Autonomic Cardiovascular Tests in Children with Obstructive Sleep Apnea Syndrome

Montesano, Marilisa; Miano, Silvia; Paolino, Maria Chiara; Massolo, Anna Claudia; Ianniello, Filomena; Forlani, Martina; Villa, Maria Pia

doi:10.1093/sleep/33.10.1349

Cited by 56 publications

(33 citation statements)

References 48 publications

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“…In recent years, OSA has emerged as a chronic low-grade inflammatory disease (1–5), and increasing evidence supports a causative link between pediatric OSA and cardiovascular diseases (CVD), including hypertension, endothelial dysfunction, and atherosclerosis (6–15). …”

mentioning

confidence: 99%

Circulating Adropin Concentrations in Pediatric Obstructive Sleep Apnea: Potential Relevance to Endothelial Function

Gozal

Kheirandish‐Gozal

Bhattacharjee

et al. 2013

The Journal of Pediatrics

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Objective To test the hypothesis that levels of adropin, a recently discovered peptide that displays important metabolic and cardiovascular functions, are lower in obstructive sleep apnea (OSA), especially when associated with endothelial dysfunction. Study design Age-, sex- and ethnicity-matched children (mean age: 7.2±1.4 years) were included into one of three groups based on the presence of OSA in an overnight sleep study, and on the time to post-occlusive maximal reperfusion (Tmax>45 sec) with a modified hyperemic test. Plasma adropin levels were assayed using a commercial ELISA kit. Results Among controls, mean morning adropin levels were 7.4 ng/ml (95% confidence intervals: 5.2–16.3 ng/ml) OSA children with abnormal endothelial function (OSA+/EF+) had significantly lower adropin levels (2.7±1.1 ng/ml, n=35) compared with matched controls (7.6±1.4 ng/ml; n=35; p<0.001), and to children with OSA and normal endothelial function (OSA+/EF−: 5.8±1.5 ng/ml, n=47; p<0.001). Plasma adropin <4.2 ng/ml reliably predicted endothelial functional status, but individual adropin levels were not significantly correlated with age, BMI-z score, obstructive apnea-hypopnea index (AHI) or nadir SpO2. Adropin levels were assessed after adenotonsillectomy in a subset of children with OSA (n=22), and showed increases in OSA+/EF+ (2.5±1.4 ng/ml to 6.4±1.9 ng/ml, n=14; p<0.01) but remained unchanged in OSA+EF− (5.7±1.3 ng/ml to 6.4±1.1 ng/ml, n=8; p>0.05). Conclusion Plasma adropin levels are reduced in pediatric OSA when endothelial dysfunction is present, and return to within normal values after adenotonsillectomy. Assessment of adropin circulating levels may provide a reliable indicator of vascular injury in the context of OSA on children.

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mentioning

confidence: 99%

Circulating Adropin Concentrations in Pediatric Obstructive Sleep Apnea: Potential Relevance to Endothelial Function

Gozal

Kheirandish‐Gozal

Bhattacharjee

et al. 2013

The Journal of Pediatrics

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“…The most accepted explanation proposes that chronic intermittent hypoxia produces oxidative stress, inflammation, and sympathetic hyperactivity, which led to endothelial dysfunction and hypertension [19,25,28,41,43,52,53,65,99,100], but it is likely that intrathoracic pressure changes causing excessive mechanical stress on large artery walls and the heart, and arousal-induced sympathetic hyperactivity may also contribute to the endothelial dysfunction [47]. OSA is characterized by repeated episodes of total or partial airflow detention during sleep produced by the pharyngeal collapse, eliciting intermittent hypoxia and hypercapnia, negative intrathoraxic pressure, sleep fragmentation and arousal.…”

Section: Pathogenic Mechanisms Of the Hypertension Induced By Osamentioning

confidence: 99%

“…Reactive oxygen species (ROS) and reactive nitrogen species (RNS), and pro-inflammatory agents have been proposed as mediators of cardiovascular and cognitive alterations in OSA patients [7,13,33,45,52,65,102] and animal models [10, 15-18, 44, 48, 82, 84, 106]. Studies performed in OSA patients and animals exposed to intermittent hypoxia showed that the hypoxia-reoxygenation episodes produce systemic oxidative stress due to the accumulation of ROS and RNS, which are potential sources of cellular damage.…”

Section: Mediators Of Enhanced Carotid Body Chemosensory Responses Tomentioning

confidence: 99%

“…Among the molecules upregulated in the carotid body by intermittent hypoxia, such as endotelin-1 (ET-1), vascular endothelial growth factor (VEGF), and inducible nitric oxide synthase (iNOS) [15-18, 50, 89-91], pro-inflammatory cytokines have been proposed as mediators of the carotid body chemosensory potentiation induced by intermittent hypoxia [16,18,43,44,50] and cardiovascular pathologies in OSA patients [7,65,108,104]. We found that chronic intermittent hypoxia induced a ROS-dependent increases of tumor necrosis factor (TNF) and Interleukin 1β (IL-1β) in the carotid body, suggesting that these pro-inflammatory cytokines may mediate the ROS-induced carotid body potentiation [16,18].…”

Section: Mediators Of Enhanced Carotid Body Chemosensory Responses Tomentioning

confidence: 99%

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Contribution of Autonomic Nervous System to the Hypertension Induced by Obstructive Sleep Apnea

Iturriaga¹,

Idiáquez²

2014

Sleep and Its Disorders Affect Society

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“…Therefore, early detection of ANS abnormalities in children with untreated OSA may help to identify candidates who are at increased risk for developing morbidity, and thus provide them with timely and effective treatment. To this effect, alterations in ANS have been evaluated using different methodologies including heart rate variability (HRV), blood pressure (BP) and blood pressure variability (BPV) peripheral arterial tonometry, and catecholamine assays (12-16). However, a simple office-based test would be highly desirable.…”

Section: Introductionmentioning

confidence: 99%

Pupillometric findings in children with obstructive sleep apnea

et al. 2015

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Background Obstructive sleep apnea (OSA) leads to intermittent hypoxia, activation of the sympathetic nervous system, and eventually cardiovascular morbidity. Alterations in autonomic nervous system (ANS) tone and reflexes are likely to play major roles in OSA-associated morbidities, and have been identified in a subset of children with OSA. Objectives To evaluate whether pupillometry, a noninvasive and rapid bedside test for the assessment of autonomic nervous system dysfunction (ANS), would detect abnormal ANS function in children with OSA. Methods Children ages 2-12 years underwent polysomnography (PSG), and were divided based on PSG findings into two groups; Habitual Snorers (HS; AHI <1 h/TST, n=17) and OSA (AHI>1 h/TST, n=49), the latter then sub-divided into AHI severity categories (>1 but <5, >5 but <10, and >10 h/TST). Pupillometric measurements were performed during the clinic visit in a dark room using an automated pupillometer device. Results A total of 66 subjects with a mean age of 7.3 ±2.6 years were recruited. There were no statistically significant differences between any of the groups, even when comparing severe OSA (n=15) and HS in any of the measures related to pupillary reflexes. However, mild, yet significant increases in systolic blood pressure and morning plasma norepinephrine levels were detected in the severe OSA group. Conclusion Although ANS perturbation are clearly present in a proportion of children with OSA, particularly those with severe disease, pupillary responses do not appear to provide a sensitive method for the detection of ANS dysfunction in OSA children.

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Autonomic Cardiovascular Tests in Children with Obstructive Sleep Apnea Syndrome

Abstract: Our data point to an increase in basal sympathetic activity during wakefulness and to an impaired reaction to several physiological stimuli, which is dependent on the severity of OSAS.

Cited by 56 publications

References 48 publications

Circulating Adropin Concentrations in Pediatric Obstructive Sleep Apnea: Potential Relevance to Endothelial Function

Circulating Adropin Concentrations in Pediatric Obstructive Sleep Apnea: Potential Relevance to Endothelial Function

Contribution of Autonomic Nervous System to the Hypertension Induced by Obstructive Sleep Apnea

Pupillometric findings in children with obstructive sleep apnea

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