Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary Report


Atherosclerotic cardiovascular disease (CVD) remains the leading cause of death in North Americans but manifest disease in childhood and adolescence is rare. By contrast, risk factors and risk behaviors that accelerate the development of atherosclerosis begin in childhood and there is increasing evidence that risk reduction delays progression towards clinical disease. In 2006, the Director of the National Heart, Lung and Blood Institute (NHLBI), Dr. Elizabeth Nabel, appointed an Expert Panel to develop cardiovascular (CV) health guidelines for pediatric care providers based on a formal evidence review of the science, with an integrated format addressing all the major CV risk factors simultaneously.

State of the Science: Cardiovascular risk Factors and the Development of Atherosclerosis in Childhood

Atherosclerosis begins in youth and this process, from its earliest phases, is related to the presence and intensity of the known CV risk factors shown in Table 1?1. Clinical events such as myocardial infarction, stroke, peripheral arterial disease, and ruptured aortic aneurysm are the culmination of the lifelong vascular process of atherosclerosis. Pathologically, the process begins with the accumulation of abnormal lipid in the vascular intima, a reversible stage, progresses to an advanced stage in which a core of extracellular lipid is covered by a fibromuscular cap, and culminates in thrombosis, vascular rupture, or acute ischemic syndromes.

Integrated Cardiovascular Health Schedule

Table 3?1. Integrated Cardiovascular Health Schedule

Risk Factor

Birth-12 m

1-4 y

5-9 y

9-11 y

12-17 y

18-21 y



At age 3 y, evaluate FHx for early CVD: parents, grandparents, aunts/uncles,

M ? 55 y, F ? 65 y. Review with parents, refer prn.

(+) FHx identifies children for intensive CVD RF attention.

Update at each nonurgent health encounter.

Reevaluate FHx for early CVD in parents, grandparents, aunts/uncles,

M ? 55 y,

F ? 65 y.

Update at each nonurgent health encounter.

Repeat FHx evaluation with patient.


Advise smoke-free home; offer smoking cessation assistance or referral to parents.

Continue active antismoking advice with parents. Offer smoking cessation assistance and referral as needed.

Begin active antismoking advice with child.

Assess smoking status of child.

Active antismoking counseling or referral as needed.

Continue active antismoking counseling with patient. Offer smoking cessation assistance or referral as needed.

Reinforce strong antismoking message.

Offer smoking cessation assistance or referral as needed.


Support breast-feeding as optimal to age 12 m if possible. Add formula if breast-feeding decreases or stops before age 12 m.

Age 12-24 m, may change to cow's milk with % fat per family & pediatric care provider.

After age 2 y, fat-free milk for all; juice ? 4 oz/d; transition to CHILD 1 Diet by age 2 y.

Reinforce CHILD 1 diet messages.

Reinforce CHILD 1 diet messages as needed.

Obtain diet information from child and use to reinforce healthy diet and limitations and provide counseling as needed.

Review healthy diet with patient.


Review FHx for obesity ? Discuss wt for ht tracking, growth chart, and healthy diet.

Chart ht/ wt/ BMI ? classify wt by BMI from age 2 y; review with parent.

Chart ht/ wt/ BMI and review with parent.

BMI > 85th %ile, crossing %iles? intensify diet/ activity focus x 6m. If no change ? RD referral, manage per obesity algorithms.

BMI ? 95th %ile, manage per obesity algorithms.

Chart ht/ wt/ BMI and review with parent and child.

BMI > 85th %ile, crossing %iles? intensify diet/ activity focus x 6m. If no change ? RD referral, manage per obesity algorithms.

BMI ? 95th %ile, manage per obesity algorithms.

Chart ht/ wt/ BMI and review with child and parent.

BMI > 85th %ile, crossing %iles? intensify diet/ activity focus x 6m. If no change ? RD referral, manage per obesity algorithms.

BMI ? 95th %ile, manage per obesity algorithms.

Review ht/ wt/ BMI and norms for health with patient.

BMI > 85th %ile, crossing %iles ?intensify diet/activity focus x 6 m. If no change ? RD referral, manage per obesity algorithms.

BMI ? 95th %ile, manage per obesity algorithms.


No routine lipid screening.

Obtain fasting lipid profile only if FHx (+), parent with dyslipidemia, any other RFs (+), or high-risk condition.

Obtain fasting lipid profile only if FHx (+), parent with dyslipidemia, any other RFs (+), or high-risk condition.

Obtain universal lipid screen with nonfasting non-HDL = TC ? HDL, or fasting lipid profile ? manage per lipid algorithms as needed.

Obtain fasting lipid profile if FHx newly (+), parent with dyslipidemia, any other RFs (+), or high-risk condition; manage per lipid algorithms as needed.

Measure nonfasting non-HDL-C or fasting lipid profile in all x 1 ? Review with patient; manage with lipid algorithms per ATP as needed.


Measure BP in infants with renal/urologic/ cardiac diagnosis or Hx of neonatal ICU.

Measure annual BP in all from age 3 y; chart for age/gender/ht %ile and review with parent.

Check BP annually and chart for age/gender/ht ? Review with parent; work up and/or manage per BP algorithm as needed.

Check BP annually and chart for age/gender/ht ? Review with parent, work up and/or manage per BP algorithm as needed.

Check BP annually and chart for age/gender/ht ? Review with adolescent and parent, work up and/or manage per BP algorithm as needed.

Measure BP ? Review with patient. Evaluate and treat as per JNC guidelines.


Encourage parents to model routine activity. No screen time before age 2 y.

Encourage active play; limit sedentary/ screen time to ? 2 h/d. No TV in bedroom.

Recommend MVPA ? 1h/d; limit screen/sedentary time to ? 2 h/d.

Obtain activity Hx from child ? recommend MVPA ? 1 h/d; screen/ sedentary time ? 2 h/d.

Use activity Hx with adolescent to reinforce MVPA ? 1 h/d, leisure screen time ? 2 h/d.

Discuss lifelong activity, sedentary time limits with patient.



Measure fasting glucose per ADA guidelines, refer to endocrinologist as needed.

Measure fasting glucose per ADA guidelines, refer to endocrinologist as needed.

Obtain fasting glucose if indicated, refer to endocrinologist as needed.

ABBREVIATIONS: m = months; y = years; FHx = family history; M = male; F = female; RF = risk factor; % = percent; BMI = body mass index; %ile = percentile; ADA = American Diabetes Association; MVPA = moderate-to-vigorous physical activity; ATP = Adult Treatment Panel III (Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults); CHILD 1= Cardiovascular Health Integrated Lifestyle Diet; JNC = The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; BP = blood pressure; h/d = hours per day

The Full and Summary Report of the Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents may also be found on the NHLBI website at:

Family History of Early Atherosclerotic Cardiovascular Disease

A family history of CVD represents the net effect of shared genetic, biochemical, behavioral and environmental components. In adults, epidemiologic studies have demonstrated that a family history of premature coronary heart disease in a first degree relative ? heart attack, treated angina, percutaneous coronary catheter interventional procedure, coronary artery bypass surgery, stroke or sudden cardiac death in a male parent or sibling before the age of 55 years or a female parent or sibling before the age of 65 years ? is an important independent risk factor for future CVD. The process of atherosclerosis is complex and involves many genetic loci and multiple environmental and personal risk factors. Nonetheless, the presence of a positive parental history has been consistently shown to significantly increase baseline risk for CVD. The risk for CVD in offspring is strongly inversely related to the age of the parent at the time of the index event. The association of a positive family history with increased CV risk has been confirmed for men, women and siblings and in different racial and ethnic groups. The evidence review identified all randomized controlled trials (RCTs), systematic reviews, meta-analyses and observational studies that addressed family history of premature atherosclerotic disease and the development and progression of atherosclerosis from childhood into young adult life.

Conclusions and Grading of the Evidence Review for the Role of Family History in Cardiovascular Health

  • Evidence from observational studies strongly supports inclusion of a positive family history of early coronary heart disease in identifying children at risk for accelerated atherosclerosis and for the presence of an abnormal risk profile. (Grade B)
  • For adults, a positive family history is defined as a parent and/or sibling with a history of treated angina, myocardial infarction, percutaneous coronary catheter interventional procedure coronary artery bypass grafting, stroke or sudden cardiac death before 55 years in men or 65 years in women. Because the parents and siblings of children and adolescents are usually young themselves, it was the panel consensus that when evaluating family history in a child, history should also be ascertained for the occurrence of cardiovascular disease in grandparents, aunts and uncles although the evidence supporting this is insufficient to date. (Grade D)
  • Identification of a positive family history for CV disease and/or CV risk factors should lead to evaluation of all family members, especially parents, for CV risk factors. (Grade B)
  • Family history evolves as a child matures so regular updates are necessary as part of routine pediatric care. (Grade D)
  • Education about the importance of accurate and complete family health information should be part of routine care for children and adolescents. As genetic sophistication increases, linking family history to specific genetic abnormalities will provide important new knowledge about the atherosclerotic process. (Grade D)

Table 4?1. Evidence-Based Recommendations for Use of Family History in Cardiovascular Health Promotion

Grades reflect the findings of the evidence review.
Recommendation levels reflect the consensus opinion of the Expert Panel.
Supportive actions represent expert consensus suggestions from the Expert Panel provided to support implementation of the recommendations; they are not graded.

Birth - 18 y Take detailed family history (FHx) of CVDa at initial encounter and/or at 3y, 9-11y & 18 y members Grade B
Birth - 18 y (cont.d) If (+) FHx identified, evaluate patient for other CV risk factors, including dyslipidemia, hypertension, diabetes, obesity, history of smoking, and sedentary lifestyle  
Birth - 18 y (cont.d) If (+) FHx and/or CV risk factors identified, evaluate family, especially parents, for CV risk factors Grade B
Birth - 18 y (cont.d) Update FHx at each non-urgent health encounter Grade D
Birth - 18 y (cont.d) Use FHx to stratify risk for CVD risk as risk profile evolves Grade D
Birth - 18 y (cont.d) Supportive actions:
Educate parents about the importance of FHx in estimating future health risks for all family members
18 - 21 y Review FHx of heart disease with young adult patient Grade B
Strongly recommend
18 - 21 y (cont.d) Supportive actions:
Educate patient about family/ personal risk for early heart disease including need for evaluation for all CV risk factors

a Parent, grandparent, aunt, uncle, or sibling with heart attack, treated angina, CABG/stent/angioplasty, stroke, or sudden cardiac death at < 55 y in males, < 65 y in females

Nutrition and Diet

The 2010 Dietary Guidelines for Americans (2010 DGA) include important recommendations for the population over the age of two. The National Cholesterol Education Program Pediatric Panel Report in 1992 provided dietary recommendations for all children as part of a population-based approach to reducing cardiovascular risk. Evidence relative to diet and the development of atherosclerosis in childhood and adolescence was identified by the evidence review for this guideline, and collectively, this provides the rationale for new dietary prevention efforts initiated early in life.

These new pediatric CV guidelines not only build upon the recommendations for achieving nutrient adequacy in growing children as stated in the 2010 DGA but also add evidence regarding the efficacy of specific dietary changes to reduce CV risk from the current evidence review for the use of pediatric care providers in the care of their patients. Because the focus of these guidelines is on CV risk reduction, the evidence review specifically evaluated dietary fatty acid and energy components as major contributors to hypercholesterolemia and obesity, as well as dietary composition and micronutrients as they affect hypertension. New evidence from multiple dietary trials addressing CV risk reduction in children provides important information for these recommendations.

Physical Activity

Physical activity is any bodily movement produced by contraction of skeletal muscle that increases energy expenditure above a basal level. Physical activity can be focused on strengthening muscles, bones and joints but because these guidelines address CV health, the evidence review concentrated on aerobic activity and on the opposite of activity, sedentary behavior. There is strong evidence for beneficial effects of physical activity and disadvantageous effects of a sedentary lifestyle on the overall health of children and adolescents across a broad array of domains. Our review focused on the effects of activity on CV health because physical inactivity has been identified as an independent risk factor for coronary heart disease in adults. Over the last several decades, there has been a steady decrease in the amount of time that children spend being physically active and an accompanying increase in time spent in sedentary activities. The evidence review identified many studies in youth ranging in age from 4 to 21 years that strongly link increased time spent in sedentary activities with reduced overall activity levels and with disadvantageous lipid profiles, higher systolic blood pressure, higher levels of obesity and higher levels of all the obesity-related cardiovascular risk factors including hypertension, insulin resistance and type 2 diabetes.

Tobacco Exposure

Tobacco dependence is responsible for approximately 4 million annual deaths worldwide, and in utero exposure to tobacco products, involuntary tobacco smoke exposure (second hand smoke), and tobacco use directly impair health in fetuses, infants, children, and adolescents. Based on an analysis of published causes of death, tobacco use is the leading actual cause of death in the U. S. The evidence that cigarette use is harmful and addictive is unequivocal. In childhood, nicotine is highly addicting with symptoms of tobacco dependence demonstrated after brief intermittent use. Cigarette use among high school students declined from 1997 to 2003. Rates were stable from 2003 to 2007 with more than 20% of high school students reporting daily smoking. From a public health standpoint, the need to reduce tobacco exposure is compelling, and a role for pediatric health care providers is essential.

A clinical practice guideline update from the U.S. Public Health Service published in May, 2008 systematically reviewed almost 9,000 publications and concluded that smoking prevention and cessation interventions are effective in adults. These same methods should be safely applicable in childhood and adolescence since behavioral interventions to alter smoking behaviors have little if any morbidity, and since morbidity with pharmacologic treatment is limited. Physicians who care for children are well positioned to provide prevention and treatment interventions for their patients. Youth interventions must target parents as well as children since parental smoking is both a risk factor for child smoking and provides second hand smoke exposure to fetuses and children. The evidence review assessed prevention and treatment interventions in each of these areas.

High Blood Pressure

In 2004, an NHLBI Task Force published The Fourth Report on the Diagnosis, Evaluation and Treatment of High Blood Pressure in Children and Adolescents. This report included a complete review of the current evidence on this subject and detailed recommendations for managing blood pressure throughout childhood. These recommendations were used as the basic recommendations for these guidelines, considered complete until 2003 when the review for the report ended. This evidence review for blood pressure for these guidelines was therefore limited to studies published between January 1, 2003, and June 30, 2007, with the addition of selected studies through June 30, 2008, identified by the Expert Panel that meet all the criteria for inclusion. Repeating the review performed by the Fourth Report Task Force was not felt to be necessary, given the short time since publication of that report, nor a judicious use of the resources available for development of these guidelines. Recommendations regarding blood pressure are all graded as expert opinion (Grade D) as they are based on the expert consensus conclusions of the Fourth Report.

Lipids and Lipoproteins

Since the last NHLBI guidelines for lipid management in children and adolescents were published in 1992, both the knowledge base surrounding dyslipidemia in childhood and clinical picture have changed. A series of critical observational studies have demonstrated a clear correlation between lipoprotein disorders and the onset and severity of atherosclerosis in children, adolescents and young adults. A major increase in the prevalence of obesity has led to a much larger population of children with dyslipidemia. At the time of the original guidelines, the focus was almost exclusively on identification of children with elevated low density lipoprotein cholesterol (LDL-C). Since then, the predominant dyslipidemic pattern in childhood is a combined pattern associated with obesity, with moderate to severe elevation in triglycerides (TG), normal to mild elevation in LDL-C and reduced high density lipoprotein cholesterol (HDL-C). Both dyslipidemic patterns have been shown to be associated with initiation and progression of atherosclerotic lesions in children and adolescents as demonstrated by pathology and imaging studies. Identification of children with dyslipidemias, which place them at increased risk for accelerated early atherosclerosis, must include a comprehensive assessment of serum lipids and lipoproteins.

The evidence review for lipids and lipoproteins addressed the association between dyslipidemia and atherosclerosis in childhood, lipid assessment in childhood and adolescence with tables of normative results provided, the dyslipidemias, dietary treatment of dyslipidemia and medication therapy.

Overweight and Obesity

Dramatic increases in childhood overweight and obesity in the United States since 1980 are an important public health focus. Despite efforts over the last decade to prevent and control obesity, recent reports from NHANES show sustained high prevalence with 17% of children and adolescents with a BMI above the 95th percentile for age and gender. The presence of obesity in childhood and adolescence is associated with increased evidence of atherosclerosis at autopsy and of subclinical measures of atherosclerosis on vascular imaging. Because of its strong association with many of the other established risk factors for CV disease, obesity is even more powerfully correlated with atherosclerosis; this association has been shown for blood pressure, dyslipidemia and insulin resistance in each of the major pediatric epidemiologic studies. Of all the risk factors, obesity tracks most strongly from childhood into adult life. Improvement in weight status and decrease in body fatness have been shown to be associated with improvement in all the obesity-related risk factors and in sub-clinical vascular changes. Higher BMI during childhood is directly associated with increased coronary heart disease in adult life. Extrapolation from current data suggests that adolescent obesity will likely increase adult CHD by 5 to 16% over the next 25 years with more than 100,000 excess cases of CHD attributable to increased obesity in childhood. The evidence review included RCTs, systematic reviews, meta-analyses and observational studies assessing the prevention and treatment of overweight and obesity in childhood and adolescence.

Diabetes Mellitus and Other Conditions Predisposing to the Development of Accelerated Atherosclerosis

Diabetes mellitus is an established risk factor for early CVD. Metabolically, diabetes is characterized by hyperglycemia due to defects in insulin secretion (type 1 diabetes [T1DM]) and insulin function and/or secretion (type 2 diabetes [T2DM]). Both T1DM and T2DM are associated with vascular disease. Autopsy and noninvasive imaging studies suggest that the extent of vascular involvement reflects the duration of the disease and the severity of the chronic metabolic derangement. The epidemiologies of the two types differ significantly. T1DM presents at a younger age, with 25% of patients diagnosed between ages 5 and 10 years and another 40% between ages 10 and 15 years. If not treated adequately, the degree of hyperglycemia is severe, and patients are highly symptomatic. By contrast, in T2DM, the majority of patients present in adult life, but a small and growing number present in adolescence, and most are relatively asymptomatic, with only mild to moderate hyperglycemia in combination with obesity. Regardless of these differences, children with diabetes, type 1 or type 2, are at significantly increased risk for accelerated atherosclerosis and early cardiovascular disease.

In certain other pediatric disease states, the process of atherosclerosis is dramatically accelerated with clinical coronary events occurring in childhood and very early adult life. These conditions were the subject of a recent guideline from the American Heart Association (AHA). The Expert Panel elected to use the AHA guideline as the template for developing recommendations for children with conditions like diabetes that predispose them to very accelerated atherosclerosis since the evidence review identified only a very small number of studies addressing these conditions in a randomized trial format.

Risk Factor Clustering and the Metabolic Syndrome

Traditional CV risk factors such as obesity, hypertension and dyslipidemia demonstrate clustering in youth. Risk behaviors like smoking, suboptimal diet and sedentary behavior also demonstrate clustering as do advantageous diet and exercise habits. Becoming obese increases the prevalence of the risk factor cluster in adults called the metabolic syndrome. The metabolic syndrome is defined as 3 or more of the following risk factors: elevated waist circumference, triglyceride levels, BP, and/or fasting glucose, and reduced HDL-cholesterol. In the U.S., the metabolic syndrome is said to affect between 34% and 39% of adults including 7% of men and 6% of women in the 20- to 30-year old age group. The Expert Panel reviewed all the RCTs, SRs, meta-analyses and observational studies that addressed the childhood association between the risk factor cluster known as the metabolic syndrome and the development of atherosclerosis, and the identification and management of the cluster in children and adolescents.

There is a lack of consensus on how to define metabolic syndrome in youth, which has led to widely varying estimates of its frequency. A recent analysis of National Health and Nutrition Examination Survey data from 1999 to 2002 yielded prevalence estimates for all teens from 2.0-9.4% and for obese teens from 12.4-44.2%. Regardless of the definition used, the prevalence of the metabolic syndrome risk factor cluster is higher in older (12- to 14-year-old) children compared with younger (8- to-11-year-old) children. The specific etiology for metabolic syndrome is unknown; however, it is most likely caused by the expression of various genotypes modified by environmental interactions and mediated through abdominal obesity and insulin resistance. Longitudinal studies of cohorts where the metabolic syndrome cluster was present in childhood identify an increased incidence of both T2DM and clinical CV events over a followup of 25 years. A strong association between obesity with or without elevated insulin levels and /or hypertension in early childhood and subsequent development of the metabolic syndrome constellation in adulthood has been consistently demonstrated. Treatment of CV risk factor clustering in youth has not been thoroughly evaluated but maintenance of low levels of CV risk factors starting in childhood is associated with a lower prevalence of cardiovascular disease and with increased longevity in adult life.

Perinatal Factors

Increasing evidence links prenatal exposures to adverse health outcomes. Perinatal risk reduction is an area where pediatric care providers can potentially be effective since they are often the only physicians that a mother sees between pregnancies. The Expert Panel identified three potential areas for consideration: maternal obesity, choice of neonatal feeding method, and maternal smoking cessation. Maternal obesity is associated with gestational diabetes, higher birth weight, childhood obesity measured by increased body mass index, and increased risk of the metabolic syndrome and T2DM in offspring. However, the Expert Panel could not identify any pre-pregnancy or post-partum studies addressing maternal obesity in a pediatric care setting, and more general approaches to preventing or treating obesity in women of reproductive age are beyond the scope of this report. A detailed discussion of childhood obesity itself is the subject of Section 10. Overweight and Obesity. With regard to choice of neonatal feeding method, the CV advantages of breastfeeding as the primary source of nutrition for infants are emphasized in the Section 5. Nutrition and Diet. The evidence review for this section therefore focused on maternal smoking cessation.