The Journal of Pediatrics
Volume 155, Issue 2 , Pages 159-161, August 2009

Childhood Prevention of Hypertensive Cardiovascular Disease

  • Matthew W. Gillman, MD, SM

      Affiliations

    • Corresponding Author InformationReprint requests: Matthew W. Gillman, MD, SM, Obesity Prevention Program, Department of Ambulatory Care and Prevention, Harvard Medical School/Harvard Pilgrim Health Care, Boston, MA 02134.

Obesity Prevention Program, Department of Ambulatory Care and Prevention Harvard Medical School/Harvard Pilgrim Health Care, Boston, Massachusetts

Article Outline

BP, Blood pressure

 

See related articles, p 165 and p 170

Let's say you are a primary care pediatric clinician. The Pediatric Blood Pressure Task Force1 recommends that you measure blood pressure (BP) routinely on all of your patients age 3 years or older. That sounds simple. Put on the cuff, get your stethoscope in place, use the bulb to pump up the bladder, and listen as you let the air out slowly. The patient's BP is low—great! But if the patient's BP is on the high side, it gets more complicated.

You may ask yourself: Did I use the right size cuff? Inflate to the correct pressure? Let out the air at the optimal rate? Read the aneroid sphygmomanometer correctly? (I sure miss those mercury ones that we were not supposed to calibrate every 6 months.) Was the patient situated correctly? At rest? Did he or she eat in the last hour?2 I know I'm supposed to get additional readings, but how many more? When—today, tomorrow, next week, next year? OK, now I've found those charts with the age, sex, height, and blood pressure percentiles. Do I use systolic or diastolic? What am I supposed to do if BP exceeds the 90th percentile? The 95th percentile?1 At what point do I order ambulatory blood pressure monitoring? How do I order it? How will the family with no insurance pay for it, or for referral to a specialist? How many of these kids will actually develop a heart attack or stroke in the next 50 years anyway? Do they really think I have some magic to induce this adolescent to get more physical activity and lose weight? Do I need a dietitian and behavior specialist on my staff?3 Why don't the food manufacturers just take most of the salt out of the food supply and be done with it?4 Could the UK have it right in not recommending that doctors measure BP in well children?

Measurement variability, tracking, prediction, intervention, cost, and harm—these are the tough issues that clinicians and policy-makers face when trying to decide whether and how to screen BP, or any other risk factor, in healthy children and adolescents. The best way to answer a question about screening is to mount a randomized controlled trial of screening itself. Randomly allocate half the children to BP screening, followed by intervention for persistently high readings, and the other half to no screening. Follow them all for decades to compare the rates of cardiovascular outcomes in each group. Try to do the study in a real-world setting, so that it is generalizable to your practice. Measure the effectiveness and cost-effectiveness. Because of time and cost constraints, as well as the likelihood that at this point few providers and parents would consent to the no-screening arm, no such trial will ever exist. Even if it did, we might be measuring BP differently 50 years from now, and the results could be moot.

In the absence of results from this chimerical randomized trial, we must piece together the evidence from disparate sources, such as the natural history of BP and its consequences. At this point, most of what we know about the natural history of BP in children emanates from studies of tracking, that is, how well BP in childhood predicts BP in adulthood. Given the inherent variability of BP readings over time in an individual, it is not surprising that tracking improves with multiple readings.5 Variability is greater over days and weeks than over minutes (and greater in children than in adults), so that measuring BP not only a few times at each sitting but also at several sittings over days, weeks, or months provides the most reliable estimate of a child's “true” underlying BP.6 This is the reasoning behind Task Force's recommendation to obtain multiple readings at multiple times before extensive evaluation or intensive treatment.

In this issue of The Journal, Collins and Alpert7 appropriately call for better information about natural history, that is, the relationship between BP and pathological changes. This information is accumulating. Atherosclerosis, arterial stiffness, endothelial dysfunction, and, as highlighted by Li et al8 in this issue of The Journal, left ventricular hypertrophy can emerge in childhood and adolescence, and elevated BP predicts them all, either cross-sectionally or longitudinally.9, 10, 11, 12 Collins and Alpert rightly assert that additional information of this type will help us make better choices about which children to evaluate further and possibly treat. However, their argument goes beyond such an agnostic statement, because even “white coat hypertension” in children may be associated with pathological changes, they apparently suggest acting on fewer readings than recommended by the Task Force (eg, 2 rather than 3 readings), which is tantamount to lowering the BP percentile cutpoints for evaluation and treatment.

A problem with the argument for treating children at lower BP levels—and thus more children overall—is that clinical decision making depends not merely on the existence of associations of BP with pathological changes (or, even better, with long-term cardiovascular outcomes) measured by relative or attributable risk, but also on how strong the associations are in terms of absolute individual risk. Often what we consider a strong association on a population scale translates into weak absolute risk; for example, even with relatively high tracking correlations, the resulting sensitivity, specificity, and predictive values for predicting adult hypertension from childhood BP values are modest.13

Under the current guidelines, to achieve a benefit for the truly affected children, we accept that we will identify and treat many “hypertensive” or “prehypertensive” children who will never go on to develop a clinical cardiovascular event as middle-aged adults. Lowering BP cutpoints for treatment means that many more children will be treated, causing an even greater proportion to fall into this false-positive category, leading in turn to excess cost and potential harm of long-term interventions with little value.

Evaluating screening programs involves weighing benefits against harms and costs. Recent studies on screening for prostate cancer in adult men underscore how a seemingly innocuous test can result in physical harm without benefit for the large majority of screen-positive individuals.14 In the case of childhood BP, harm is one potential issue, especially for the few children eligible for medication, but cost is likely a more important consideration, because the recommended interventions for the vast majority will entail behavior change strategies, which are costly but probably incur relatively little harm. Achieving even small BP reductions through lifestyle modification requires a great deal of resources. If BP cutpoints are lowered, then a smaller proportion of screen-positive children will benefit from these costly and only modestly effective interventions. Overall, the result is a high societal cost for little relative benefit. My colleagues and I recently addressed this issue by performing a cost-effectiveness analysis comparing the recommendations of the current Task Force guidelines with other hypertension prevention strategies. The model incorporated estimates of measurement, tracking, and treatment efficacy from the literature along with lifetime risks of coronary heart disease, stroke, and renal disease. Our preliminary analysis suggests that compared with population-wide policy approaches, such as reducing the salt content of food and promoting physical education, universal BP screening at age 15 years or even screening of only overweight adolescents both costs more and is less effective. Therefore, in contrast to the assertion of Collins and Alpert, new data may indicate that it is more reasonable to limit treatment to children with BP at higher, rather than lower, percentiles than those recommended by the Task Force. Given the current evidence, it would be unwise for the next Task Force to recommend lowering the cutpoints.

As Collins and Alpert emphasize, more studies on natural history are needed, especially if they use left ventricular hypertrophy, measures of atherosclerosis, and/or other surrogate outcomes as study endpoints. At least as important are long-term studies of behavior change interventions to lower BP in real-world settings. In settings where routine BP screening is being considered but is not yet widespread, it would be advantageous to incorporate these interventions into studies of screening itself, for example, a randomized trial of screening/treatment with surrogate outcomes like left ventricular hyopertrophy and atherosclerosis. In the United States, where screening is already nearly universal, modeling approaches are appropriate and can address issues that even a randomized trial cannot, such as the marginal cost-effectiveness of BP screening in childhood versus waiting until early adulthood, whether limiting treatment to children with severe hypertension is an attractive alternative to the current guidelines, and the utility of evaluation and treatment at lower BP levels than the Task Force currently recommends.

Childhood prevention of hypertensive cardiovascular disease is a worthy goal; however, even after decades of research, the optimal approaches to controlling BP levels from early life on are not clear.15 Policy approaches like mandating lower salt content in foods, once only theoretical but now tangible, are likely to shift the entire population distribution of BP to lower levels, a particularly powerful way to prevent cardiovascular disease.16, 17, 18 The extent to which any screening approach adds value is a key question. The best avenue to clarity is for researchers and guideline panels to incorporate the tenets of clinical decision making and policy analysis in addition to etiology and pathogenesis.

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References 

  1. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004;114:555–576
  2. Gillman MW, Cook NR. Blood pressure measurement in childhood epidemiological studies. Circulation. 1995;92:1049–1057
  3. Couch SC, Saelens BE, Levin L, Dart K, Falciglia G, Daniels SR. The efficacy of a clinic-based behavioral nutrition intervention emphasizing a DASH-type diet for adolescents with elevated blood pressure. J Pediatr. 2008;152:494–501
  4. Asaria P, Chisholm D, Mathers C, Ezzati M, Beaglehole R. Chronic disease prevention: health effects and financial costs of strategies to reduce salt intake and control tobacco use. Lancet. 2007;370:2044–2053
  5. Gillman MW, Cook NR, Rosner B, Beckett LA, Evans DA, Keough ME, et al. Childhood blood pressure tracking correlations corrected for within-person variability. Stat Med. 1992;11:1187–1194
  6. Cook NR, Gillman MW, Rosner BA, Taylor JO, Hennekens CH. Combining annual blood pressure measurements in childhood to improve young adult blood pressure. Stat Med. 2000;19:2625–2640
  7. Collins RT, Alpert BS. Prehypertension and hypertension in pediatrics: don't let the statistics hide the pathology. J Pediatr. 2009;155:165–169
  8. Li R, Richey PA, Sessa TG, Jones DP. Blood aldosterone-to-renin ratio, ambulatory blood pressure, and left ventricular mass in children. J Pediatr. 2009;155:170–175
  9. Brady TM, Fivush B, Flynn JT, Parekh R. Ability of blood pressure to predict left ventricular hypertrophy in children with primary hypertension. J Pediatr. 2008;152:73–78
  10. Li S, Chen W, Srinivasan SR, Berenson GS. Childhood blood pressure as a predictor of arterial stiffness in young adults: the Bogalusa Heart Study. Hypertension. 2004;43:541–546
  11. McGill HC, McMahan CA, Tracy RE, Oalmann MC, Cornhill JF, Herderick EE, et al. Relation of a postmortem renal index of hypertension to atherosclerosis and coronary artery size in young men and women. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 1998;18:1108–1118
  12. Aggoun Y, Farpour-Lambert NJ, Marchand LM, Golay E, Maggio AB, Beghetti M. Impaired endothelial and smooth muscle functions and arterial stiffness appear before puberty in obese children and are associated with elevated ambulatory blood pressure. Eur Heart J. 2008;29:792–799
  13. Gillman MW, Cook NR, Rosner B, Evans DA, Keough ME, Taylor JO, et al. Identifying children at high risk for the development of essential hypertension. J Pediatr. 1993;122:837–846
  14. Barry MJ. Screening for prostate cancer: the controversy that refuses to die. N Engl J Med. 2009;360:1351–1354
  15. Gillman MW, Ellison RC. Childhood prevention of essential hypertension. Ped Clin North Am. 1993;40:179–194
  16. Severson K. Throwing the book at salt. Available from: http://www.nytimes.com/2009/01/28/dining/28salt.html/2009. Accessed April 8, 2009.
  17. Rose G. Strategy of Preventive Medicine. London: Oxford University Press; 1993;
  18. Cook NR, Cohen JD, Hebert PR, Taylor J, Hennekens CH. Implications of small reductions in diastolic blood pressure for primary prevention. Arch Intern Med. 1995;155:701–709

 Supported by the National Institutes of Health (Grant HL 68041), Harvard Medical School, and the Harvard Pilgrim Health Care Foundation

PII: S0022-3476(09)00468-5

doi:10.1016/j.jpeds.2009.04.062

Refers to article:

  • Pre-hypertension and Hypertension in Pediatrics: Don't Let the Statistics Hide the Pathology

    R. Thomas Collins, Bruce S. Alpert
    The Journal of Pediatrics August 2009 (Vol. 155, Issue 2, Pages 165-169)

  • Blood Aldosterone-to-Renin Ratio, Ambulatory Blood Pressure, and Left Ventricular Mass in Children , 22 May 2009

    Rongling Li, Phyllis A. Richey, Thomas G. DiSessa, Bruce S. Alpert, Deborah P. Jones
    The Journal of Pediatrics August 2009 (Vol. 155, Issue 2, Pages 170-175)

The Journal of Pediatrics
Volume 155, Issue 2 , Pages 159-161, August 2009

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