hansen ML, Gunn PW, Kaelber DC. Underdiagnosis of hypertension in
children and adolescents. JAMA. 2007;298:874 – 879.
65. Daniels SR, Loggie JM, Khoury P, Kimball TR. Left ventricular
geometry and severe left ventricular hypertrophy in children and ado-
lescents with essential hypertension. Circulation. 1998;97:1907–1911.
66. Lande MB, Adams H, Falkner B, Waldstein SR, Schwartz GJ, Szilagyi
PG, Wang H, Palumbo D. Parental assessment of executive function and
internalizing and externalizing behavior in primary hypertension after
anti-hypertensive therapy. J Pediatr. 2010;157:114 –119.
67. Couch SC, Saelens BE, Levin L, Dark K, Falcigila G, Daniels SR. The
efficacy of a clinic-based behavioral nutrition intervention emphasizing
a DASH-type diet for adolescents with elevated blood pressure.
J Pediatr. 2008;152:494 –501.
68. Kupferman JC, Paterno K, Mahgerefteh J, Pagala M, Golden M, Lytrivi
ID, Ramaswamy P. Improvement of left ventricular mass with antihy-
pertensive therapy in children with hypertension. Pediatr Nephrol. 2010;
24:1513–1518.
69. McGill HC Jr, McMahan CA, Zieske AW, Sloop GD, Walcott JV,
Troxclair DA, Malcolm GT, Tracy RE, Oalmann MC, Strong JP. Asso-
ciations of coronary heart disease risk factors with the intermediate
lesion of atherosclerosis in youth: the Pathobiological Determinants of
Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb
Vasc Bio. 2000;20:1998 –2004.
70. McMahan CA, Gidding SS, Malcolm GT, Tracy RE, Strong JP, McGill
HC Jr. Pathobiological determinants of atherosclerosis in youth risk
scores in youth are associated with early and advanced atherosclerosis.
Pediatrics. 2006;118:1447–1455.
71. Li S, Chen W, Srinivasan SR, Bond MG, Tang R, Urbina EM, Berenson.
Childhood cardiovascular risk factors and carotid vascular changes in
adulthood: the Bogalusa Heart Study. JAMA. 2003;290:2271–2276.
72. 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.
73. Tonstad S, Joakimsen O, Sternsland-Bugge E, Leren TP, Ose L, Russell
D, Bonaa KH. Risk factors related to carotid intima media thickness and
plaque in children with familial hypercholesterolemia and control
subjects. Arterioscler Thromb Vas Biol. 1996;16:984 –991.
74. Treiber F, Papavassiliou D, Gutin B, Malpass D, Yi W, Islam S, Davis
H, Strong W. Determinants of endothelium-dependent femoral artery
vasodilation in youth. Psychom Med. 1997;59:376 –381.
75. US Department of Health and Human Services, Centers for Disease
Control and Prevention. Prevalence of abnormal lipid levels among
youths: United States, 1999 –2006. Morbidity and Mortality Weekly
Report. 2010;59:2. www.cdc.gov/mmwr.
76. Daniels SR, Greer FR; Committee on Nutrition. Lipid screening and
cardiovascular health in childhood. Pediatrics. 2008;122:198 –208.
77. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between
childhood and adult cholesterol levels: the Muscatine Study. Pediatrics.
1988;82:309 –318.
78. Lauer RM, Clarke WR. Use of cholesterol measurements in childhood
for the prediction of adult hypercholesterolemia: the Muscatine Study.
JAMA. 1990;264:3034 –3038.
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on March 11, 2015
Reduction of Risk for CVD in Childhood 1685
79. 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.
80. 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.
81. American Academy of Pediatrics. National Cholesterol Education Pro-
gram: report of the Expert Panel on Blood Cholesterol Levels in
Children and Adolescents. Pediatrics. 1992;89:525–584.
82. Tamir L, Heiss G, Glueck CJ, Christensen B, Kwiterovich P, Rifkind B.
Lipid and lipoprotein distributions in white children ages 6 –19 years:
the Lipid Research Clinics Program Prevalence Study. J Chronic Dis.
1981;34:27–39.
83. 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.
84. 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. Circulation. 2007;115:1948 –1967.
85. Dennison BA, Jenkins PL, Pearson TA. Challenges to implementing the
current pediatric cholesterol screening guidelines into practice. Pedi-
atrics. 1994;94:296 –302.
86. Rifai N, Neufeld E, Ahlstrom P, Rimm E, D’Angelo L, Hicks JM.
Failure of current guidelines for cholesterol screening in urban African-
American adolescents. Pediatrics. 1996;98:383–388.
87. Rastam L, Hannan PJ, Puepker RV, Mittelmark MB, Murray DM, Slater
JS. Seasonal variation in plasma cholesterol distributions: implications
for screening and referral. Am J Prev Med. 1992;8:360 –366.
88. Williams RR, Hunt SC, Barlow GK, Wu LL, Hopkins PN, Schumacher
MC, Hasstedt SJ, Ware J, Chamberlain RM, Weinberg AD. Prevention
of familial cardiovascular disease by screening for family history and
lipids in youths. Clin Chem. 1992;38:1555–1560.
89. Bachman RP, Schoen EJ, Stembridge A, Jurecki ER, Imagire RS.
Compliance with childhood cholesterol screening among members of a
prepaid health plan. Am J Dis Child. 1993;147:382–385.
90. Ritchie SK, Murphy ECS, Ice C, Cottrell LA, Minor V, Elliott E, Neal
W. Universal versus targeted blood cholesterol screening among youth:
the CARDIAC Project. Pediatrics. 2010;126:260 –265.
91. Diller PM, Huster GA, Leach AD, Laskarzewski PM, Sprecher DL.
Definition and application of the discretionary screening indicators
according to the National Cholesterol Education Program for Children
and Adolescents. J Pediatr. 1995;126:345–352.
92. Griffin TC, Christoffel KK, Binns HJ, Mc Guire PA. Family history
evaluation as a predictive screen for childhood hypercholesterolemia:
Pediatric Practice Research Group. Pediatrics. 1989;84:365–373.
93. 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 Prev-
alence Program Follow-Up Study. Pediatrics. 2006;118:165–172.
94. Rose G. Sick individuals and sick populations. Int J Epidemiol. 1985;
14:32–38.
95. Hakanen M, Lagström H, Kaitosaari T, Niinikoski H, Näntö-Salonen K,
Jokinen E, Sillanmäki L, Viikari J, Rönnemaa T, Simell O. Development
of overweight in an atherosclerosis prevention trial starting in early
childhood: the STRIP study. Int J Obes (Lond). 2006;30:618 – 626.
96. Gidding SS, Dennison BA, Birch LL, Daniels SR, Gillman MW, Lich-
tenstein AH, Rattay KT, Steinberger J, Stettler N, Van Horn L. Dietary
recommendations for children and adolescents: a guide for practitioners:
consensus statement from the American Heart Association. Circulation.
2005;112:2061–2075.
97. Gidding SS, Lichtenstein AH, Faith MS, Karpyn A, Menella JA, Popkin
B, Rowe J, Van Horn L, Whitsel L. Implementing American Heart
Association pediatric and adult nutrition guidelines: a scientific
statement from the American Heart Association Nutrition Committee of
the Council on Nutrition, Physical Activity and Metabolism, Council on
Cardiovascular Disease in the Young. Circulation. 2009;119:
1161–1175.
98. Stein EA, Marais AD, Szamosi T, Raal FJ, Schurr D, Urbina EM,
Hopkins PN, Karki S, Xu J, Misir S, Melino M. Colesevelam hydro-
chloride: efficacy and safety in pediatric subjects with heterozygous
familial hypercholesterolemia. J Pediatr. 2010;156:231–236.
1686 Circulation October 11, 2011
99. US Department of Health and Human Services. The Health Conse-
quences of Smoking: A Report of the Surgeon General. Atlanta, GA: US
Department of Health and Human Services, CDC. http://www.cdc.gov/
tobacco/data_statistics/sgr/2004/index.htm. Accessed May 6, 2011.
100. Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of
death in the United States. 2000. JAMA. 2004;291:1238 –1245.
101. Substance Abuse and Mental Health Services Administration. Results
From the 2008 National Survey on Drug Use and Health: National
Findings. Rockville, MD: US Department of Health and Human
Services, Substance Abuse and Mental Health Services Administration:
2009. http://www.oas.samhsa.gov/nsduh/2k8nsduh/2k8results.pdf.
Accessed May 6, 2011.
102. US Department of Health and Human Services. The Health Conse-
quences of Involuntary Exposure to Tobacco Smoke: A Report of the
Surgeon General. Atlanta, GA: Department of Health and Human
Services, Public Health Service, Centers for Disease Control and Pre-
vention, National Center for Chronic Disease Prevention and Health
Promotion, Office of Smoking and Health; 2006.
103. Treating Tobacco Use and Dependence: 2008 Update. Rockville, MD:
US Department of Health and Human Services, Public Health Service;
May 2008. http://www. ahrq.gov/path/tobacco.htm. Accessed May 6,
2011.
104. Centers for Disease Control and Prevention. Tobacco use among middle
and high school students: United States, 2000 –2009. MMWR Morb
Mortal Wkly Rep. 2010;59:1063–1067.
105. Mowery PD, Farrelly MC, Haviland ML, Gable JM, Wells HE. Pro-
gression to established smoking among US youth. Am J Public Health.
2004;94:331–337.
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on March 11, 2015
106. Centers for Disease Control and Prevention. Best Practices for Compre-
hensive Tobacco Control Programs: 2007. Atlanta, GA: US Department of
Health and Human Services, Centers for Disease Control and Prevention;
2007. http://www.cdc.gov/tobacco/tobacco_control_programs/state and
community/bestpractices/index.htm.
107. National Cancer Institute. The Role of the Media in Promoting and
Reducing Tobacco Use. Bethesda, MD: US Department of Health and
Human Services, National Institutes of Health, National Cancer Insti-
tute; 2008. Tobacco Control Monograph No. 19.
108. American Academy of Pediatrics Committee on Environmental Health.
Environmental tobacco smoke: a hazard to children. Pediatrics. 1997;
99:639 – 642.
109. Fiore MC, Jaen CR. A clinical blueprint to accelerate the elimination of
tobacco use. JAMA. 2008;299:2083–2085.
110. Christakis DA, Garrison MM, Ebel BE, Wiehe SE, Rivara FP. Pediatric
smoking interventions delivered by care providers: a systematic review.
Am J Prev Med. 2003;25:358 –362.
111. Thomas RE, Baker P, Lorenzetti D. Family-based programmes for
preventing smoking by children and adolescents. Cochrane Database
Syst Rev. 2007:CD004493.
112. Pbert L, Flint AJ, Fletcher KE, Young MH, Drucker S, DiFranza JR.
Effect of a pediatric practice-based smoking prevention and cessation
intervention for adolescents: a randomized controlled trial. Pediatrics.
2008;121:e738 – e747.
113. Grimshaw GM, Stanton A. Tobacco cessation interventions for young
people. Cochrane Database Syst Rev. 2006:CD003289.
KEY WORDS: atherosclerosis 䡲 diet 䡲 hypertension 䡲 obesity
Supplemental Table 1. Strong- and moderately-rated evidence linking diet and CVD
Evidence from the 2010 Dietary Guidelines Advisory Committee
Topic
MACRONUTRIENTS
AND ENERGY
Is intake of dietary fat
associated with adiposity
in children?
Is total energy intake
associated with adiposity
in children?
Is dietary energy density
associated with adiposity
in children?
Is intake of sugar-
sweetened beverages
associated with adiposity
in children?
MICRO NUTRIENTS
What is the effect of a
reduced sodium intake on
blood pressure in children
from birth to age 18 years?
Is intake of calcium and/or
dairy (milk and milk
products) related to
adiposity in children?
FOODS AND FOOD
ENVIRONMENT
What is the relationship
between the environment,
body weight and
fruit/vegetable
consumption?
risk:
Conclusion Grade
Moderate evidence from prospective cohort Moderate
studies suggests that increased intake of dietary
fat is associated with greater adiposity in
children. However, there were no studies
conducted under isocaloric conditions.
Moderately strong evidence from recent Moderate-
prospective cohort studies that identified Strong
plausible reports of energy intake, support a
positive association between total energy
(caloric) intake and adiposity in children.
Moderately strong evidence from Moderate-
methodologically rigorous longitudinal cohort Strong
studies of children and adolescents suggests
that there is a positive association between
dietary energy density and increased adiposity
in children.
Strong evidence supports the conclusion that Strong
greater intake of sugar-sweetened beverages is
associated with increased adiposity in children.
A moderate body of evidence has documented Moderate
that as sodium intake decreases, so does blood
pressure in children, birth to 18 years of age.
Moderate evidence suggests that there is no Moderate
relationship between intake of calcium and/or
dairy (milk and milk products) and adiposity in
children and adolescents.
An emerging body of evidence has documented Moderate
the impact of the food environment and select
behaviors on body weight in both children and
adults.
Moderately strong evidence now indicates that
the food environment is associated with dietary
intake, especially less consumption of
 vegetables and fruits and higher body weight.
The presence of supermarkets in local
neighborhoods and other sources of vegetables
and fruits are associated with lower body mass
index (BMI), especially for low-income
Americans, while lack of supermarkets and
long distances to supermarkets are associated
with higher BMI. Finally, limited but
consistent evidence suggests that increased
geographic density of fast food restaurants and
convenience stores is also related to increased
BMI.
What is the relationship Strong and consistent evidence indicates that Strong
between eating out and children and adults who eat fast food are at
body weight? increased risk of weight gain, overweight and
obesity. The strongest documented relationship
between fast food and obesity is when one or
more fast food meals are consumed per week.
There is not enough evidence at this time to
similarly evaluate eating out at other types of
restaurants and risk of weight gain, overweight
and obesity.
What is the relationship Moderate evidence suggests that children who Moderate
between breakfast and do not eat breakfast are at increased risk of
body weight? overweight and obesity. The evidence is
stronger for adolescents. There is inconsistent
evidence that adults who skip breakfast are at
increased risk for overweight and obesity.
Is breakfast intake Moderate evidence supports a positive Moderate
associated with achieving relationship between the behavior of breakfast
recommended nutrient consumption and intakes of certain nutrients in
intakes? children, adolescents and adults.
What is the relationship Strong evidence documents a positive Strong
between portion size and relationship between portion size and body
body weight? weight.

What is the relationship Strong and consistent evidence in both children Strong
between screen time and and adults shows that screen time is directly
body weight? associated with increased overweight and
obesity. The strongest association is with
television screen time.
Source: Selected from the Report of the Dietary Guidelines Advisory Committee on the
Dietary Guidelines for Americans, 2010 (http://www.cnpp.usda.gov/DGAs2010-
DGACReport.htm) http://www.nutritionevidencelibrary.com/category.cfm?cid=21 (13)

Grading criteria used in the 2010 U.S. Dietary Guidelines was adapted from the
American Dietetic Association Evidence Analysis Library® and based upon: Greer N,
Mosser G, Logan G, Wagstrom Halaas G. A practical approach to evidence grading. The
Joint Commission Journal on Quality Improvement. 2000;26:700-712.
Supplemental Table 2. Examples of obesity prevention and treatment interventions in children and adolescents

Reference Population Intervention Outcomes (e.g., Diet, food pattern,

nutrients/weight/BMI/blood pressure/blood
lipids/glucose /sedentary behavior-TV viewing,
physical activity)
Diaz RG et al. Mexican youth, Shape Down program adapted for Mexican Mean changes in body weight for the lifestyle
Lifestyle 9-17 years; RCT; youth with culturally appropriate topics. 12 group and the control group were -0.8 kg (-3.2,
intervention in
primary care
12 months, BMI weekly 2-hour sessions on improving self- 1.5) vs. +5.6 kg (3, 8.2; P<0.001).
settings or weight esteem, emotions, communication, and
improves circumference lifestyle behaviors—nutrition, weight Mean changes in BMI were -1.8 (-2.6, -0.9) vs.
obesity >90th percentile regulation, energy balance, physical activity. +0.4 (-0.5, 1.3; P<0.001), intervention vs.
parameters in Dietitian advice and physician consult. control, respectively.
Mexican youth.
J Am Diet
Assoc. Control condition: 10-15 consult with Significant differences in primary outcomes
2010;110:285- physician, encouraged 30 min PA, food guide (weight -3.5 kg, P=0.02; BMI -1.2, P=0.03) in
90. (53) pyramid suggestions. favor of the lifestyle group at 12 months.

Kalarchian MA 192 children 8-12 Family-based intervention; 20 group meetings, Significant decreases in child percent
et al. Family- years old (mean 1 hr each, for 6 mo. Lifestyle coach, 6 group overweight, relative to usual care, at 6 months.
based treatment
of severe +/- SD: 10.2 +/- sessions and telephone calls. Intervention Intervention vs. Usual Care - 7.58% vs. 0.66%
pediatric 1.2 years). The focused on Stop Light eating plan ranging decrease in child percent overweight at 6
obesity: average BMI from 1200 to 1800 kcal; strategies to increase months.
randomized percentile for age PA, decreased sedentary hours, decreased
controlled trial. and gender was emotional eating, goal setting. .
Pediatrics.
2009;124:1060-
99.18 (SD: 0.72)
8. Control condition-2 nutrition consults. Offered
intervention after 18 mo.
Vitola BE et al. 8 obese Four-week behavioral therapy sessions; 5% stable weight loss for 4 weeks improved
Weight loss adolescents, BMI Healthy Habits weight loss program used to hepatic triglycerides by 61.6% , insulin
reduces liver fat
and improves >95th percentile, decrease caloric intake and increase physical sensitivity in the liver by 56% and in skeletal
hepatic and mean age 15.3, activity. 1200 kcal to 1500 kcal/d. muscle by 97% .
skeletal muscle
insulin
tanner stage 4.4.
sensitivity in
obese
adolescents.
Obesity.
2009;17:1744-
8.
Reinehr T et al. 288 obese ”Obeldicks” is 12-month outpatient physical Lifestyle intervention significantly reduced
Lifestyle children, mean activity, nutrition and behavior therapy BMI-z score (mean -0.22; 95%CI -0.18 to -
intervention in
obese children
age 12.5 years. intervention Psychological care for3 mo 0.26), compared to control (mean +0.15; 95%CI
is associated (10-16 yrs). intensive—nutrition course 1.5 hrs for 6 +0.13 to +0.18), and metabolic syndrome
with a decrease Metabolic months, 30min/mo of psychological therapy prevalence (from 19% to 9%).
of the metabolic syndrome with family, 3 mo of individual care. Physical
syndrome components at activity 1/wk for 12 mo, ball games, jogging,
prevalence.
Atherosclerosis. baseline and 1 yr. trampoline jumping, and TV reduction. Food
2009;207:174- Control group based dietary guidance- 15% pro, 55% CHO,
80. 186 obese 5% sugar, 30% fat.
children- no
intervention.
Marcus et al. A 3135 boys and 30 min physical activity daily, elimination of The prevalence of overweight and obesity
4-year, cluster- girls in grades 1-4 sweets and sweetened beverages, increase in decreased by 3.2% (from 20.3 to 17.1) in
randomized,
controlled
(Sweden). School whole grains. Low-fat dairy products and intervention schools compared with an increase
childhood children- N= 5 whole-grain bread were promoted and all of 2.8% (from 16.1 to 18.9) in control schools
obesity intervention sweets and sweetened drinks were eliminated (P<0.05). A larger proportion of the children
prevention schools, and N=5 in intervention schools.. Duration: 4 years, who were initially overweight reached normal
study: STOPP. control schools. 8/2001 to 6/2005 weight in the intervention group (14%)
Int J Obes
(Lond). compared with the control group (7.5%),
2009;33:408- P=0.017.
17. (52)
Nowicka P et 72 obese Family based intervention consisting of a Intervention group with initial BMI z-score < 3.5
al. Family adolescents 12-19multidisciplinary team-pediatrician, RD, sports significantly reduced BMI z-scores in both
weight school
treatment: 1-
years old. trainer, nurse, family therapist. Whole family genders (-0.09 +/- 0.04, p = 0.039) compared
year results in Referred by approach; focus on solutions and family goals. with those in the control group with initial BMI
obese pediatrician and Four group meetings; family meeting with z-score < 3.5.
adolescents. Int school nurses. Pediatrician for 10 min; intervention tool box
J Pediatr Obes. with nutrition messages, portion sizes, limited
2008;3:141-7.
Duration: 1 year. intake of nutrient poor foods, increase in fruits
and vegetables, 60 min physical activity.
Woo J et al. Fifty-five subjects Lifestyle modification program or to usual care Intervention group maintained their weight loss
Effectiveness of with and without after 6 months' treatment with Orlistat. and favorable anthropometric, metabolic, dietary
a lifestyle
modification diabetes mellitus. Nutritionist-led intervention consisted of intake, physical activity and quality of life
programme in dietary management, physical activity, peer profiles, while most parameters deteriorated in
weight group support and discussion using techniques the usual care group, being more marked in
management in of self-monitoring, stimulus control and subjects with diabetes.
obese subjects cognitive restructuring.
after cessation
of treatment
with Orlistat. J
Eval Clin Pract.
2007;13:853-9.
Saelens BE et 204 healthy 7- to 5 months weight loss treatment followed BSM or SFM maintained relative weight
al. Efficacy of 12-year-olds, randomization into 1 of 3 maintenance significantly better than children assigned to the
maintenance
treatment
20% to 100% conditions-- control group, 4 months of control group (P< =.01 for all; effect sizes d =
approaches for above median behavioral skills maintenance (BSM), or social 0.72-0.96; mean changes in BMI z scores = -
childhood body mass index facilitation maintenance (SFM) treatment. 0.04, -0.04, -0.05, and 0.05 for BSM alone, SFM
overweight: a (BMI) for age and Follow-up assessments 1 and 2 years following alone, BSM and SFM together, and the control
randomized sex, with at least randomization. . group, respectively). Active maintenance
controlled trial.
JAMA.
1 overweight treatment efficacy relative to the control group
2007;298:1661- parent. declined during follow-up, but the effects of
73. SFM alone (P = .03; d = 0.45; mean change in
BMI z score = -0.24) and when analyzed
 together with BSM (P = .04; d = 0.38; mean
change in BMI z score = -0.22) were
significantly better than the control group (mean
change in BMI z score = -0.06) when examining
BMI z score outcomes from baseline to 2-year
follow-up.
Savoye M et al. 209 overweight Participants were randomly assigned to either a Six-month improvements were sustained at 12
Effects of a children (body control (n=69, traditional clinical weight months in weight management vs. control,
weight
management
mass index [BMI] management counseling every 6 months), or a including changes in the following (mean [95%
program on >95th percentile weight management group (n = 105, an confidence interval]): weight (+0.3 kg [-1.4 to
body for age and sex), intensive family-based program including 2.0] vs. +7.7 kg [5.3 to 10.0]); BMI (-1.7 [-2.3 to
composition ages 8 to 16 years exercise, nutrition, and behavior modification). -1.1] vs. +1.6 [0.8 to 2.3]); body fat (-3.7 kg [-
and metabolic of mixed ethnic Intervention occurred biweekly the first 6 5.4 to -2.1] vs. +5.5 kg [3.2 to 7.8]); and
parameters in
overweight groups. months, bimonthly thereafter. HOMA-IR (-1.52 [-1.93 to -1.01] vs. +0.90 [-
children: a 0.07 to 2.05]).
controlled trial.
JAMA.
2007;297:2697-
704.
Kalavainen MP 70 obese children Two-arm intervention: 1) routine counseling Children attending the group treatment lost more
et al. Clinical (weight for height (two appointments for children) or 2) family- weight for height (6.8%) than children receiving
efficacy of
group-based
115-182%) aged based group treatment (15 separate sessions for routine counseling (1.8%) (P=0.001). The
treatment of 7-9 years. parents). Sessions included nutrition education, respective decreases in BMI were 0.8 vs. 0.0
childhood children).. physical activity education and behavioral (P=0.003) and in BMI-SDS 0.3 vs. 0.2
obesity therapy Children's weights and heights were (P=0.022).
compared with measured at baseline, after the 6-month
routinely given
individual
intervention and after the 6-month follow-up.
counseling. Int
J Obes (Lond).
2007;31:1500-
8.
Supplemental Table 3. Lipid and Lipoprotein Distributions in Children and Adolescents, Aged 5-19 Years

Males Females
5-9y 10-14y 15-19y 5-9y 10-14y 15-19y
Total Cholesterol, mg/dL
50th percentile 153 161 152 164 159 157
75th percentile 168 173 168 177 171 176
90th percentile 183 191 183 189 191 198
95th percentile 186 201 191 197 205 208
Triglyceride, mg/dL
50th percentile 48 58 68 57 68 64
75th percentile 58 74 88 74 85 85
90th percentile 70 94 125 103 104 112
95th percentile 85 111 143 120 120 126
LDL, mg/dL
50th percentile 90 94 93 98 94 93
75th percentile 103 109 109 115 110 110
90th percentile 117 123 123 125 126 129
95th percentile 129 133 130 140 136 137
HDL, mg/dL
5th percentile 38 37 30 36 37 35
10th percentile 43 40 34 38 40 38
25th percentile 49 46 39 48 45 43
50th percentile 55 55 46 52 52 51

Adapted from the Lipid Research Clinics Pediatric Prevalence Study (83).
 Reduction of Risk for Cardiovascular Disease in Children and Adolescents
Stephen R. Daniels, Charlotte A. Pratt and Laura L. Hayman

Circulation. 2011;124:1673-1686
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