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Original Research: Sleep Disorders |

A 4-Year Prospective Follow-up Study of Childhood OSA and Its Association With BPChildhood OSA and BP: A Follow-up Study FREE TO VIEW

Albert M. Li, MD; Chun T. Au, MPhil; Crystal Ng, MPhil; Hugh S. Lam, MB; Crover K. W. Ho, RPSGT; Yun K. Wing, MB
Author and Funding Information

From the Department of Pediatrics (Drs Li and Lam, Mr Au, and Ms Ng) and Department of Psychiatry (Mr Ho and Dr Wing), Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong.

Correspondence to: Albert M. Li, MD, Department of Pediatrics, Prince of Wales Hospital, 30-32 Ngan Shing St, Shatin, Hong Kong; e-mail: albertmli@cuhk.edu.hk


Part of this article has been presented in abstract form at the 8th Congress of Asian Society for Pediatric Research, May 17-19, 2012, Seoul, Korea.

Funding/Support: This study was funded by the Research Grants Council of the Hong Kong Special Administrative Region, China [CUHK470108].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(6):1255-1263. doi:10.1378/chest.13-1333
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Background:  Childhood OSA is a prevalent condition associated with raised BP as documented in cross-sectional studies. This study aimed to determine whether baseline or change in OSA severity was associated with ambulatory BP at 4-year follow-up.

Methods:  Children who participated in our previous OSA prevalence research were invited to undergo a repeat overnight sleep study and 24-h ambulatory BP monitoring in this 4-year follow-up study. BP parameters of subjects with differing baseline OSA severity, that is, obstructive apnea-hypopnea index (OAHI) < 1/h, 1 to 5/h, and > 5/h, were compared. Overweight and normal-weight children were analyzed separately.

Results:  One hundred eighty-five of 306 subjects (60%) were included in the analysis, of whom 58 were overweight at baseline. Linear increasing trends of wake systolic BP (SBP), wake diastolic BP (DBP), and sleep SBP z scores at follow-up were found across groups of increasing baseline OSA severity in the normal weight but not in the overweight subgroup. After adjusting for BMI z score, baseline OAHI was independently associated with all BP z scores at follow-up but not associated with changes in BP z scores across 4 years. On the other hand, change in OAHI was independently associated with sleep SBP and DBP z scores at follow-up and with changes in sleep SBP and DBP z scores across 4 years.

Conclusions:  This study provides longitudinal data as additional proof that childhood OSA is associated with elevated BP independent of obesity.

Figures in this Article

Childhood OSA is a common condition, with prevalence ranging from 0.1% to 13%.13 In adults, OSA is an independent risk factor for hypertension.4 Data for the pediatric population present conflicting results.514 A meta-analysis concluded that inadequate evidence exists for an association between raised BP and childhood OSA.15 The authors also found marked heterogeneity among published series and emphasized the need for further studies to clarify this important issue. Furthermore, all the published studies were limited by their cross-sectional design.

Children with elevated BP are at higher risk of adulthood hypertension, metabolic syndrome, and abnormal cardiovascular rhythmicity.1621 A significant association has been established between hypertension and atherosclerotic lesions in adolescents and young adults.19 Robust evidence also indicates that elevated BP during childhood is associated with increased carotid artery intima-media thickness in young adults.17,21 Exposure to high BP early in life would significantly increase one’s risk of cardiovascular adverse events. Thus, early identification of elevated BP and hypertension in children is important to avoid long-term complications.

In this study, we aimed to assess the association between OSA and BP in a prospective analysis of data obtained from subjects recruited from the community for an OSA prevalence study. The subjects returned at 4-year follow-up, providing longitudinal data of the natural history of OSA and changes in BP. It was expected that obesity would be the major confounder of the association between BP and OSA; therefore, normal-weight and overweight subjects were analyzed separately. We hypothesized that baseline OSA severity and change in OSA severity over the 4-year period are associated with BP z scores and their changes, respectively, at follow-up in both normal-weight and overweight subjects.

Subjects

This prospective follow-up study was in a cohort established between 2003 and 2005 for a childhood OSA prevalence project for Hong Kong Chinese.2 A 2-year assessment of the natural progression of children with mild OSA from this cohort has been previously reported.22 There were 306 children (199 boys [65%]) involved in the baseline study, of whom 127 were normal control subjects, 133 had mild OSA (obstructive apnea-hypopnea index [OAHI] of 1-5/h), and 46 had moderate to severe OSA (OAHI > 5/h). Subjects with mild OSA were followed up at our sleep disorder clinic every 4 to 6 months for disease progression, whereas all subjects with moderate to severe OSA were referred to our ear, nose, and throat colleagues with a view to surgery. Subjects who refused surgery or were assessed to be not suitable for surgery (tonsil grading ≤ 1 based on a standardized scale of 0-4)23 were offered CPAP therapy. All were invited to return for the present follow-up. Subjects were excluded if they had structural heart disease, were taking medications that could alter BP control, and had facial dysmorphology, congenital or acquired neurologic diseases, history of premature delivery, intrauterine growth retardation, and acute illness within 2 weeks of the scheduled visit. This study was approved by the Joint Chinese University of Hong Kong-New Territories East Cluster Clinical Research Ethics Committee (CREC-2007.363). Written informed consent and assent were obtained from the parents and subjects, respectively.

Measurements

All subjects underwent anthropometric measurements, self-reported pubertal assessment,24 overnight polysomnography (PSG), and 24-h ambulatory BP (ABP) monitoring. Anthropometric parameters, including weight, height, and waist and hip circumferences, were measured on the day of PSG. BMI was converted to a BMI z score according to local reference.25 Overweight was defined as BMI z score > 1.036 (ie, 85th percentile). A modified Epworth Sleepiness Scale was used to assess daytime sleepiness.26 History of hypertension in the subjects’ first-degree relatives was also obtained.

Polysomnography

All baseline PSG studies were performed in a dedicated sleep laboratory with CNS 1000P polygraph (CNS Inc). At follow-up, most of the subjects (90.5%) underwent PSG in the same laboratory with the same machine. The remaining who refused hospital admission were offered home PSG. A portable sleep recorder (MediPalm; Braebon Medical Corp) was used to collect data with the same montage as that applied in the sleep laboratory. For details of recording methods and definition of PSG parameters, see e-Appendix 1.

ABP Monitoring

Twenty-four-hour ABP was monitored on the same day of overnight PSG with a validated oscillometric monitor (Spacelabs 90217; Spacelabs Healthcare).27 The proper-sized cuff was placed on the nondominant arm. Systolic BP (SBP) and diastolic BP (DBP) were measured every one-half hour during the period from 21:30 to 07:30 (sleep period) and every 15 min outside this period (wake period). The exact cutoff time dividing wake and sleep BP was defined according to the PSG tracings. Individual mean SBP and DBP were calculated for wake and sleep periods. Recordings were accepted when they had a minimum of 14 and seven successful readings during active wakefulness and sleep, respectively.27 All mean BP variables were converted to a BP z score according to reference values (relative to sex and height) published by Wühl et al.28 Nocturnal SBP and DBP dipping was defined as the percentage drop of BP levels from wakefulness to sleep [(wake BP − sleep BP)/wake BP × 100%].

Statistical Analysis

Normal-weight subjects and overweight subjects were analyzed separately. Comparisons between subjects with differing baseline OSA severity (ie, OAHI < 1/h, 1-5/h, > 5/h) were made to investigate the effect of baseline OSA severity on ABP at follow-up. Continuous data were compared with one-way analysis of variance (ANOVA) with post hoc pairwise comparisons. Analyses of linear trends of continuous variables across the various baseline OSA severity groups were also obtained from one-way ANOVA. χ2 tests were used to assess the linear trends of categorical variables across groups. Paired t tests were used to assess the within-group changes from baseline to follow-up. Repeated-measures ANOVAs were used to examine the between-group differences in ABP changes over time. To determine the effect of OSA severity and BMI on ABP over 4 years, multiple linear regression models were constructed with ABP z scores at follow-up or change in ABP z score over 4 years as the dependent variable and baseline OAHI, change in OAHI, baseline BMI z score, and change in BMI z score as the independent variables; together, these were adjusted for sex, pubertal status at baseline and follow-up, baseline age, change in age, and parental history of hypertension simultaneously. Partial η2 was calculated to measure the effect size of the independent variables. SPSS, version 13.0 for Windows (IBM) was used for all statistical analyses. Significance was set at P < .05, except for pairwise comparisons for which Bonferroni correction was made.

One hundred ninety-one subjects (126 boys [66.0%]) agreed to take part in this follow-up study. Six subjects with OAHI > 5/h at baseline had undergone adenotonsillectomy, and no subjects received CPAP therapy. Because the number of subjects who had received intervention for OSA was so small that subgroup analysis was impossible, the six subjects who underwent surgery were excluded from the final analysis (Fig 1). The mean age of the remaining 185 subjects (120 boys, 58 overweight at baseline) increased from 10.2 ± 1.7 to 14.3 ± 1.8 years over a time interval of 4.1 ± 0.6 years between the two visits. There were no significant differences in baseline BMI z scores, OAHI, and ABP measures between those who did and those who did not participate in this study (e-Table 1).

Figure Jump LinkFigure 1. Consort diagram. OAHI = obstructive apnea-hypopnea index.Grahic Jump Location
Normal-Weight Subgroup

The normal-weight subgroup comprised 53 children with baseline OAHI < 1/h, 63 with baseline OAHI between 1 and 5/h, and 11 with baseline OAHI > 5/h. There were increasing trends in the proportion of boys (P for trend = .028) and family history of hypertension (P for trend = .041) across groups of increasing baseline OSA severity. No significant differences or linear trends in age, height, and BMI z score could be found across groups (Fig 2, Table 1). Over the period of 4 years, no significant changes in BMI z score and OAHI were found within each baseline OSA severity group (Fig 2). Change in OSA severity of each individual is detailed in Table 2.

Figure Jump LinkFigure 2. BMI z scores and OAHI of varying baseline OSA severity groups at baseline and follow-up. A, BMI z score. B, OAHI z score. Error bars represent mean (95% CI). Data from normal-weight and overweight subgroups are shown separately, with subjects from the overweight subgroup presented in the shaded region. *Significant within-group change from baseline to follow-up (P < .05). See Figure 1 legend for expansion of abbreviation.Grahic Jump Location
Table Graphic Jump Location
Table 1 —Demographic and Anthropometric Data of Children With Varying OSA Severity at Baseline

Data are presented as median (interquartile range), mean ± SD, or No. (%) unless otherwise indicated. ESS = Epworth Sleepiness Scale; fHTN = family history of hypertension; OAHI = obstructive apnea-hypopnea index.

Table Graphic Jump Location
Table 2 —Change in OSA Severity Across 4 y

See Table 1 legend for expansion of abbreviation.

Increasing trends were demonstrated in wake and sleep BP at both baseline and follow-up across groups of increasing baseline OSA severity (Table 3). Similar trends were also observed for the BP z scores (Fig 3). No significant differences or trends in nocturnal dipping could be found between groups. There were no significant differences in the changes in BP, BP z scores, and nocturnal dipping over the follow-up period among groups with varying baseline OSA severity (Table 3).

Table Graphic Jump Location
Table 3 —Ambulatory BP Measures in Children With Varying Baseline OSA Severity

Data are presented as mean ± SD. DBP = diastolic BP; SBP = systolic BP; SDBP = sleep diastolic BP; SSBP = sleep systolic BP; WDBP = wake diastolic BP; WSBP = wake systolic BP. See Table 1 legend for expansion of other abbreviation.

a 

Significant P < .05.

Overweight Subgroup

The overweight subgroup comprised 19, 25, and 14 children with baseline OAHI < 1/h, between 1 and 5/h, and > 5/h, respectively. No significant differences or linear trends in age, sex, family history of hypertension, height, and BMI z score could be observed among groups. Across 4 years, significant reductions in BMI z score were found in the groups of baseline OAHI < 1/h and 1 to 5/h (both P < .05), but no significant change in OAHI was found (Fig 2). Change in OSA severity of each individual is detailed in Table 2.

There were no significant differences or linear trends in any ABP parameters among groups with varying baseline OSA severity (Fig 3, Table 3). The BP z scores tended to decrease over 4 years (Fig 3), which is probably attributable to the decrease in BMI z score (Fig 2).

Figure Jump LinkFigure 3. BP z scores of varying baseline OSA severity groups at baseline and follow-up. A, WSBP z scores. B, WDBP z scores. C, SSBP z scores. D, SDBP z scores. Error bars represent mean (95% CI). Data from normal-weight and overweight subgroups are shown separately, with those from the overweight subgroup presented in the shaded region. For the normal-weight subgroup, linear increasing trends across groups of increasing baseline OSA severity were found in baseline WDBP, SSBP, and SDBP z scores and follow-up WSBP, WDBP, and SSBP z scores (all P < .05). No increasing trends were found in the overweight subgroup. *Significant change from baseline to follow-up (P < .05). †Significant difference between groups in baseline OAHI < 1/h and 1-5/h at the corresponding visit (P < .05). ‡Significant difference between groups in baseline OAHI 1-5/h and > 5/h at the corresponding visit (P < .05). SDBP = sleep diastolic BP; SSBP = sleep systolic BP; WDBP = wake diastolic BP; WSBP = wake systolic BP. See Figure 1 legend for expansion of other abbreviation.Grahic Jump Location

Multiple linear regression analyses revealed that baseline OAHI was independently associated with all BP z scores at follow-up (all P < .02) but not associated with changes in BP z scores across 4 years. On the other hand, change in OAHI was independently associated with sleep SBP (P = .005) and DBP (P = .013) z scores at follow-up and changes in sleep SBP (P < .001) and DBP (P = .012) z scores across 4 years. In contrast, both baseline BMI z score and change in BMI z score were associated only with wake and sleep SBP z scores at follow-up (all P<.02) but not associated with any changes in BP z scores across 4 years (Table 4). No significant interactions between OAHI and BMI z scores were found.

Table Graphic Jump Location
Table 4 —Results From Linear Regression Models Determining Correlates of BP z Scores at 4-y Follow-up

All regression models were constructed with BP z score or change in BP z score as the dependent variables. Independent variables were sex, pubertal status at baseline and follow-up, parental hypertension status, baseline age, change in age, baseline BMI z score, change in BMI z score, baseline OAHI, and change in OAHI. ηp2 = partial η2. See Table 1 and 3 legends for expansion of other abbreviations.

a 

Significant P < .05.

To our knowledge, this prospective longitudinal study is the first to demonstrate an association between ABP and OSA severity in children. The results showed that baseline OSA severity was independently and positively associated with wake and sleep BP 4 years later in children of normal weight. This finding is novel wherein normal-weight children with OSA could be predicted to have higher BP at 4 years than children without OSA. This is consistent with findings from the Wisconsin Sleep Cohort Study, which showed that the OR for hypertension is higher in subjects with higher baseline OSA severity.29 The present data also demonstrate that change in OAHI over 4 years is positively associated with change in sleep SBP z scores in the normal-weight subjects, whereas in overweight subjects, it is associated with sleep SBP and DBP z scores at follow-up as well as their changes over 4 years, independent of baseline and change in BMI z score. All these findings further support the causal relationship between OSA and BP elevation in children.

A separate analysis for normal-weight children and overweight children aimed to minimize the confounding effect of obesity to provide a clearer picture of the association between OSA and BP. The data reveal differences in the association between OSA severity and BP between the normal-weight and overweight subgroups. Baseline OAHI was independently associated with BP z scores both at baseline and at follow-up in normal weight subjects only, suggesting that the effect of obesity on BP overshadows the effect of OSA in overweight children. However, change in OAHI was significantly associated with change in sleep BP z scores in both the normal-weight and the overweight subgroups, implying that OSA, and especially a change in its severity, remains an important factor in BP regulation irrespective of one’s body weight status.

We did not document a significant association between change in OAHI and change in wake BP z scores, which may suggest that sleep BP in children is more liable to elevate as a result of sleep-disordered breathing. Our research group has previously shown that children with more severe OSA are at higher risk of nighttime hypertension.11 Leung et al10 also demonstrated that the desaturation index is significantly associated with sleep DBP but not with wake BP, which is also consistent with findings reported in adult studies.30 Nocturnal BP provides a more direct reflection of acute insults, such as intermittent hypoxia, changes to pulmonary volume, intrathoracic pressure, and arousals, as a result of OSA.30 On the other hand, the increasing trend of wake BP among OSA severity progression groups could be explained by sympathetic activation that spills over into wakefulness.31 In other words, in assessing children with OSA, measurement of nocturnal BP is essential in providing a better reflection of cardiovascular disturbances.

It is still unclear whether OSA exerts an adverse effect on SBP alone, DBP alone, or both. Studies in adults suggested that subjects with OSA have higher SBP and that effective CPAP treatment would lead to a decrease in SBP instead of DBP in both normotensive and hypertensive individuals.32,33 On the other hand, several studies in children suggested that DBP but not SBP is affected by OSA.5,7,12 Of note, one of the studies found that DBP during wakefulness is lower in children with OSA than in primary snorers.5 The current study reveals that both SBP and DBP during sleep are independently associated with baseline OAHI and change in OAHI. The reason for the discrepancy between studies is unclear. The data suggest that baseline and change in BMI z score are associated with wake and sleep SBP z scores but not with DBP z scores. In other words, the association between OSA and SBP is more likely affected by obesity because childhood OSA is highly associated with obesity.34 This implies that if the effect of obesity is not adequately adjusted, the association between OSA severity and SBP may be either overestimated or underestimated, depending on the prevalence and degree of obesity of various samples and, as a result, yielding inconsistent conclusions.

This study has a few limitations. First, the rate of follow-up was relatively modest. However, there were no significant differences in baseline variables between those who did and those who did not return for follow-up (e-Table 1). Second, only a single-night PSG was done in each subject, and first-night effect together with night-to-night PSG variability could lead to misclassification of OSA severity. As previously shown, a single-night study could, however, correctly identify 80% of all OSA cases.35 Third, only a small proportion of subjects with OSA at baseline received treatment. The high refusal rate of treatment might be explained by the fact that the subjects were recruited from the community, and the parents might not have been aware of sleep problems before their children joined the study. Hence, the parents might have wanted to wait and observe for a longer period before committing to an intervention. This has restricted us from further investigating the treatment effect on ABP. Fourth, ABP could be largely affected by activity level during ABP monitoring, which was not assessed in this study. However, because all subjects had to stay in our sleep laboratory during the time when ABP was being monitored, their activities were limited; hence, there should be no significant difference in activity level among subjects. Fifth, the subjects were undergoing various stages of puberty over the follow-up period. Because it has been suggested that pubertal growth is associated with BP changes,36 the observed BP changes might be partly attributable to puberty. However, the possible effect of pubertal status on BP was adjusted in the multiple regression analyses. Finally, this study recruited only Hong Kong Chinese children; hence, the results may not be applicable to other populations.

In summary, baseline OAHI > 5/h and increase in OAHI could partially explain the elevated ABP in the 4-year follow-up, independent of obesity and weight gain. The association was particularly significant for normal-weight subjects. This study provided novel findings of a longitudinal association of childhood OSA with elevated BP. The results are clinically relevant because elevated BP in childhood is a well-known risk factor for future cardiovascular adverse events. Early diagnosis and active intervention should, thus, be advocated in the management of childhood OSA. In a locality where parents might have great concern about the risk and benefits of the intervention for childhood OSA, as in Hong Kong, the current data add a relevant and important message to guide our counseling on the long-term deleterious effects of OSA.

Author contributions: Dr Li had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Li: contributed to the study concept and design, data interpretation, drafting and revision of the manuscript for important intellectual content, and final approval of the manuscript.

Mr Au: contributed to the study concept and design; data collection, analysis, and interpretation; drafting and revision of the manuscript for important intellectual content; and final approval of the manuscript.

Ms Ng: contributed to the data collection, analysis, and interpretation; drafting and revision of the manuscript for important intellectual content; and final approval of the manuscript.

Dr Lam: contributed to the study concept and design, data interpretation, drafting and revision of the manuscript for important intellectual content, and final approval of the manuscript.

Mr Ho: contributed to the data collection and interpretation and final approval of the manuscript.

Dr Wing: contributed to the study concept and design, data interpretation, drafting and revision of the manuscript for important intellectual content, and final approval of the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Wing has received grant sponsorship from the Government of Hong Kong SAR and received an honorarium by serving as a part-time consultant for Renascence Therapeutics Limited. Drs Li and Lam, Messrs Au and Ho, and Ms Ng have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

Additional information: The e-Appendix and e-Table can be found in the “Supplemental Materials” area of the online article.

ABP

ambulatory BP

ANOVA

analysis of variance

DBP

diastolic BP

OAHI

obstructive apnea-hypopnea index

PSG

polysomnography

SBP

systolic BP

Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc. 2008;5(2):242-252. [CrossRef]
 
Li AM, So HK, Au CT, et al. Epidemiology of obstructive sleep apnoea syndrome in Chinese children: a two-phase community study. Thorax. 2010;65(11):991-997. [CrossRef]
 
Marcus CL, Brooks LJ, Draper KA, et al; American Academy of Pediatrics. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):576-584. [CrossRef]
 
Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. 2003;290(14):1906-1914. [CrossRef]
 
Amin RS, Carroll JL, Jeffries JL, et al. Twenty-four-hour ambulatory blood pressure in children with sleep-disordered breathing. Am J Respir Crit Care Med. 2004;169(8):950-956. [CrossRef]
 
Enright PL, Goodwin JL, Sherrill DL, Quan JR, Quan SF; Tucson Children’s Assessment of Sleep Apnea study. Blood pressure elevation associated with sleep-related breathing disorder in a community sample of white and Hispanic children: the Tucson Children’s Assessment of Sleep Apnea study. Arch Pediatr Adolesc Med. 2003;157(9):901-904. [CrossRef]
 
Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med. 1998;157(4):1098-1103. [CrossRef]
 
Kohyama J, Ohinata JS, Hasegawa T. Blood pressure in sleep disordered breathing. Arch Dis Child. 2003;88(2):139-142. [CrossRef]
 
Guilleminault C, Khramsov A, Stoohs RA, et al. Abnormal blood pressure in prepubertal children with sleep-disordered breathing. Pediatr Res. 2004;55(1):76-84. [CrossRef]
 
Leung LCK, Ng DK, Lau MW, et al. Twenty-four-hour ambulatory BP in snoring children with obstructive sleep apnea syndrome. Chest. 2006;130(4):1009-1017.
 
Li AM, Au CT, Sung RY, et al. Ambulatory blood pressure in children with obstructive sleep apnoea: a community based study. Thorax. 2008;63(9):803-809. [CrossRef]
 
Ng DK, Wong JC, Chan CH, Leung LC, Leung SY. Ambulatory blood pressure before and after adenotonsillectomy in children with obstructive sleep apnea. Sleep Med. 2010;11(7):721-725. [CrossRef]
 
Horne RS, Yang JS, Walter LM, et al. Elevated blood pressure during sleep and wake in children with sleep-disordered breathing. Pediatrics. 2011;128(1):e85-e92. [CrossRef]
 
Xu Z, Li B, Shen K. Ambulatory blood pressure monitoring in Chinese children with obstructive sleep apnea/hypopnea syndrome. Pediatr Pulmonol. 2013;48(3):274-279. [CrossRef]
 
Zintzaras E, Kaditis AG. Sleep-disordered breathing and blood pressure in children: a meta-analysis. Arch Pediatr Adolesc Med. 2007;161(2):172-178. [CrossRef]
 
Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics. 1989;84(4):633-641.
 
Li S, Chen W, Srinivasan SR, et al. Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study. JAMA. 2003;290(17):2271-2276. [CrossRef]
 
Raitakari OT, Juonala M, Kähönen M, et al. Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA. 2003;290(17):2277-2283. [CrossRef]
 
Strong JP. Atherosclerosis in the young: risk and prevention. Hosp Pract (1995). 1999;34(10):15–-16,19.
 
Sun SS, Grave GD, Siervogel RM, Pickoff AA, Arslanian SS, Daniels SR. Systolic blood pressure in childhood predicts hypertension and metabolic syndrome later in life. Pediatrics. 2007;119(2):237-246. [CrossRef]
 
Sorof JM, Alexandrov AV, Cardwell G, Portman RJ. Carotid artery intimal-medial thickness and left ventricular hypertrophy in children with elevated blood pressure. Pediatrics. 2003;111(1):61-66. [CrossRef]
 
Li AM, Au CT, Ng SK, et al. Natural history and predictors for progression of mild childhood obstructive sleep apnoea. Thorax. 2010;65(1):27-31. [CrossRef]
 
Ng SK, Lee DL, Li AM, Wing YK, Tong MC. Reproducibility of clinical grading of tonsillar size. Arch Otolaryngol Head Neck Surg. 2010;136(2):159-162. [CrossRef]
 
Chan NP, Sung RY, Nelson EA, So HK, Tse YK, Kong AP. Measurement of pubertal status with a Chinese self-report Pubertal Development Scale. Matern Child Health J. 2010;14(3):466-473. [CrossRef]
 
Leung SS, Cole TJ, Tse LY, Lau JT. Body mass index reference curves for Chinese children. Ann Hum Biol. 1998;25(2):169-174. [CrossRef]
 
Melendres MC, Lutz JM, Rubin ED, Marcus CL. Daytime sleepiness and hyperactivity in children with suspected sleep-disordered breathing. Pediatrics. 2004;114(3):768-775. [CrossRef]
 
O’Brien E, Asmar R, Beilin L, et al; European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens. 2003;21(5):821-848. [CrossRef]
 
Wühl E, Witte K, Soergel M, Mehls O, Schaefer F; German Working Group on Pediatric Hypertension. Distribution of 24-h ambulatory blood pressure in children: normalized reference values and role of body dimensions. J Hypertens. 2002;20(10):1995-2007. [CrossRef]
 
Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-1384. [CrossRef]
 
Sekizuka H, Kida K, Akashi YJ, et al. Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension. J Cardiol. 2010;55(1):92-98. [CrossRef]
 
Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995;96(4):1897-1904. [CrossRef]
 
Dimsdale JE, Loredo JS, Profant J. Effect of continuous positive airway pressure on blood pressure: a placebo trial. Hypertension. 2000;35(1):144-147. [CrossRef]
 
Hla KM, Skatrud JB, Finn L, Palta M, Young T. The effect of correction of sleep-disordered breathing on BP in untreated hypertension. Chest. 2002;122(4):1125-1132. [CrossRef]
 
Wing YK, Hui SH, Pak WM, et al. A controlled study of sleep related disordered breathing in obese children. Arch Dis Child. 2003;88(12):1043-1047. [CrossRef]
 
Li AM, Wing YK, Cheung A, et al. Is a 2-night polysomnographic study necessary in childhood sleep-related disordered breathing? Chest. 2004;126(5):1467-1472. [CrossRef]
 
Shankar RR, Eckert GJ, Saha C, Tu W, Pratt JH. The change in blood pressure during pubertal growth. J Clin Endocrinol Metab. 2005;90(1):163-167. [CrossRef]
 

Figures

Figure Jump LinkFigure 1. Consort diagram. OAHI = obstructive apnea-hypopnea index.Grahic Jump Location
Figure Jump LinkFigure 2. BMI z scores and OAHI of varying baseline OSA severity groups at baseline and follow-up. A, BMI z score. B, OAHI z score. Error bars represent mean (95% CI). Data from normal-weight and overweight subgroups are shown separately, with subjects from the overweight subgroup presented in the shaded region. *Significant within-group change from baseline to follow-up (P < .05). See Figure 1 legend for expansion of abbreviation.Grahic Jump Location
Figure Jump LinkFigure 3. BP z scores of varying baseline OSA severity groups at baseline and follow-up. A, WSBP z scores. B, WDBP z scores. C, SSBP z scores. D, SDBP z scores. Error bars represent mean (95% CI). Data from normal-weight and overweight subgroups are shown separately, with those from the overweight subgroup presented in the shaded region. For the normal-weight subgroup, linear increasing trends across groups of increasing baseline OSA severity were found in baseline WDBP, SSBP, and SDBP z scores and follow-up WSBP, WDBP, and SSBP z scores (all P < .05). No increasing trends were found in the overweight subgroup. *Significant change from baseline to follow-up (P < .05). †Significant difference between groups in baseline OAHI < 1/h and 1-5/h at the corresponding visit (P < .05). ‡Significant difference between groups in baseline OAHI 1-5/h and > 5/h at the corresponding visit (P < .05). SDBP = sleep diastolic BP; SSBP = sleep systolic BP; WDBP = wake diastolic BP; WSBP = wake systolic BP. See Figure 1 legend for expansion of other abbreviation.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —Demographic and Anthropometric Data of Children With Varying OSA Severity at Baseline

Data are presented as median (interquartile range), mean ± SD, or No. (%) unless otherwise indicated. ESS = Epworth Sleepiness Scale; fHTN = family history of hypertension; OAHI = obstructive apnea-hypopnea index.

Table Graphic Jump Location
Table 2 —Change in OSA Severity Across 4 y

See Table 1 legend for expansion of abbreviation.

Table Graphic Jump Location
Table 3 —Ambulatory BP Measures in Children With Varying Baseline OSA Severity

Data are presented as mean ± SD. DBP = diastolic BP; SBP = systolic BP; SDBP = sleep diastolic BP; SSBP = sleep systolic BP; WDBP = wake diastolic BP; WSBP = wake systolic BP. See Table 1 legend for expansion of other abbreviation.

a 

Significant P < .05.

Table Graphic Jump Location
Table 4 —Results From Linear Regression Models Determining Correlates of BP z Scores at 4-y Follow-up

All regression models were constructed with BP z score or change in BP z score as the dependent variables. Independent variables were sex, pubertal status at baseline and follow-up, parental hypertension status, baseline age, change in age, baseline BMI z score, change in BMI z score, baseline OAHI, and change in OAHI. ηp2 = partial η2. See Table 1 and 3 legends for expansion of other abbreviations.

a 

Significant P < .05.

References

Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc. 2008;5(2):242-252. [CrossRef]
 
Li AM, So HK, Au CT, et al. Epidemiology of obstructive sleep apnoea syndrome in Chinese children: a two-phase community study. Thorax. 2010;65(11):991-997. [CrossRef]
 
Marcus CL, Brooks LJ, Draper KA, et al; American Academy of Pediatrics. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):576-584. [CrossRef]
 
Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. 2003;290(14):1906-1914. [CrossRef]
 
Amin RS, Carroll JL, Jeffries JL, et al. Twenty-four-hour ambulatory blood pressure in children with sleep-disordered breathing. Am J Respir Crit Care Med. 2004;169(8):950-956. [CrossRef]
 
Enright PL, Goodwin JL, Sherrill DL, Quan JR, Quan SF; Tucson Children’s Assessment of Sleep Apnea study. Blood pressure elevation associated with sleep-related breathing disorder in a community sample of white and Hispanic children: the Tucson Children’s Assessment of Sleep Apnea study. Arch Pediatr Adolesc Med. 2003;157(9):901-904. [CrossRef]
 
Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med. 1998;157(4):1098-1103. [CrossRef]
 
Kohyama J, Ohinata JS, Hasegawa T. Blood pressure in sleep disordered breathing. Arch Dis Child. 2003;88(2):139-142. [CrossRef]
 
Guilleminault C, Khramsov A, Stoohs RA, et al. Abnormal blood pressure in prepubertal children with sleep-disordered breathing. Pediatr Res. 2004;55(1):76-84. [CrossRef]
 
Leung LCK, Ng DK, Lau MW, et al. Twenty-four-hour ambulatory BP in snoring children with obstructive sleep apnea syndrome. Chest. 2006;130(4):1009-1017.
 
Li AM, Au CT, Sung RY, et al. Ambulatory blood pressure in children with obstructive sleep apnoea: a community based study. Thorax. 2008;63(9):803-809. [CrossRef]
 
Ng DK, Wong JC, Chan CH, Leung LC, Leung SY. Ambulatory blood pressure before and after adenotonsillectomy in children with obstructive sleep apnea. Sleep Med. 2010;11(7):721-725. [CrossRef]
 
Horne RS, Yang JS, Walter LM, et al. Elevated blood pressure during sleep and wake in children with sleep-disordered breathing. Pediatrics. 2011;128(1):e85-e92. [CrossRef]
 
Xu Z, Li B, Shen K. Ambulatory blood pressure monitoring in Chinese children with obstructive sleep apnea/hypopnea syndrome. Pediatr Pulmonol. 2013;48(3):274-279. [CrossRef]
 
Zintzaras E, Kaditis AG. Sleep-disordered breathing and blood pressure in children: a meta-analysis. Arch Pediatr Adolesc Med. 2007;161(2):172-178. [CrossRef]
 
Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics. 1989;84(4):633-641.
 
Li S, Chen W, Srinivasan SR, et al. Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study. JAMA. 2003;290(17):2271-2276. [CrossRef]
 
Raitakari OT, Juonala M, Kähönen M, et al. Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA. 2003;290(17):2277-2283. [CrossRef]
 
Strong JP. Atherosclerosis in the young: risk and prevention. Hosp Pract (1995). 1999;34(10):15–-16,19.
 
Sun SS, Grave GD, Siervogel RM, Pickoff AA, Arslanian SS, Daniels SR. Systolic blood pressure in childhood predicts hypertension and metabolic syndrome later in life. Pediatrics. 2007;119(2):237-246. [CrossRef]
 
Sorof JM, Alexandrov AV, Cardwell G, Portman RJ. Carotid artery intimal-medial thickness and left ventricular hypertrophy in children with elevated blood pressure. Pediatrics. 2003;111(1):61-66. [CrossRef]
 
Li AM, Au CT, Ng SK, et al. Natural history and predictors for progression of mild childhood obstructive sleep apnoea. Thorax. 2010;65(1):27-31. [CrossRef]
 
Ng SK, Lee DL, Li AM, Wing YK, Tong MC. Reproducibility of clinical grading of tonsillar size. Arch Otolaryngol Head Neck Surg. 2010;136(2):159-162. [CrossRef]
 
Chan NP, Sung RY, Nelson EA, So HK, Tse YK, Kong AP. Measurement of pubertal status with a Chinese self-report Pubertal Development Scale. Matern Child Health J. 2010;14(3):466-473. [CrossRef]
 
Leung SS, Cole TJ, Tse LY, Lau JT. Body mass index reference curves for Chinese children. Ann Hum Biol. 1998;25(2):169-174. [CrossRef]
 
Melendres MC, Lutz JM, Rubin ED, Marcus CL. Daytime sleepiness and hyperactivity in children with suspected sleep-disordered breathing. Pediatrics. 2004;114(3):768-775. [CrossRef]
 
O’Brien E, Asmar R, Beilin L, et al; European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens. 2003;21(5):821-848. [CrossRef]
 
Wühl E, Witte K, Soergel M, Mehls O, Schaefer F; German Working Group on Pediatric Hypertension. Distribution of 24-h ambulatory blood pressure in children: normalized reference values and role of body dimensions. J Hypertens. 2002;20(10):1995-2007. [CrossRef]
 
Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-1384. [CrossRef]
 
Sekizuka H, Kida K, Akashi YJ, et al. Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension. J Cardiol. 2010;55(1):92-98. [CrossRef]
 
Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995;96(4):1897-1904. [CrossRef]
 
Dimsdale JE, Loredo JS, Profant J. Effect of continuous positive airway pressure on blood pressure: a placebo trial. Hypertension. 2000;35(1):144-147. [CrossRef]
 
Hla KM, Skatrud JB, Finn L, Palta M, Young T. The effect of correction of sleep-disordered breathing on BP in untreated hypertension. Chest. 2002;122(4):1125-1132. [CrossRef]
 
Wing YK, Hui SH, Pak WM, et al. A controlled study of sleep related disordered breathing in obese children. Arch Dis Child. 2003;88(12):1043-1047. [CrossRef]
 
Li AM, Wing YK, Cheung A, et al. Is a 2-night polysomnographic study necessary in childhood sleep-related disordered breathing? Chest. 2004;126(5):1467-1472. [CrossRef]
 
Shankar RR, Eckert GJ, Saha C, Tu W, Pratt JH. The change in blood pressure during pubertal growth. J Clin Endocrinol Metab. 2005;90(1):163-167. [CrossRef]
 
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