Adolescent Health Care: A Practical Guide

Chapter 13

Systemic Hypertension

Joseph T. Flynn

Although more than 58 million American adults, or approximately 29% of the population, have systemic hypertension, screening studies in children and adolescents have demonstrated a prevalence of persistent hypertension of between 1% and 2%. Given the impact of the obesity epidemic on the prevalence of hypertension in adolescents, more recent studies, however, have demonstrated a higher prevalence of approximately 5% in obese minority adolescents (Sorof et al., 2004). Most adolescents and adults with hypertension have primary hypertension—that is, no identifiable underlying cause can be found for their blood pressure (BP) elevation. Most hypertensive adolescents, particularly those with primary hypertension, are asymptomatic. Therefore, it is imperative that BP is measured whenever an adolescent is seen for health care. Detection and treatment of hypertension in the adolescent years may prevent later cardiovascular diseases, with their catastrophic consequences (Kavey et al., 2003).

Definition of Hypertension in Adolescence

Definition

The cardiovascular endpoints used to define hypertension in adults (myocardial infarction, stroke, etc.) do not occur in children and adolescents. Therefore, the definition of hypertension in the young is a statistical one derived from analysis of a large database of BPs obtained from healthy children (National High Blood Pressure Education Program Working Group, 2004). The most recent classification of BP in the young is summarized in Table 13.1.

Normative BP values for adolescents ≤17 years of age are listed in Tables 13.2 and 13.3. For these children, height should first be obtained and plotted on a standard growth curve to determine the child's height percentile. Then the gender-appropriate chart should be used to determine the BP percentile. For adolescents ≥18 years of age, the adult BP classification scheme issued by the Joint National Commission (Chobanian et al., 2003) should be followed (Table 13.4).

Prehypertension

Common to both the pediatric and adult BP classification schemes is the recent concept of “prehypertension”. This refers to BPs that would have been classified as “high-normal” in prior consensus recommendations. Although the term prehypertension has proved to be controversial, it is meant to serve as a means of alerting patients and physicians alike of the potential for later development of hypertension, and of the need to make lifestyle changes that might prevent this from occurring. The same BP value of >120/80 mm Hg is used in both adolescents and adults to designate prehypertension.

TABLE 13.1
Classification of Blood Pressure in Adolescents 17 years and Younger

Blood Pressure Classification

Systolic or Diastolic Blood Pressure Percentilea

a See Tables 13.2 and 13.3. taken from National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute, Bethesda, Maryland. NIH Publication 05-5267, 2005.

Normal

<90th

Prehypertension

90th–95th; or if BP is >120/80 mm Hg even if <90th

Stage 1 hypertension

95th to 99th plus 5 mm Hg

Stage 2 hypertension

>99th plus 5 mm Hg

Staging

Also common to both the pediatric and adult BP classification schemes is the concept of “staging” the degree of hypertension. For children and adolescents, this replaces the older terms of denoting higher levels of hypertension, such as “significant” and “severe”. As will be discussed later, the staging system also plays a role in determining how rapidly a hypertensive adolescent should be

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evaluated, and when antihypertensive drug therapy should be instituted.

TABLE 13.2
Blood Pressure Values for Adolescent Boys 17 Years or Younger

   

Systolic BP (mm Hg)

Diastolic BP (mm Hg)

   

Percentile of Height

Percentile of Height

Age (yr)

BP Percentile

5th

10th

25th

50th

75th

90th

95th

5th

10th

25th

50th

75th

90th

95th

BP, blood pressure.
To use the table, first plot the child's height on a standard growth curve (www.cdc.gov/growthcharts). The child's measured systolic blood pressure and diastolic blood pressure are compared with the numbers provided in the table according to the child's age and height percentile.
National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute, Bethesda, Maryland. NIH Publication 05-5267, 2005.

10

50th

97

98

100

102

103

105

106

58

59

60

61

61

62

63

 

90th

111

112

114

115

117

119

119

73

73

74

75

76

77

78

 

95th

115

116

117

119

121

122

123

77

78

79

80

81

81

82

 

99th

122

123

125

127

128

130

130

85

86

86

88

88

89

90

11

50th

99

100

102

104

105

107

107

59

59

60

61

62

63

63

 

90th

113

114

115

117

119

120

121

74

74

75

76

77

78

78

 

95th

117

118

119

121

123

124

125

78

78

79

80

81

82

82

 

99th

124

125

127

129

130

132

132

86

86

87

88

89

90

90

12

50th

101

102

104

106

108

109

110

59

60

61

62

63

63

64

 

90th

115

116

118

120

121

123

123

74

75

75

76

77

78

79

 

95th

119

120

122

123

125

127

127

78

79

80

81

82

82

83

 

99th

126

127

129

131

133

134

135

86

87

88

89

90

90

91

13

50th

104

105

106

108

110

111

112

60

60

61

62

63

64

64

 

90th

117

118

120

122

124

125

126

75

75

76

77

78

79

79

 

95th

121

122

124

126

128

129

130

79

79

80

81

82

83

83

 

99th

128

130

131

133

135

136

137

87

87

88

89

90

91

91

14

50th

106

107

109

111

113

114

115

60

61

62

63

64

65

65

 

90th

120

121

123

125

126

128

128

75

76

77

78

79

79

80

 

95th

124

125

127

128

130

132

132

80

80

81

82

83

84

84

 

99th

131

132

134

136

138

139

140

87

88

89

90

91

92

92

15

50th

109

110

112

113

115

117

117

61

62

63

64

65

66

66

 

90th

122

124

125

127

129

130

131

76

77

78

79

80

80

81

 

95th

126

127

129

131

133

134

135

81

81

82

83

84

85

85

 

99th

134

135

136

138

140

142

142

88

89

90

91

92

93

93

16

50th

111

112

114

116

118

119

120

63

63

64

65

66

67

67

 

90th

125

126

128

130

131

133

134

78

78

79

80

81

82

82

 

95th

129

130

132

134

135

137

137

82

83

83

84

85

86

87

 

99th

136

137

139

141

143

144

145

90

90

91

92

93

94

94

17

50th

114

115

116

118

120

121

122

65

66

66

67

68

69

70

 

90th

127

128

130

132

134

135

136

80

80

81

82

83

84

84

 

95th

131

132

134

136

138

139

140

84

85

86

87

87

88

89

 

99th

139

140

141

143

145

146

147

92

93

93

94

95

96

97

There are several important considerations in evaluating BP in children and adolescents of any age. They are as follows:

  1. Although various methods are available to measure BP, auscultation is the most accurate and is the method of choice. Because of the removal of mercury sphygmomanometers from most health care settings, aneroid devices should be made available and utilized. The stethoscope bell should be used for auscultation, as it is better suited to detect soft, low-pitched Korotkoff sounds than the diaphragm.
  2. BP in the young is labile; therefore, hypertension should not be diagnosed on the basis of a single measurement. At least three elevated readings on separate occasions are necessary to diagnose hypertension. Using one isolated measurement may lead to mislabeling of an individual, with adverse consequences.
  3. Proper cuff bladder size is critical. The length of the cuff bladder should be at least 80% of the mid-arm circumference. For practical purposes, use the largest cuff that fits the arm while leaving the antecubital fossa free for auscultation. It is better to choose a cuff slightly too big than one too small, as a cuff that is too small will give a falsely elevated BP, but one that is slightly large will not give a falsely low reading.
  4. BP measurements should be taken with the adolescent in the sitting position, with the sphygmomanometer at heart level. The arm (preferably the right) used for the measurement should be recorded in the chart. Ideally,

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the adolescent should have rested for several minutes and should not have smoked or ingested caffeine within 30 minutes before measurement.

  1. For apprehensive patients, BP measurements obtained outside of the office setting, such as by a school nurse or at home using a calibrated over-the-counter device may provide insight as to the existence of “white coat” hypertension. However, ambulatory monitoring, in which BP measurements are obtained over a 24-hour period with an automated device, is the preferred technique for diagnosing white coat hypertension. Given the high prevalence of white coat hypertension in recent studies (Sorof and Portman, 2000), ambulatory BP monitoring should be considered as part of the initial evaluation of an adolescent or young adult with elevated BPs in the office setting.

TABLE 13.3
Blood Pressure Values for Adolescent Girls 17 Years or Younger

   

Systolic BP (mm Hg)

Diastolic BP (mm Hg)

   

Percentile of Height

Percentile of Height

Age (yr)

BP Percentile

5th

10th

25th

50th

75th

90th

95th

5th

10th

25th

50th

75th

90th

95th

BP, blood pressure.
To use the table, first plot the child's height on a standard growth curve (www.cdc.gov/growthcharts). The child's measured systolic blood pressure and diastolic blood pressure are compared with the numbers provided in the table according to the child's age and height percentile.
From National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute, Bethesda, Maryland. NIH Publication 05-5267, 2005.

10

50th

98

99

100

102

103

104

105

59

59

59

60

61

62

62

 

90th

112

112

114

115

116

118

118

73

73

73

74

75

76

76

 

95th

116

116

117

119

120

121

122

77

77

77

78

79

80

80

 

99th

123

123

125

126

127

129

129

84

84

85

86

86

87

88

11

50th

100

101

102

103

105

106

107

60

60

60

61

62

63

63

 

90th

114

114

116

117

118

119

120

74

74

74

75

76

77

77

 

95th

118

118

119

121

122

123

124

78

78

78

79

80

81

81

 

99th

125

125

126

128

129

130

131

85

85

86

87

87

88

89

12

50th

102

103

104

105

107

108

109

61

61

61

62

63

64

64

 

90th

116

116

117

119

120

121

122

75

75

75

76

77

78

78

 

95th

119

120

121

123

124

125

126

79

79

79

80

81

82

82

 

99th

127

127

128

130

131

132

133

86

86

87

88

88

89

90

13

50th

104

105

106

107

109

110

110

62

62

62

63

64

65

65

 

90th

117

118

119

121

122

123

124

76

76

76

77

78

79

79

 

95th

121

122

123

124

126

127

128

80

80

80

81

82

83

83

 

99th

128

129

130

132

133

134

135

87

87

88

89

89

90

91

14

50th

106

106

107

109

110

111

112

63

63

63

64

65

66

66

 

90th

119

120

121

122

124

125

125

77

77

77

78

79

80

80

 

95th

123

123

125

126

127

129

129

81

81

81

82

83

84

84

 

99th

130

131

132

133

135

136

136

88

88

89

90

90

91

92

15

50th

107

108

109

110

111

113

113

64

64

64

65

66

67

67

 

90th

120

121

122

123

125

126

127

78

78

78

79

80

81

81

 

95th

124

125

126

127

129

130

131

82

82

82

83

84

85

85

 

99th

131

132

133

134

136

137

138

89

89

90

91

91

92

93

16

50th

108

108

110

111

112

114

114

64

64

65

66

66

67

68

 

90th

121

122

123

124

126

127

128

78

78

79

80

81

81

82

 

95th

125

126

127

128

130

131

132

82

82

83

84

85

85

86

 

99th

132

133

134

135

137

138

139

90

90

90

91

92

93

93

17

50th

108

109

110

111

113

114

115

64

65

65

66

67

67

68

 

90th

122

122

123

125

126

127

128

78

79

79

80

81

81

82

 

95th

125

126

127

129

130

131

132

82

83

83

84

85

85

86

 

99th

133

133

134

136

137

138

139

90

90

91

91

92

93

93

Epidemiology

As noted in the introduction, the prevalence of hypertension in children and adolescents in screening studies is generally between 0.5% and 2%. The importance of repeated measurements is demonstrated in a study of

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3,537 adolescents in New York (Kilcoyne et al., 1974). In this study, 5.4% of adolescents had systolic hypertension and 7.8% had diastolic BPs of >140/90 mm Hg on the first screening. The prevalence dropped to 1.2% and 2.4%, respectively, after a second screening. More recently, screenings conducted in Houston, Texas, public schools have also demonstrated a decreased prevalence of hypertension after repeated measurements (Sorof et al., 2004). Table 13.5 lists various prevalence studies of hypertension in children and adolescents.

TABLE 13.4
Classification of Blood Pressure in Adolescents 18 Years or Older

Blood Pressure classification

Systolic Blood Pressure (mm Hg)

 

Diastolic Blood Pressure (mm Hg)

From Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report. JAMA 2003;289:2560.

Normal

<120

and

<80

Prehypertension

120–139

or

80–89

Hypertension:

     

 Stage 1

140–159

or

90–99

 Stage 2

≥160

or

≥100

TABLE 13.5
Prevalence of Hypertension in Children and Adolescents

Study Location

Number Screened

Age (yr)

Number of Screenings

Threshold BP Value

Prevalence

Reference

BP, blood pressure; dHTN, diastolic hypertension; sHTN, systolic hypertension; TF, Second Task Force Report (1987); WG, Working Group Report (1996).

Muscatine, IA, United States

1,301

14–18

1

140/90

8.9% sHTN 12.2% dHTN

Lauer et al., 1975

Edmonton, Canada

15,594

15–20

1

150/95

2.2%

Silverberg et al., 1975

Dallas, TX, United States

10,641

14

3

95th percentile

1.2% sHTN 0.4% dHTN

Fixler et al., 1979

Minneapolis, MN, United States

14,686

10–15

1

1987 TF

4.2%

Sinaiko et al., 1989

Tulsa, OK, United States

5,537

14–19

1

1987 TF

6.0%

O'Quin et al., 1992

Buraidah, Saudi Arabia

3,299

3–18

1

1996 WG

10.6%

Soyannwo et al., 1997

Minneapolis, MN, United States

14,686

10–15

2

1996 WG

0.8% sHTN 0.4% dHTN

Androgue and Sinaiko, 2001

Houston, TX, United States

5,102

12–16

3

1996 WG

4.5%

Sorof et al., 2004

Factors that Influence Blood Pressure

Height and Weight

Height has already been mentioned as part of the definition of normative BP in childhood and adolescence (Rosner et al., 1993; National High Blood Pressure Education Program Working Groups, 1996, 2004); this conclusion was based on statistical analysis of the childhood BP database. Others hold that weight is the most important factor in determining BP. Weight has long been held to have a positive relationship with BP, as demonstrated in a study of Minneapolis school children (Luepker et al., 1999). More than half of hypertensive young people are obese. Higgins et al. (1984) suggested that if weight could be reduced in young people to below-obesity levels the prevalence of hypertension would decrease by one third.

Age

BP increases with age in a nonlinear manner through adolescence; this is likely related to growth. Beyond adolescence, BP continues to increase in a significant percentage of individuals as the result of genetic and environmental factors.

Sodium and Other Dietary Constituents

Controversy prevails over the numerous studies concerning the relationship of sodium intake to BP. For most individuals, little correlation exists. However, in certain

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salt-sensitive individuals, sodium restriction appears beneficial. For example, it has been suggested (Hohn et al., 1983) that African-American children from hypertensive families may be salt sensitive. Obese adolescents also have heightened responsiveness to sodium intake (Rocchini et al., 1989).

Other studies have found a link between potassium intake and both elevated and low BP. However, efforts to correlate calcium and other divalent cations with BP have been equivocal. Similarly, correlations between BP and vitamins A, C, and E, although suggestive, remain to be proved. Falkner et al. (2000) noted that dietary modification of certain nutrients when instituted at an early age could contribute to the prevention of hypertension in urban minority adolescents at risk for hypertension.

Stress

Both physical stress and mental stress evoke changes in BP. Indeed, the degree of change has been thought by some to be useful in predicting later-life hypertension. Early studies by Falkner demonstrated that hypertensive adolescents had significantly greater increases in heart rate, systolic BP, and diastolic BP during mental stress (performance of difficult arithmetic problems) than normotensive adolescents (Falkner et al., 1981). Increased cardiovascular reactivity to the cold pressor test has also been shown to predict the subsequent development of hypertension (Menkes et al., 1989).

Race

Although a significant determinant in adult BP, race is not a factor in teens. Hohn et al. (1983) suggested that certain subgroups of African-American youths have higher BPs than their white counterparts, and Rabinowitz et al. (1993) found a higher prevalence of hypertension among African-American females than among non-Hispanic females. However, Baron et al. (1986) found no significant differences in BP among white, black, and Mexican-American youths. Ethnicity and socioeconomic status have also been related to BP and cardiovascular reactivity (Barnes et al., 2000).

Genetics

Both familial aggregation BP studies, such as those of Lascaux-Lefebvre et al. (1999), and twin studies, such as those of Schieken (1993), indicate a strong positive correlation between hereditary influences and BP measurements. Colhoun (1999) estimated that approximately one third of variations in BP among individuals are due to genetic factors most likely from several genes. Additionally, several single-gene defects have also been recently described (Lifton et al., 2001), which account for hypertension in a small number of children and adolescents, especially those with a family history of severe hypertension of early onset.

Birth Weight and Other Perinatal Factors

The so-called “fetal origins” hypothesis maintains that low birth weight is a risk factor for the subsequent development of primary hypertension in adulthood. This hypothesis is based on the findings of large population studies that demonstrate an inverse correlation between birth weight and adult BP (Barker et al., 1993; Zureik et al., 1996). Proposed explanations for this effect include deficient maternal nutrition, possibly leading to acquisition of a reduced number of nephrons in utero. Other investigators have demonstrated that maternal smoking during pregnancy and bottle-feeding of newborns also may lead to hypertension later in life (Beratis et al., 1996; Singhal et al., 2001), thereby widening the spectrum of possible influences on later BP to include postnatal factors as well. On the other hand, other epidemiological studies have found that adult BP is more closely related to early childhood growth (Falkner et al., 1998) than to birth weight. While more research is clearly needed, it is apparent that at least in some individuals, perinatal and early childhood factors may play an important role in the later development of hypertension.

Etiology

The causes of hypertension vary among different age-groups. In adolescents, the prevalence of primary hypertension is increased in comparison with younger children. This is particularly true for mild hypertension. Table 13.6 shows an estimation of the causes of hypertension in adolescents from data gathered from a number of population studies. This information shows that primary hypertension is by far the most common cause of hypertension in the adolescent. As in younger children, renal parenchymal diseases are the most common secondary cause in the adolescent age-group.

TABLE 13.6
Estimated Causes of Hypertension in Children and Adolescents

 

School-aged Children

Adolescents

a Breakdown of causes is generally similar to that for school-aged children.

Primary/essential

15%–30%

80%–90%

Secondary

70%–85%

10%–20%a

 Renal parenchymal disease

60%–70%

 

 Renovascular

5%–10%

 

 Endocrine

3%–5%

 

 Aortic coarctation

10%–20%

 

 Reflux nephropathy

5%–10%

 

 Neoplastic

1%–5%

 

 Miscellaneous

1%–5%

 

At least 80% of hypertensive adolescents have no known cause for their disorder and are labeled as having primary or essential hypertension. Primary hypertension in adolescents is frequently characterized by isolated systolic BP elevation (Flynn and Alderman, 2005), whereas diastolic

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BP elevation is more likely to be present in secondary hypertension. Obesity and a positive family history of hypertension are also common in adolescents with primary hypertension.

Diagnosis

Confirmation of Hypertension

Adolescents make fewer visits per year to health care practitioners than other age-groups. However, each visit presents an opportunity to assess the BP. Approximately 10% of these young people will have a high initial BP (at or above the 95th percentile). They should be labeled as having an elevated BP, and not given a diagnosis of hypertension. Before a diagnosis of hypertension can be made, two subsequent BP determinations on different days must also show a high systolic or diastolic pressure or both (National High Blood Pressure Education Program Working Group, 2004). Only 1% to 2% of adolescents will fulfill these criteria and, by definition, have hypertension.

Additionally, determination of “out-of-office BP” to assess possible “white coat hypertension” is increasingly advocated. Recently, however, Vaindirlis et al. (2000) presented data supporting the hypothesis that such “white coat” hypertension may actually be a prelude to permanent hypertension.

Once the diagnosis of hypertension has been confirmed, a diagnostic evaluation and management plan can be initiated. The algorithm in Figure 13.1, although originally designed for children ≤17 years of age, is appropriate for all adolescents and should be followed.

 

FIGURE 13.1 Algorithm for the identification, diagnosis, and management of hypertension in adolescents. BMI, body mass index; BP, blood pressure; Rx, Treatment.
*See tables 13.2, 13.3 and 13.4.
†Diet modification and physical activity.
‡Especially if younger, very high BP, little or no family history, diabetic, or other risk factors.
Reprinted from National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute, Bethesda, Maryland. NIH Publication 05-5267, 2005.

Diagnostic Evaluation

The diagnostic evaluation must be tailored to the individual patient, taking into account the age, sex, race, family history, and level of hypertension. For example, a 12-year-old white female with a past medical history of recurrent urinary tract infections, no family history of hypertension, and a BP of 150/115 mm Hg would be a candidate for an aggressive evaluation for secondary causes, particularly renal parenchymal disease, specifically reflux nephropathy.

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In contrast, invasive studies to look for a secondary cause are unlikely to be helpful in a 17-year-old obese African-American boy with a family history of hypertension and a BP of 150/78 mm Hg. Consultation with someone knowledgeable about hypertension in young people can often be helpful to pursue the most cost-effective and safest diagnostic evaluation.

TABLE 13.7
Substances That May Elevate Blood Pressure in Adolescents

Prescription Medications

Nonprescription Medications

Others

a These cause elevated blood pressure relatively infrequently compared with the other agents in the table.

Calcineurin inhibitors (cyclosporine, tacrolimus)

Caffeine

Cocaine

 

Ephedrine

Ethanol

Dexedrinea

Nonsteroidal anti-inflammatory drugsa

Heavy metals (lead, mercury)

Erythropoietin

 

MDMA (“Ecstasy”)

Glucocorticoids

Pseudoephedrine

Tobacco

Methylphenidatea

 

Herbal preparations (Ephedra, Glycyrrhiza)

Oral contraceptives

   

Phenylpropanolamine

   

Pseudoephedrine

   

Tricyclic antidepressantsa

   
  1. History: Investigating a young person for hypertension requires that a detailed history be elicited. The history should aim at eliciting clues of possible secondary causes, target-organ damage, and other cardiovascular risk factors. Look for symptoms of urinary tract infections or renal disease and for a family history of hypertension or other cardiovascular disease. Activity, dietary, and other habits should be sought. The adolescent with an elevated BP should also be questioned about alcohol, tobacco, and substance use, as many substances may elevate BP (Table 13.7). Also ask about ergogenic aids such as anabolic steroids as well as any complementary or alternative medicine products that they might be using. Clues from the history suggestive of secondary hypertension are listed in Table 13.8.
  2. Physical examination: A thorough examination is also an essential part of the diagnostic study. The adolescent in question will often be obese. The examination should include an exploration for evidence of a secondary cause or end-organ damage and an evaluation of the following:
  3. Height, weight, and body mass index (BMI) (calculated)
  4. BP in both arms and a lower extremity
  5. Femoral pulses
  6. Neck: Carotid bruits or an enlarged thyroid gland
  7. Fundi: Arteriolar narrowing, arteriovenous nicking, hemorrhages, exudates
  8. Abdomen: Bruits, hepatosplenomegaly, flank masses
  9. Heart: Rate, precordial heave, clicks, murmurs, arrhythmias
  10. Extremities: Pulses, edema
  11. Nervous system
  12. Skin: Striae, acanthosis nigricans, café au lait spots, neurofibromas

Physical examination findings suggestive of secondary causes of hypertension are listed in Table 13.8. In addition, the clinician should remember that severe hypertension in an adolescent suggests a secondary cause, particularly renal disease. Acute onset may also suggest acute renal disease.

  1. Laboratory testing: Some basic/screening studies should be performed in all adolescents with confirmed BP elevation, whereas others should be reserved for those in whom secondary hypertension is suspected or in those with stage 2 hypertension.
  2. Screening tests—should be done in all patients and these include:
  • Electrolytes
  • Blood urea nitrogen (BUN) and creatinine
  • Urinalysis
  • Fasting lipid profile
  • Complete blood cell (CBC) count
  • Urine cultures should be done as appropriate based on the history and urinalysis findings. Add a fasting glucose with or without a fasting insulin in obese adolescents to screen for impaired glucose tolerance/hyperinsulinemia.
  1. Specific laboratory testsshould be done as appropriate to follow up on clues from the history and physical examination, or from the screening test results. These might include an antinuclear antibody (ANA) test and sedimentation rate in a hypertensive female adolescent with a malar rash, thyroid studies if there is a history of thyroid dysfunction for example, heat/cold intolerance, menstrual dysfunction, and so on.
  2. Echocardiogramsare now recommended to be obtained in all adolescents with confirmed hypertension (National High Blood Pressure Education Program Working Group, 2004). This is to detect left ventricular hypertrophy (LVH), which is a risk factor for sudden cardiac death and an indication to initiate or intensify antihypertensive drug therapy. Recent studies have shown that LVH occurs commonly in hypertensive adolescents (Hanevold et al., 2004; Flynn, 2005).
  3. Advanced testingshould only be done to confirm suspected secondary causes of hypertension, for

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example, plasma normetanephrine to norepinephrine ratio if pheochromocytoma is suspected, or a 24-hour urine collection for proteinuria if there is persistent proteinuria on the urinalysis.

  1. Imaging studiesshould only be obtained in specific circumstances. Renal ultrasonography should be obtained in all adolescents with stage 2 hypertension, or in those with stage 1 hypertension and an abnormal urinalysis. Chest x-rays should only be obtained if the cardiac examination is abnormal. More advanced studies such as renal scans or angiography are useful in a very small percentage of hypertensive adolescents and should only be obtained under the direction of the appropriate subspecialist.

TABLE 13.8
History and Physical Examination Findings Suggestive of Secondary Causes of Hypertension

UTI, urinary tract infection; BP, blood pressure; SLE, systemic lupus erythematosus; RAS, renal artery stenosis; HTN, hypertension.

Present in History

Suggests

Known UTI/UTI symptoms

Reflux nephropathy

Joint pains, rash, fever

Vasculitis, SLE

Acute onset of gross hematuria

Glomerulonephritis, renal thrombosis

Renal trauma

Renal infarct, RAS

Abdominal radiation

Radiation nephritis, RAS

Renal transplant

Transplant RAS

Precocious puberty

Adrenal disorder

Muscle cramping, constipation

Hyperaldosteronism

Excessive sweating, headache, pallor and/or flushing

Pheochromocytoma

Known illicit drug use

Drug-induced hypertension

Present on Examination

Suggests

BP >140/100 mm Hg at any age

Secondary hypertension

Leg BP < arm BP

Aortic coarctation

Poor growth, pallor

Chronic renal disease

Turner syndrome

Aortic coarctation

Café au lait spots

Renal artery stenosis

Delayed leg pulses

Aortic coarctation

Precocious puberty

Adrenal disorder

Bruits over upper abdomen

Renal artery stenosis

Edema

Renal disease

Excessive sweating

Pheochromocytoma

Excessive pigmentation

Adrenal disorder

Striae in a male

Drug-induced HTN

Therapy

Prevention

Optimally, measures to prevent or minimize the effects of hypertension should be applied to those adolescents at risk of developing hypertension later in life. The difficulty lies in finding those at risk and deciding what measures to apply. Data from young people for this purpose are lacking, and long-term follow-up information is unavailable. Nevertheless, a starting point for such a strategy is to consider those with the findings listed in the subsequent text as being at risk. They should be counseled about nonpharmacologic approaches to maintain lower BP and should be periodically monitored:

  1. Those with prehypertension (>120/80 mm Hg)
  2. Those with BMI >85th percentile, particularly if parents are obese
  3. Those with hyperlipidemia or a family history of the disorder, particularly if there is a known family history of coronary artery disease or stroke
  4. Those with type 1 or type 2 diabetes mellitus
  5. Those with two or more family members with treated hypertension, particularly African-Americans and Hispanics

Nonpharmacologic Interventions

Although the magnitude of change in BP may be modest, weight loss, aerobic exercise, and dietary modifications have all been shown to successfully reduce BP in children and adolescents, at least in research settings. Such “therapeutic lifestyle changes” should therefore be incorporated into the treatment plan for any hypertensive adolescent, whether a secondary cause has been identified, and whether there is an indication to initiate antihypertensive drug therapy (Fig. 13.1).

  1. Weight reduction: Excess body weight is correlated closely with increased BP. Weight reduction reduces BP in a large proportion of hypertensive individuals who are >10% above ideal weight.

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  1. Dietary changes: Moderate sodium restriction in hypertensive individuals has been shown, on average, to reduce systolic BP by 4.9 mm Hg and diastolic BP by 2.6 mm Hg. The benefits of sodium restriction are probably greatest in those with renal disease, those with long-standing hypertension, and possibly also African-Americans. Although there has been some evidence to suggest that potassium, calcium, or magnesium supplementation might theoretically be of benefit, studies have not always confirmed a beneficial effect of supplementing the diet with these minerals. On the other hand, the so-called “DASH diet,” which is lower in sodium content and enhanced in potassium and calcium intake, has been demonstrated to be of benefit in hypertensive adults (Appel et al., 1997) and should probably be recommended for hypertensive adolescents.
  2. Regular physical exercise: Regular aerobic physical activity, adequate to achieve at least a moderate level of physical fitness, may be beneficial for both prevention and treatment of hypertension. Regular aerobic physical activity (≥30 minutes/session, 4–5 days/week) can reduce systolic BP in hypertensive patients by approximately 10 mm Hg.
  3. Other Lifestyle changes: Discontinuance of smoking and avoidance of alcohol excess, medications (except as directed by health care providers), and drugs (e.g., cocaine, amphetamines). In addition to elevating BP, cigarette smoking is a major risk factor for cardiovascular disease and therefore should be avoided by hypertensive individuals. Excessive alcohol intake can raise BP and cause resistance to antihypertensive therapy.

Pharmacologic Treatment

  1. Antihypertensive medications are definitely indicated for those who have the following:
  2. Symptoms of hypertension
  3. Stage 2 hypertension
  4. Evidence of hypertensive end-organ damage
  5. Type 1 or type 2 diabetes
  6. Secondary hypertension
  7. Persistent hypertension despite lifestyle changes
  8. If none of the above indications are present, drug treatment can be withheld. Lifestyle modifications as discussed in the preceding text should be recommended. If these measures fail to lower BP after a reasonable period of time, then medication should be prescribed.
  9. Drug therapy should be simple so that compliance will be increased in what may be a lifelong but asymptomatic problem.
  10. Explicit education should be given regarding hypertension and the reasons for therapy.
  11. The adolescent should generally be responsible for taking his or her own medication.
  12. Antihypertensive agents should be chosen to obtain the maximum benefit with the fewest and least-severe side effects. The ideal hypertensive agent would
  13. Lower BP in almost all hypertensive individuals
  14. Address specific pathogenic mechanisms
  15. Improve hemodynamics
  16. Be associated with few biochemical changes
  17. Be associated with few or no adverse reactions
  18. Be dosed once or, at most, twice daily
  19. Be inexpensive
  20. Unfortunately, the ideal antihypertensive agent does not exist. Initial therapeutic regimens have been debated. In adults, diuretics have been advocated as first-line therapy based on the results of the ALLHAT trial (ALLHAT Collaborative Research Group, 2002). However, the findings of this study are not directly applicable to otherwise healthy adolescents with hypertension. Instead, individualized stepped-care approach, as suggested by the National High Blood Pressure Education Program Working Group (2004) and as illustrated in Figure 13.1, should be followed. In this approach, a monotherapy drug regimen is superimposed on nonpharmacologic therapy as initial treatment. Advocates of this approach recommend the following:
  21. Begin with a low dose of the chosen initial drug. Because all classes of antihypertensive agents have now been studied in adolescents, either a diuretic, β-blocker, angiotensin-converting enzyme (ACE) inhibitor, or calcium channel blocker may be chosen as the initial agent. Preparations with once- or twice-daily dosing are available for members of all drug classes and can improve compliance. Increases in the dose of the initial medication may be used to achieve BP control if necessary. If BP control is still not achieved, proceed to combination treatment.
  22. Add a low dose of another drug with a complementary mechanism of action. In many cases, the second agent will be a diuretic. Combination antihypertensive drug treatment with one of the medications being a diuretic is being advocated increasingly in adolescents (Wells and Stowe, 2001). Proceed to a full dose if necessary.
  23. If BP control is still not achieved, one may choose to add a third antihypertensive drug, usually a vasodilator or renin-angiotensin inhibitor, or preferably obtain consultation from an expert on hypertension in adolescents.
  24. Suggested initial and maximum doses of various antihypertensive agents are given in Table 13.9. Many of these now have pediatric-specific Food and Drug Administration (FDA)-approved labeling as a result of recent trials in children and adolescents. More comprehensive references, specifically published clinical trial results, should be consulted for detailed discussion of the specific adverse effects of these medications.
  25. For adolescents younger than 18 years with uncomplicated primary hypertension, target BP should be the 95th percentile for age, gender, and height; for those with secondary hypertension, diabetes, or chronic kidney disease, target BP should be the 90th percentile. In those 18 years or older, BP targets should be <140/90 mm Hg for those with uncomplicated primary hypertension, and <130/80 mm Hg for those with secondary hypertension, diabetes, or chronic kidney disease.
  26. Step-down therapy, or drug withdrawal, should not be forgotten. After an extended course of drug therapy and sustained BP control, a gradual reduction in or withdrawal of medication can be attempted. This requires close observation and continuation of nonpharmacologic therapy, and will probably be successful only in the adolescent who has been successful with lifestyle modification.

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TABLE 13.9
Antihypertensive Agents for Use in Chronic Treatment of Hypertension in Adolescents

Class

Drug

Starting Dose

Interval

Maximum Dosea

q.d., once-daily; b.i.d., twice-daily; t.i.d., three times daily; q.i.d., four times daily; HCTZ, hydrochlorothiazide.
a The maximum recommended adult dose should never be exceeded.

Angiotensin-converting enzyme (ACE) inhibitors

Benazepril

0.2 mg/kg/d up to 10 mg/d

q.d.

0.6 mg/kg/d up to 40 mg q.d.

 

Captopril

0.3–0.5 mg/kg/dose

b.i.d.–t.i.d.

6 mg/kg/d up to 450 mg/d

 

Enalapril

0.08 mg/kg/d

q.d.

0.6 mg/kg/d up to 40 mg/d

 

Fosinopril

0.1 mg/kg/d up to 10 mg/d

q.d.

0.6 mg/kg/d up to 40 mg/d

 

Lisinopril

0.07 mg/kg/d up to 5 mg/d

q.d.

0.61 mg/kg/d up to 40 mg/d

 

Quinapril

5–10 mg/d

q.d.

80 mg/d

 

Ramipril

2.5 mg/d

q.d.

20 mg/d

Angiotensin-receptor blockers
α-and β-Antagonists

Candesartan

4 mg/d

q.d.

32 mg q.d.

 

Irbesartan

75–150 mg/d

q.d.

300 mg/d

 

Losartan

0.75 mg/kg/d up to 50 mg/d

q.d.–b.i.d.

1.44 mg/kg/d up to 100 mg/d

 

Labetalol

2–3 mg/kg/d

b.i.d.

10–12 mg/kg/d up to 2.4 g/d

 

Carvedilol

0.1 mg/kg/dose up to 12.5 mg b.i.d.

b.i.d.

0.5 mg/kg/dose up to 25 mg b.i.d.

β-Antagonists

Atenolol

0.5–1 mg/kg/d

q.d.–b.i.d.

2 mg/kg/d up to 100 mg/d

 

Bisoprolol/HCTZ

0.04 mg/kg/d up to 2.5/6.25 mg/d

q.d.

10/6.25 mg q.d.

 

Metoprolol

1–2 mg/kg/d

b.i.d.

6 mg/kg/d up to 200 mg/d

 

Propranolol

1 mg/kg/d

b.i.d.–t.i.d.

16 mg/kg/d Calcium channel blockers

 

Amlodipine

0.06 mg/kg/d

q.d.

0.6 mg/kg/d up to 10 mg/d

 

Felodipine

2.5 mg/d

q.d.

10 mg/d

 

Isradipine

0.05–0.15 mg/kg/dose

t.i.d.–q.i.d.

0.8 mg/kg/d up to 20 mg/d

 

Extended-release nifedipine

0.25–0.5 mg/kg/d

q.d.–b.i.d.

3 mg/kg/d up to 120 mg/d

Central α-agonists

Clonidine

5–10 µg/kg/d

b.i.d.–t.i.d.

25 µg/kg/d up to 0.9 mg/d

 

Methyldopa

5 mg/kg/d

b.i.d.-q.i.d.

40 mg/kg/d up to 3 g/d

Diuretics

Amiloride

5–10 mg/d

q.d.

20 mg/d

 

Chlorthalidone

0.3 mg/kg/d

q.d.

2 mg/kg/d up to 50 mg/d

 

Furosemide

0.5–2.0 mg/kg/dose

q.d.–b.i.d.

6 mg/kg/d

 

HCTZ

1 mg/kg/d

b.i.d.

3 mg/kg/d up to 50 mg/d

 

Spironolactone

1 mg/kg/d

q.d.–b.i.d.

3.3 mg/kg/d up to 100 mg/d

 

Triamterene

1–2 mg/kg/d

b.i.d.

3–4 mg/kg/d up to 300 mg/d

Peripheral α-antagonists

Doxazosin

1 mg/d

q.d.

4 mg/d

 

Prazosin

0.05–0.1 mg/kg/d

t.i.d.

0.5 mg/kg/d

 

Terazosin

1 mg/d

q.d.

20 mg/d

Vasodilators

Hydralazine

0.25 mg/kg/dose

t.i.d.–q.i.d.

7.5 mg/kg/d up to 200 mg/d

 

Minoxidil

0.1–0.2 mg/kg/d

b.i.d.–t.i.d.

1 mg/kg/d up to 50 mg/d

Special Populations

  1. African-Americans: The frequency of hypertension in African-Americans is among the highest in the world. Hypertension develops at an earlier age and is more severe in African-Americans than in whites. In African-Americans, diuretics have been proved to reduce hypertensive morbidity and mortality rates, so diuretics should be seriously considered for use in the absence of other conditions that prohibit their use. ACE inhibitors used to be considered less effective in African-Americans than in whites, although recent research indicates otherwise (Bakris et al., 2005). Calcium channel blockers and α-receptor blockers are as effective in African-Americans as in whites.
  2. Females who take oral contraceptives: Most females who take oral contraceptives have a small increase in systolic and diastolic BPs but usually within the reference range. Hormonal contraceptives, mainly those that contain estrogen, can increase angiotensinogen, leading to an increase in angiotensin II and an increase in BP in some individuals. The risk of overt hypertension appears to increase with age, duration of use, and body mass. Many of the studies of BP and oral contraceptive agents involved higher doses of both estrogen and progesterone than are used currently. If concurrent treatment with an oral contraceptive and antihypertensive medication is needed, consideration should be given to using a low-estrogen or progestin-only contraceptive.
  3. Adolescents with asthma: In teens with asthma and hypertension, β-blocking drugs can worsen bronchoconstriction and are therefore relatively contraindicated. Some of the newer, β1receptor selective agents such as metoprolol or bisoprolol may be tried, especially in adolescents with mild asthma.

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  1. Diabetes: As noted in the preceding text, the diagnosis of hypertension or even prehypertension in an adolescent with either type 1 or type 2 diabetes is an indication to initiate antihypertensive drug therapy. ACE inhibitors or angiotensin-receptor blockers should be used as the initial agent in hypertensive diabetic patients because of their potential benefit in slowing the progression of or even preventing diabetic nephropathy.

Hypertensive Emergencies

Rarely an adolescent will have signs of encephalopathy or heart failure at presentation and be found to have extraordinarily high BP, at levels well above stage 2 hypertension. This constitutes a true emergency and may have disastrous consequences unless efforts to lower the BP are begun at once. Assistance from an expert in hypertension should be sought. Meanwhile, the patient should be hospitalized and an intravenous line placed. Usually, a continuous infusion of either nicardipine or labetalol should be started at a low dose and then titrated up as needed to slowly reduce the BP. The initial reduction should be no more than 25% over the first 8 hours in order to prevent cerebral, cardiac, or renal ischemia from overly rapid BP reduction (Adelman et al., 2000). BP can be further lowered to the 95th percentile over the next 24 hours. When adequate pressure control has been achieved, oral antihypertensive agents can be gradually introduced and the intravenous agents discontinued. A vigorous search for the cause of the hypertension, if not known, must be made once the patient's condition has been stabilized.

Summary

As adolescents mature toward full adulthood, an increasing number will be found to have hypertension. Perhaps this progression can be delayed or avoided through the applications of the principles outlined in this chapter. At the very least, BP should be taken when adolescents are seen for health care, regardless of the complaint.

When pressures are found to be repeatedly elevated, nonpharmacologic antihypertensive measures should be started. They are good general health rules. Initially, in the absence of severe hypertension, a set of basic diagnostic studies should be obtained. Depending on the history, physical examination, and results of the initial studies, other tests may or may not be necessary.

For selected adolescents, drug therapy is indicated. The individualized stepped-care approach displayed in Figure 13.2 is recommended. When hypertension is resistant to initial drug therapies, consultation with an expert on hypertension in adolescents should be sought.

 

FIGURE 13.2 Stepped-care approach to antihypertensive therapy. BP, blood pressure.

Web Sites

For Teenagers and Parents

http://www.americanheart.org/presenter.jhtml?identifier=4609. American Heart Association site on childhood hypertension. Free.

http://pediatrichypertension.org. Home of the International Pediatric Hypertension Association. Includes links to additional patient education Web sites about hypertension. Free.

http://www.nhlbi.nih.gov/hbp/index.html. NIH patient education site on hypertension. Free.

http://www.medscape.com/pages/editorial/patiented/index/index-hypertension. WebMD/Medscape patient education site on hypertension. Requires free registration.

http://www.nlm.nih.gov/medlineplus/highbloodpressure.html. “Medline Plus” site on hypertension. Free.

http://www.mayoclinic.com/health/high-blood-pressure/DS00100. Mayo Clinic patient education site on hypertension. Free.

http://monitorbloodpressure.com/. Commercial site to buy home BP monitors.

For Health Care Professionals

http://www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_ped.htm. Home of The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents. Includes link to downloadable PDA application. Free.

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http://pediatrichypertension.org. Home of the International Pediatric Hypertension Association. Includes links to additional Web sites about hypertension for health care professionals. Free; membership available for health care professionals.

http://www.who.int/topics/cardiovascular_diseases/en/. World Health Organization site containing links to various cardiovascular disease-related WHO initiatives and resources. Free.

http://www.hdcn.com/fhh.htm. Nephrology-oriented site on hypertension. Contains links to educational lectures and other materials. Requires paid annual subscription to access all content.

References and Additional Readings

Adelman RD, Coppo R, Dillon MJ. The emergency management of severe hypertension. Pediatr Nephrol 2000;14:422.

Adrogue HE, Sinaiko AR. Prevalence of hypertension in junior high school-aged children: effect of new recommendations in the 1996 Updated Task Force Report. Am J Hypertens2001;14(5 Pt 1):412.

ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs. diuretic: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). J Am Med Assoc 2002;288:2981.

Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117.

Bakris GL, Smith DH, Giles TD, et al. Comparative antihypertensive efficacy of angiotensin receptor blocker-based treatment in African-American and white patients. J Clin Hypertens 2005;7:587.

Barker DJP, Gluckman PD, Godfrey KM, et al. Fetal nutrition and cardiovascular disease in adult life. Lancet 1993;341:941.

Barnes VA, Treiber FA, Musante L, et al. Ethnicity and socioeconomic status: impact on cardiovascular activity at rest and during stress in youth with a family history of hypertension. Ethn Dis 2000;10:4.

Baron AE, Freyer B, Fixler DE. Longitudinal blood pressures in blacks, whites, and Mexican Americans during adolescence and early adulthood. Am J Epidemiol 1986;123:809.

Bartosh SM, Aronson AJ. Childhood hypertension: an update on etiology, diagnosis, and treatment. Pediatr Clin North Am 1999;46:235.

Beratis NG, Panagoulias D, Varvarigou A. Increased blood pressure in neonates and infants whose mothers smoked during pregnancy. J Pediatr 1996;128:806.

Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report. JAMA 2003;289:2560.

Colhoun H. Commentary: confirmation needed for genes for hypertension. Lancet 1999;353:1200.

Couch SC, Daniels SR. Diet and blood pressure in children. Curr Opin Pediatr 2005;17:642.

Dickinson HO, Mason JM, Nicolson DJ, et al. Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials. J Hypertens 2006;24:215.

Falkner B, Kushner H, Onesti G, et al. Cardiovascular characteristics in adolescents who develop essential hypertension. Hypertension 1981;3:521.

Falkner B, Hulman S, Kushner H. Birth weight versus childhood growth as determinants of adult blood pressure. Hypertension 1998;31(part 1):145.

Falkner B, Sherif K, Michel S, et al. Dietary nutrients and blood pressure in urban minority adolescents at risk for hypertension. Arch Pediatr Adolesc Med 2000;154:918.

Falkner B, Gidding SS, Ramirez-Garnica G, et al. The relationship of body mass index and blood pressure in primary care pediatric patients. J Pediatr 2006;148:195.

Fernandes E, McCrindle BW. Diagnosis and treatment of hypertension in children and adolescents. Can J Cardiol 2000;16:801.

Fixler DE, Laird WP, Fitzgerald V, et al. Hypertension screening in schools: results of the Dallas study. Pediatrics 1979;63:32.

Flynn JT. Impact of ambulatory blood pressure monitoring on the management of hypertension in children. Blood Press Monit 2000;5:211.

Flynn JT. Evaluation and management of hypertension in childhood. Prog Pediatr Cardiol 2001;12:177.

Flynn JT. Drug therapy of childhood hypertension: current status, future challenges. Am J Hypertens 2002;15(2 Part 2):30S.

Flynn JT. Hypertension in adolescents. Adolesc Med Clin 2005;16:11.

Flynn JT, Alderman MH. Characteristics of children with primary hypertension seen at a referral center. Pediatr Nephrol 2005;20:961.

Hanevold C, Waller J, Daniels S, et al. The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the International Pediatric Hypertension Association. Pediatrics 2004;113:328.

Higgins MW, Hinton PC, Keller JB. Weight and obesity as a predictor of blood pressure and hypertension. In: Loggie JMH, Horan MJ, Gruskin AB, et al, eds. National Heart, Lung, and Blood Institute workshop on juvenile hypertension. Proceedings of a symposium. New York: Biomedical Information, 1984:125.

Hohn AR, Riopel DA, Keil JE, et al. Childhood familial and racial differences in physiologic and biochemical factors related to hypertension. Hypertension 1983;5:56.

Kaplan NM. Maximally reducing cardiovascular risk in the treatment of hypertension. Ann Intern Med 1988;109:36.

Kavey REW, Daniels SR, Lauer RM, et al. American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood.Circulation 2003;107:1562.

Kilcoyne MM, Richter RW, Alsup PA. Adolescent hypertension. I. Detection and prevalence. Circulation. 1974;50:758.

Lascaux-Lefebvre V, Ruidavets J, Arveiler D, et al. Influence of parental history of hypertension on blood pressure. J Hum Hypertens 1999;13:631.

Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine study. Pediatrics 1989;84:633.

Lauer RM, Conner WE, Leaverton PE, et al. Coronary heart disease risk factors in school children: the Muscatine study. J Pediatr 1975;86:697.

Luepker RV, Jacobs DR, Prineas RJ, et al. Secular trends of blood pressure and body size in a multi-ethnic adolescent population: 1986 to 1996. J Pediatr 1999;134:668.

Lieberman E. Pediatric hypertension, clinical perspective. Mayo Clin Proc 1994;69:1098.

Lifton RP, Gharavi AG, Geller DS. Molecular mechanisms of human hypertension. Cell 2001;104:545.

Menkes MS, Mathhews KA, Krantz DS, et al. Cardiovascular reactivity to the cold pressor test as a predictor of hypertension. Hypertension 1989;14:524.

P.219

 

National High Blood Pressure Education Program Working Group. Update on the 1987 task force report on high blood pressure in children and adolescents: a working group report from the National High Blood Pressure Education Program. Pediatrics 1996;98:649.

National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute, Bethesda, Maryland. Pediatrics 2004;114:555.

Neaton JD, Grimm RH Jr, Prineas RJ, et al. Treatment of mild hypertension study: final results. JAMA 1993;270:713.

O'Quin M, Sharma BB, Miller KA, et al. Adolescent blood pressure survey: Tulsa, Oklahoma, 1987 to 1989. South Med J 1992;85:487.

Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood pressure measurement in humans and experimental animals: part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Hypertension2005;45:142.

Portman RJ, McNiece KL, Swinford RD, et al. Pediatric hypertension: diagnosis, evaluation, management, and treatment for the primary care physician. Curr Probl Pediatr Adolesc Health Care 2005;35:262.

Rabinowitz A, Kushner H, Falkner B. Racial differences in blood pressure among urban adolescents. J Adolesc Health 1993;14:314.

Reed WL. Racial differences in blood pressure levels of adolescents. Am J Public Health 1981;71:1165.

Rocchini AP, Key J, Bondie D, et al. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. N Engl J Med 1989;321:580.

Rocchini AP. Obesity hypertension. Am J Hypertens 2002;15(2 Pt 2):50S.

Rosner B, Prineas RJ, Loggie JMH, et al. Blood pressure nomograms for children and adolescents, by height, sex and age, in the United States. J Pediatr 1993;123:871.

Schieken RM. Genetic factors that predispose the child to develop hypertension. Pediatr Clin North Am 1993;40:1.

Silverberg DS, Nostrand CV, Juchli B, et al. Screening for hypertension in a high school population. Can Med Assoc J 1975;113:103.

Sinaiko AR, Gomez-Marion O, Prineas RJ. Prevalence of “significant” hypertension in junior high school-aged children: the Children and Adolescent Blood Pressure Program. J Pediat 1989;114(4 Pt 1):664.

Sinaiko AR, Gomez-Marin O, Prineas RJ. Effect of low sodium diet or potassium supplementation on adolescent blood pressure. Hypertension 1993;21:989.

Singhal A, Cole TJ, Lucas A. Early nutrition in preterm infants and later blood pressure: two cohorts after randomized trials. Lancet 2001;357:413.

Sorof JM, Portman RJ. White coat hypertension in children with elevated casual blood pressure. J Pediatr 2000;137:493.

Sorof JM, Lai D, Turner J, et al. Overweight, ethnicity, and the prevalence of hypertension in school-aged children. Pediatrics 2004;113:475.

Soyannwo MAO, Gadallah M, Kurashi NY, et al. Studies on preventative nephrology: Systemic hypertension in the pediatric and adolescent population of Gassim, Saudi Arabia. Ann Saudi Med 1997;17:47.

Task Force on Blood Pressure Control in Children. Report of the second task force on blood pressure control in children—1987. National Heart, Lung, and Blood Institute, Bethesda, Maryland. Pediatrics 1987;79:1.

Vaindirlis I, Peppa Patrikiou M, Dracopoulou M, et al. “White coat hypertension” in adolescents: increased values of urinary cortisol and endothelin. J Pediatr 2000;136:359.

Wells T, Stowe C. An approach to the use of antihypertensive drugs in children and adolescents. Curr Ther Res Clin Exp 2001;62:329.

Zureik M, Bonithon-Kopp C, Lecomte E, et al. Weights at birth and in early infancy, systolic pressure and left ventricular structure in subjects aged 8 to 24 years. Hypertension1996;27(part 1):339.