Pediatric Preventive Cardiology





Atherosclerotic CVD is a major cause of morbidity and mortality and is responsible for more than 50% of all deaths in the United States. Although most of the clinical burden of CVD occurs in adulthood, risk factors for CVD develop during childhood and adolescence. In fact, there is now clear evidence that atherosclerosis begins during childhood, with a rapid increase in the prevalence of coronary pathology during adolescence and young adulthood. Studies have found that:



  • 1.

    Fatty streak, the earliest lesion of the atherosclerosis, occurred by 5 to 8 years of age and fibrous plaque, the advanced lesion, appeared in the coronary arteries in subjects in their late teens.


  • 2.

    Fibrous plaque was found in over 30% of 16- to 20-year-olds and the prevalence of the lesion reached nearly 70% by age 26 to 39.


  • 3.

    The extent of pathologic changes in the coronary arteries increased with age and so did the number of known CV risk factors that the individual had at the time of death.



Therefore one strategy of reducing CAD in adults would be to prevent or correct CV risk factors in children and adolescents.


Unfortunately, the importance of preventing heart disease in pediatric population is not well perceived by pediatricians and pediatric cardiologists. Although CHD is associated with the highest mortality of any congenital defects, only 0.4% of deaths from CVDs are caused by CHD. The great majority of CV death is from coronary artery disease (54%), stroke (18%), CHF (6%) and hypertension (5%). Therefore preventive cardiology is and should be pediatric domain.


The primary purpose of this chapter is to raise physicians’ attention to the emerging importance of practicing medicine to prevent future CVD (and type 2 diabetes) during childhood. This chapter discusses the topics listed below. Lipid screening for dyslipidemia and its management and hypertension, two other important CV factors, are discussed in earlier chapters (Chapters 26 and 23, respectively).



  • 1.

    Cardiovascular risk factors


  • 2.

    Metabolic syndrome in children.


  • 3.

    Diagnosis and principles of management of childhood obesity


  • 4.

    Strategies for smoke cessation.


  • 5.

    The summary table of the American Heart Association (AHA) guidelines on practice of pediatric preventive cardiology.



I. Cardiovascular Risk Factors


Well-known CV risk factors include positive family history of coronary heart disease, high levels of cholesterol, low levels of high-density lipoprotein cholesterol (HDL-C, hypertension, cigarette smoking, and diabetic or prediabetic states ( Box 27.1 ).



Box 27.1

Major Risk Factors for Coronary Heart Disease

Adapted from the 2002 Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Education, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation, 106 (25), 3143–3421.





  • Family history of premature coronary heart disease, cerebrovascular or occlusive peripheral vascular disease (with onset before age 55 years for men and 65 years for women in parents or grandparents)



  • Hypercholesterolemia



  • Low levels of high-density lipoprotein (<40 mg/100 mL)



  • Hypertension (blood pressure >140/90 mm Hg or taking antihypertensive medication)



  • Cigarette smoking



  • Diabetes mellitus (regarded as a coronary heart disease risk equivalent)




Obesity is now known to be an independent risk factor for CVD. Obese individuals have increased prevalence of clustering of multiple CV risk factors, called the metabolic syndrome, which lead to increased incidence of both type 2 diabetes and CV events (see the following text). Unfortunately, the prevalence of obesity has increased rapidly in recent decades.


II. Metabolic Syndrome


Obese individuals often have emerging risk factors, including atherogenic dyslipidemia (also known as “lipid triad,” consisting of raised level of triglycerides, and small, dense low-density lipoprotein (LDL) particles, and low levels of HDL cholesterol), insulin resistance (hyperinsulinemia), a proinflammatory state (elevation of serum high-sensitivity C-reactive protein), and a prothrombotic state (increased amount of plasminogen activator inhibitor-1 [PAI-1]). The cluster of the these risk factors occurring in one person is known as “the metabolic syndrome.” In the metabolic syndrome, LDL cholesterol (LDL-C) levels may not be elevated but apoprotein B (apoB) and small, dense LDL particles are elevated. The smallest particles in the LDL fraction are known to have the greatest atherogenicity. This syndrome occurs more commonly in individuals with abdominal (visceral) obesity. Hispanics and South Asians seem to be particularly susceptible to the syndrome.


Clinically identifiable components of the metabolic syndrome for adults are listed in Box 27.2 . The presence of at least three of the risk factors is required to make the diagnosis of the metabolic syndrome in adults according to the AHA/National Heart, Lung, and Blood Institute (NHLBI scientific statement) (Grundy et al., 2005), but the International Diabetes Federation (IDF) recommends obesity plus at least two of the remaining four criteria (Alberti et al., 2006). Evidence has supported that waist circumference (reflecting visceral adiposity) is a better predictor of CVD than body mass index (BMI). Other components of metabolic syndrome, such as proinflammatory and prothrombotic states, are not routinely measured in clinical practice.



Box 27.2

Definitions of the Metabolic Syndrome in Adults and in Children and Adolescents



































Adults a Children and adolescents b
Obesity (WC)


  • Men: WC ≥40 inches (102 cm)



  • Women: WC ≥35 inches (88 cm)




  • WC ≥90th percentile or



  • adult cutoff point

Triglycerides ≥150 mg/dL ≥150 mg/dL
HDL cholesterol


  • Men <40 mg/dL



  • Women <50 mg/dL

≤40 mg/dL
Hypertension 130/85 mm Hg or greater Systolic BP ≥130 mm Hg; diastolic BP ≥85 mm Hg
Elevated fasting glucose ≥100 mg/dL ≥100 mg/dL
Defining criteria


  • ≥3 criteria (AHA/NHLBI consensus statement) a or



  • Obesity + ≥2 remaining 4 criteria c

Obesity + ≥2 remaining 4 criteria b

BMI, body mass index; BP, blood pressure; HDL, high-density lipoprotein; NHLBI, National Heart, Lung, and Blood Institute; WC, waist circumference .

a From Grundy, S. M., Cleeman, J. I., Daniels, S. R., et al. (2005). Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation, 112 (17), 2735–2752.


b From Zimmet, P., Alberti, G., Kaufman, F., et al. (2007). Lancet, 369 (9579), 2059–2061.


c From Alberti, K. G., Zimmet, P., & Shaw, J. (2006). Metabolic syndrome—a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabetic Medicine, 23 (5), 469–480.




For children, the IDF has proposed new cutoff points for triglycerides and fasting glucose different from earlier criteria. The new criteria for children make the definition almost the same as for adults ( Box 27.2 ). Obesity and the presence of at least two of the remaining four criteria are required to make the diagnosis of the metabolic syndrome in children. As in adults, waist circumference is preferable to BMI for children as well, which represents abdominal (visceral or central) obesity. Ethnicity and gender specific waist circumference percentiles are now available for children (Fernandez et al., 2004) as presented in Appendix C (Tables C1 through C3). The prevalence of the metabolic syndrome is 30% to 50% in overweight adolescents.


Comorbidities are frequently found in patients with metabolic syndrome: (1) nonalcoholic fatty liver disease (NAFLD), (2) polycystic ovary syndrome (PCOS) in females, (3) obstructive sleep apnea (OSA), and (4) mental health disorders (Magge et al., 2017).



  • 1.

    NAFLD can be screened by measuring aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in overweight and obese children.


  • 2.

    PCOS is characterized by hyperandrogenism, menstrual irregularities and/or ovulatory dysfunction, and polycystic ovaries.


  • 3.

    OSA occurs because of enlarged soft tissues in and around the airway as well as decreased lung volumes because of increased abdominal fat.



A. Management




  • 1.

    The mainstay of the treatment of the metabolic syndrome for both adults and children is weight control through dietary intervention and promotion of active lifestyle to achieve and maintain optimum weight, normal blood pressure, and normal lipid profile for age. Reducing obesity results in decreases in insulin resistance and inflammatory markers.


  • 2.

    In addition, each component of the syndrome present should be treated aggressively, because the presence of the syndrome indicates a higher risk for CVDs and diabetes.


  • 3.

    Treatment of insulin resistance involves lifestyle modification only (Magge et al., 2017). Although some studies have revealed beneficial effects of metformin on BMI, total cholesterol levels, fasting plasma glucose, and insulin resistance, metformin is not currently recommended for treatment of insulin resistance.


  • 4.

    Treatment of dyslipidemias is presented in some detail in Chapter 26 (Dyslipidemia). The principles of managing obesity are presented in the section of obesity in this chapter.



B. Lipid Screening for Dyslipidemia


Dyslipidemia, including high levels of LDL-C, elevated triglycerides, and low levels of HDL-C, are the best-known, long-established risk factors for CAD. Therefore the most important approach to preventing CV events is to detect and treat patients with dyslipidemia. This topic has been presented in Chapter 26 (Dyslipidemia).


In the past, selective screening of children was recommended. In 2011, however, the Expert Panel convened by the NHLBI) made major changes in the recommendation (Pediatrics, 2011) (see Box 27.2 ).



  • 1.

    A universal screening for children between the ages of 9 and 11 years (late childhood)


  • 2.

    An additional universal screening between the ages of 17 and 21 years


  • 3.

    Selective screening for children in other age groups who have certain CV risk factors (see Chapter 26).



III. Obesity


Information in this section is provided only to assist health care providers in making the diagnosis of overweight and obesity, recognizing complications of obesity, and providing the basic knowledge needed in patient counseling. This section is not intended to describe in detail treatment of obesity; successful treatment of obesity requires special skills and facilities with availability of a multidisciplinary team consisting of registered dietitians, specialized nurses, psychologists, and exercise specialists.


A. Definition and Classification


The BMI (weight in kilograms divided by square of the height in meters [kg/m 2 ]) is a simple, valid measure of relative weight and is recommended in clinical diagnosis of overweight states. A large BMI does not always indicate an increase in body fat; lean muscular individuals may have a large BMI.



  • 1.

    In adults, obesity is present when BMI is >30 and overweight is present when BMI is between 25.0 and 29.9.


  • 2.

    For children, the statistical definition of overweight states is used.



    • a.

      Overweight: BMI between the 85th and 95th percentiles


    • b.

      Obese: BMI ≥95th percentile, and


    • c.

      Severely obese: BMI >99th percentile




Age- and gender-specific BMI percentile curves for the U.S. pediatric population are presented in Appendix C (Figs. C1 and C2).


B. Prevalence


Obesity is one of the most pressing public health issues today in the United States. Nearly half of all American children and adolescents are either overweight or obese. According to a recent national statistics, 16.9% of children and adolescents (2- to 19-year-olds) and 34.9% of adults in the United States are obese. In addition, approximately 32% of children and adolescents are either overweight or obese (Ogden et al., 2014).


C. Pathogenesis


The pathogenesis of obesity may be, in part, inherited, but environmental factors appear importantly related to the recent rise in the prevalence of obesity.



  • 1.

    Increased consumption of calorie-dense food and a decrease in physical activity and/or an increased time spent on television viewing and video games may be causally related to the increasing prevalence of obesity seen in children and adolescents.


  • 2.

    In recent decades, the role of high glycemic index (GI) foods has emerged as an important cause of weight gain.



1. Concept of Energy Balance


The concept of energy balance applies to the pathogenesis of obesity ( Fig. 27.1 ).



  • 1.

    When energy intake exceeds energy expenditure on a chronic basis, obesity results. When energy intake is less than energy expenditure, weight loss may result.


  • 2.

    All energy intake comes from ingestion of macronutrients. Caloric value of fat is 9 kcal/g, whereas that of protein and carbohydrate is 4 kcal/g; this is an important reason for recommending reduced-fat intake to control weight.


  • 3.

    A large portion of energy expenditure is the resting metabolic rate (RMR), accounting 60% to 75% of energy expenditure. Approximately 10% of energy expenditure is dissipated through the thermic effect of food (TEF), which is mainly the result of the energy cost for nutrient absorption, processing, and storage. Energy expenditure resulting from physical activity is relatively small, accounting for only 10% to 15% of the total energy expenditure. This component is least affected by genetics and varies greatly from individual to individual depending on the level of physical activities. The level of energy expenditure from RMR and TEF may be predominantly determined by genetic factors.


  • 4.

    By measure, 3500 calories is equivalent to 1 lb. A relatively small positive energy balance can lead to significant weight gain over time. For example, an excess intake of only 100 calories per day will lead to a 10-lb weight gain over 1 year.




Fig. 27.1


Energy balance. To maintain a stable weight, energy intake (protein, carbohydrate, and fat) of a person should be equal to energy expenditure, which is composed of resting metabolic rate (RMR), the thermic effect of food (TEF), and expenditure associated with physical activities. When intake is greater than expenditure, weight gain will result; when expenditure of energy is greater than the intake, weight loss may result.


2. High Glycemic Index Food as a Cause of Obesity and Increased CV Risks


In addition to the traditional concept of energy balance in the pathogenesis of obesity as discussed earlier, the consumption of high-GI food has emerged an important cause of obesity in recent decades.


Several decades ago, the U.S. government and scientific organizations recommended that people eat low-fat diets to reduce weight gain and improve CV health. However, low-fat diets have not had much effect on the obesity rate. Even though mean fat intake in the United States has decreased since the 1960s (from 42% to 34% of dietary energy), the prevalence of obesity has risen over the past several decades. During this period, people were eating low-fat/high-carbohydrate (CHO) diets. On the other hand, low CHO diets (with more protein and fat), such as the Atkins diet, became popular, appearing to be effective in terms of weight reduction.


Researchers started finding out that the high CHO portion in the diet was respondible for weight gain. CHOs consumed by people following low-fat diets were mostly refined and high in sugar content (i.e., high-GI food). Consumption of high-GI food results in hormonal and metabolic changes that can cause weight gain (as discussed later). A brief review of the concept of the GI (and glycemic load [GL]) follows.


The glycemic index is the number given to a food based on how quickly a CHO diet is digested and absorbed into the bloodstream (Jenkins et al., 1981). The amount of glucose absorbed into the blood a in 2-hour period after consuming 50 g of CHO in a given food is compared with the glycemic response after the consumption of 50 g of glucose, which is set at 100. The GI is classified into three categories: (1) low (a GI ≤55), (2) medium or intermediate (a GI of 55 to 69), and (3) high (a GI ≥70).


Here are some general information about the GI of various food:



  • 1.

    In general, fruits, vegetables (except potatoes), and legumes have a low-GI, whereas sweets, refined-grain products (e.g., white bread), and potatoes have a high-GI.


  • 2.

    The presence of fat lowers the GI. A baked potato has a GI of 85, but fried potatoes (French fries) have a GI of 75.


  • 3.

    The presence of soluble dietary fiber lowers the GI. Whole-wheat breads with higher amounts of fiber generally have a lower GI than white breads.


  • 4.

    The way food is prepared can change its GI. A boiled potato has a GI of 56, steamed potatoes have a GI of 65, and a microwaved potato has a GI of 82.


  • 5.

    The ripeness of fruit increases the GI. The GI of underripe bananas is 30, whereas that of overripe bananas is 52.



Glycemic load . One criticism of the GI is that it tells only how rapidly 50 g of CHO in a particular food turns into blood sugar, but it does not tell how much of that CHO is in a serving of a particular food. The GL is a new way of assessing the impact of CHO consumption that takes into account serving size. For example, although candies have a high-GI, eating a single piece of candy, which contains a small fraction of 50 g, will result in a relatively small glycemic response. Thus the GL of the candy is not high. A GL of a typical serving of food is the product of the amount of available CHO in that serving and the GI of the food (calculated by the amount of CHO contained in a specified serving size of the food × the GI of that food ÷ 100). The GL is categorized as follows: (1) high (a GL of ≥20 points) (2) medium (a GL of 11 to 19 points) and (3) low (a GL of ≤10 points).


The higher the food’s GL, the greater the expected elevation in blood glucose after consumption. A diet with a low GL has been linked to a lower risk of heart disease. A diet low in CHO automatically has a low GL. Almost all food with a low-GI has a low GL. Table 27.1 shows the GI and GL of selected food. As seen in the table, some foods with high GIs turn out to have low GLs. A more complete list of the GI is periodically published by the American Society for Clinical Nutrition (the official website for the GI is www.ajcn.org.easyaccess2.lib.cuhk.edu.hk/content/76/1/5.full ).


Apr 11, 2021 | Posted by in CARDIOLOGY | Comments Off on Pediatric Preventive Cardiology
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