The relationship between sleep-disordered breathing, blood pressure, and urinary cortisol and catecholamines in children

Abstract

Study objectives: Hypertension is a complication of obstructive sleep apnea (OSA) syndrome in adults. A correlation between OSA syndrome and elevated blood pressure (BP) is suggested in children, but its pathogenesis remains unclear. Our aim was to study the effects of sleep and sleep apnea on BP and sympathetic nervous system activation as measured by serum cortisol and urinary catecholamines. We hypothesized that children with OSA syndrome would have higher BP, urinary catecholamines, and cortisol compared with controls.

Methods: We measured BP during polysomnography in 78 children with suspected sleep-disordered breathing and 18 nonsnoring controls. BP was measured during wakefulness and every 30-60 minutes throughout the night. All participants had 24-hour urinary catecholamine and free cortisol collections 48 hours before polysomnography.

Results: BP varied with sleep stage; it was highest during wakefulness and N1 and lowest during non-rapid eye movement stage 3. Children classified as high apnea-hypopnea index (AHI) snorers (AHI >5 events/h) had a greater prevalence of systolic hypertension (57%) than low-AHI snorers (22%) and nonsnoring controls (22%; P = .04). The high-AHI snorers also had higher diastolic BP (P < .02) as well as blunted nocturnal diastolic BP changes during sleep (P = .02) compared with low-AHI snorers (AHI <5 events/h). Twenty-hour urinary free cortisol and 24-hour urinary catecholamines were not associated with BP.

Conclusions: BP in children varies with sleep stage. OSA is associated with systolic hypertension, higher BP during rapid eye movement sleep, as well as elevation of diastolic BP and blunted BP changes with sleep.

Keywords: blood pressure; catecholamines; children; cortisol; hypertension; obstructive sleep apnea.

Figure 1. Systolic blood pressure changes across sleep stages.

The pattern of change in systolic blood pressure of the 3 groups did not differ during sleep, P < 0.1163; all 3 groups showed similar changes across sleep stage. Bars represent ±1 SE. Blood pressure values were obtained from a random-effects model (random intercept) adjusted for age, sex, ethnicity, BMI, sleep state, group, and sleep stage × group interaction. Values plotted represent an 11-year-old African American whose BMI is 28 kg/m². *Significantly different from blood pressure when awake in a child of the same group, P < .05 (controls, high-AHI snorers, or low-AHI snorers). ⁺Different from blood pressure when awake in a child of the same group, P < .10 (controls, high-AHI snorers, or low-AHI snorers). ^▲High-AHI snorers differed from controls (P = .01, ANOVA). AHI = apnea-hypopnea index; BMI = body mass index; HiAHISnorers = high-AHI snorers; LowAHIsnorers = low-AHI snorers.

Figure 2. Diastolic blood pressure changes across sleep stages.

The pattern of change in systolic blood pressure of the 3 groups differed during sleep, P < .0064. Controls and low-AHI snorers show similar patterns. There was relatively little change in high-AHI snorers in stages N1, N2, and N3. Bars represent ±1 SE. Blood pressure values were derived from a random-effects model (random intercept) adjusted for age, sex, ethnicity, BMI, sleep state, group, and sleep stage × group interaction. Values plotted represent an 11-year-old African American whose BMI is 28 kg/m². *Significantly different from blood pressure when awake in a child of the same group, P < .05 (controls, high-AHI snorers, or low-AHI snorers). ^▲Different from low-AHI snorers and controls, P = .001 (ANOVA). AHI = apnea-hypopnea index; BMI = body mass index; HiAHISnorers = high-AHI snorers; LowAHIsnorers = low-AHI snorers.