Right Analysis—Wrong Conclusion: Obese Youth With higher BP Are at Risk for Target Organ Damage

See ARTICLE page 672 The sphygmomanometer was invented by Karl Ritter in the 1880s1 and was later adopted as a routine vital sign in physical examination since extremely high or low blood pressure (BP) levels were found to indicate presence of disease. In an historical review, Kotchen2 tracked the role of the insurance industry in recognizing a relationship between BP and mortality. In the early 1900s, BP measurement became part of life insurance examinations, and actuarial data developed from that era showed an effect of elevated BP on life expectancy. However, it was not until the 1950s that data from the Framingham Heart Study demonstrated that modest elevations of BP were predictive of future adverse cardiovascular (CV) events.3 The study confirmed that high BP is a risk factor for CV disease and predicts subsequent morbidity. Many later studies replicated these findings and demonstrated that as BP increases there is a linear increase in CV risk, without a threshold effect (i.e., a clear cut-point at which lower levels of BP are “safe”).4 These historical observations are important to remember because it is not the BP level itself, which confers morbidity and mortality, but it is the harm the BP elevation is causing to important body organs that leads to CV events. In fact, BP-related target organ damage such as elevated left ventricular mass (LVM), increased carotid intima-media thickness (cIMT), and pulse wave velocity (PWV) are predictors of hard CV events in adults, even after adjusting for other CV risk factors.5–7 The precise level of BP that elevates risk for future adverse events in children is less clear. With development of normative BP data on asymptomatic healthy children, it was recognized that BP levels in children and adolescents are considerably lower than in adults; and there is a progressive increase in BP level that corresponds to childhood growth and development. In adults, there are long-term outcome data that link a BP level (e.g., 140/90mm Hg) with high risk for subsequent events such as stroke, heart failure, kidney failure, or death, thus providing a numerical BP level to predict heightened risk. However, no such outcome data that link a BP level with heightened risks are available in childhood. Moreover, BP data in healthy children demonstrate a shift in the normative BP distribution curve according to age, sex, and height. For these reasons, since the late 1970s, hypertension in childhood has been defined statistically as a BP level that matches the extreme portion of the normal distribution. Therefore, hypertension in childhood is defined as BP level that is ≥95th percentile of the age, sex, and height-adjusted BP distribution.8 Thus, hypertension in children is defined statistically and, unlike adult hypertension, is not based on outcomes. Whether this childhood definition of hypertension accurately estimates risk for later CV events or for underlying CV injury has never been confirmed. The association of obesity with higher BP has been has well established in both adults and children. Several epidemiologic and clinical reports describe the strong association of overweight and obesity with high BP and prevalence of hypertension in childhood.9–11 When overweight and obese children were removed from the child BP data used in the Fourth Report,12 the BP levels at the 95th percentile were lower.13 In the report by Schwandt et al. 14 in this issue of the journal, the authors clearly demonstrate divergence in age, height, and sex-adjusted BP distribution in normal weight vs. overweight vs. obese children. The BP distributions are considerably higher in obese children. For example, the 95th percentile for a median height 15-year-old boy is 146.3/90.5mm Hg and the 85th percentile is 137.8/86.4mm Hg. These effects of overweight and obesity provide support to removing overweight and obese children from data on which the reference BP distribution percentiles are developed. However, what remains unresolved is the level of BP in children, whether percentile or numerical level, that confers an increase in risk for CV injury. There are now substantial pediatric data linking risk factors such as hypertension to intermediate measures of target organ damage.15 The Bogalusa Heart Study demonstrated increased atherosclerosis at autopsy in adolescents with hypertension.16 Later, noninvasive studies showed cardiac17 and vascular18 damage in youth with hypertension. A recent meta-analysis that evaluated 93 pediatric studies19 demonstrated significant association between ambulatory BP and LVM index with a moderate association between BP and cIMT. These relationships were consistent in both healthy and obese children. More concerning, however, is the observation that measures of LVM, cIMT, and PWV in youth with pre-hypertension are higher than their normotensive counterparts.20,21 These reports consistently describe a higher prevalence of target organ damage among obese children and adolescents. Together, these data indicate that target organ damage may already be present in youth at levels of BP even lower than the 95th percentile. Therefore, the conclusion of the well-designed study by Schwandt et al. that youth with obesity should be allowed to have a higher BP is disturbing because the data clearly demonstrate that elevated BP in childhood is linked to target organ damage that is predictive of later CV events. Therefore, allowing obese youth to have a higher BP and still be considered “normal” exposes these patients to increased risk for development of target organ damages. We agree that BP levels on average are higher in obese youth, but these should not be “forgiven” but rather, they should be evaluated and managed.