Maternal Sleep-disordered Breathing Research Articles

Fetal Heart Rate Responses to Maternal Sleep-Disordered Breathing

(Am J Obstet Gynecol. 2023;228(4):459.e1–459.e8) The physical changes inherent in pregnancy can amplify underlying comorbidities. One common problem worsened in pregnancy is sleep-disordered breathing. Sleep-disordered breathing has been investigated in relation to pregnancy and found to have a host of negative outcomes associated with it, including gestational diabetes, preeclampsia, preterm delivery, and stillbirth. Risk factors for sleep-disordered breathing often overlap with risk factors for other pregnancy complications, and thus relationships can be difficult to characterize. One area needing investigation is the effect of sleep-disordered breathing on fetal heart rate (FHR), which is an indicator of wellbeing during pregnancy. This study was designed to examine the FHR response to sleep-disordered breathing in pregnant women with obesity. The authors hypothesized that apnea or hypopnea would elicit a detectable response in FHR that would be potentiated in women with more severe symptoms.

Fetal heart rate responses to maternal sleep-disordered breathing

Maternal sleep-disordered breathing is associated with adverse pregnancy outcomes and is considered to be deleterious to the developing fetus. Maternal obesity potentiates sleep-disordered breathing, which, in turn, may contribute to the effect of maternal obesity on adverse fetal outcomes. However, only a few empirical studies have evaluated the contemporaneous effects of maternal sleep-disordered breathing events on fetal well-being. These events include apnea and hypopnea with accompanying desaturations in oxyhemoglobin. This study aimed to reconcile contradictory findings on the associations between maternal apnea or hypopnea events and clinical indicators of fetal compromise. It also sought to broaden the knowledge base by examining the fetal heart rate and heart rate variability before, during, and after episodes of maternal apnea or hypopnea. To accomplish this, we employed overnight polysomnography, the gold standard for ascertaining maternal sleep-disordered breathing, and synchronized it with continuous fetal electrocardiography. A total of 84 pregnant women with obesity (body mass index >30 kg/m2) participated in laboratory-based polysomnography with digitized fetal electrocardiography recordings during or near 36 weeks of gestation. Sleep was recorded, on average, for 7 hours. Decelerations in fetal heart rate were identified. Fetal heart rate and heart rate variability were quantified before, during, and after each apnea or hypopnea event. Event-level intensity (desaturation magnitude, duration, and nadir O2 saturation level) and person-level characteristics based on the full overnight recording (apnea-hypopnea index, mean O2 saturation, and O2 saturation variability) were analyzed as potential moderators using linear mixed effects models. A total of 2936 sleep-disordered breathing events were identified, distributed among all but 2 participants. On average, participants exhibited 8.7 episodes of apnea or hypopnea per hour (mean desaturation duration, 19.1 seconds; mean O2 saturation nadir, 86.6% per episode); nearly half (n=39) of the participants met the criteria for obstructive sleep apnea. Only 45 of 2936 apnea or hypopnea events were followed by decelerations (1.5%). Conversely, most (n=333, 88%) of the 378 observed decelerations, including the prolonged ones, did not follow an apnea or a hypopnea event. Maternal sleep-disordered breathing burden, body mass index, and fetal sex were unrelated to the number of decelerations. Fetal heart rate variability increased during events of maternal apnea or hypopnea but returned to initial levels soon thereafter. There was a dose-response association between the size of the increase in fetal heart rate variability and the maternal apnea-hypopnea index, event duration, and desaturation depth. Longer desaturations were associated with a decreased likelihood of the variability returning to baseline levels after the event. The mean fetal heart rate did not change during episodes of maternal apnea or hypopnea. Episodes of maternal sleep apnea and hypopnea did not evoke decelerations in the fetal heart rate despite the predisposing risk factors that accompany maternal obesity. The significance of the modest transitory increase in fetal heart rate variability in response to apnea and hypopnea episodes is not clear but may reflect compensatory, delimited autonomic responses to momentarily adverse conditions. This study found no evidence that episodes of maternal sleep-disordered breathing pose an immediate threat, as reflected in fetal heart rate responses, to the near-term fetus.

Maternal sleep disordered breathing during gestation produces sexually dimorphic autism‐relevant synaptic and behavioral aberrations in the offspring associated with excessive mTOR cortical signaling

Sleep disordered breathing (SDB) is characterized by recurring breathing cessations during sleep, causing intermittent hypoxia (oxygen deprivation) often several hundred times per night. Obstructive sleep apnea is the most common form of SDB in pregnancy, and confers risk for detrimental maternal‐fetal outcomes. Although many of the maternal risk factors for the onset SDB during pregnancy and the development of autism spectrum disorders (ASD) in her offspring are highly overlapping (e.g., maternal obesity, advanced maternal age), no studies to date have empirically investigated the potential link between these conditions. We subjected pregnant rat dams to intermittent hypoxia or normoxia (GIH and GNX, respectively) from gestation day 10‐21 to investigate the consequences of maternal SDB on offspring neural function. We found that male GIH offspring exhibited deficits in several behaviors which were accompanied by increased pyramidal neuron dendritic spine density in the medial prefrontal cortex (PFC). These effects appear to arise from a disruption of normal developmental synaptic pruning late in childhood and persisting into early adolescence. The mTOR kinase signal transduction pathway has emerged as a critical regulator of dendritic spine formation, and dysregulation of key components of this pathway are implicated in the etiology of the increased cortical dendritic spine density of ASD. Additionally, we found that mTOR is aberrantly activated in the prefrontal cortex of male GIH offspring. Furthermore, inhibition of mTOR by rapamycin treatment significantly reduced behavioral abnormalities within GIH offspring. These findings suggest an opportunity for clinical intervention for offspring of the SDB maternal model by targeting the mTOR signaling pathway.

Butyrate supplementation rescues sex‐specific deficits in respiratory plasticity and mean arterial pressure in adult offspring exposed to gestational intermittent hypoxia

Sleep disordered breathing (SDB) in pregnancy is increasing in parallel with the obesity epidemic, and is linked to adverse perinatal outcomes in the offspring. Consequences of maternal SDB during pregnancy on the adult offspring are not well‐understood. Preliminary data indicate that adult male, but not female, offspring of dams exposed to intermittent hypoxia during gestation (GIH ‐ gestational intermittent hypoxia), a rat model of SDB during pregnancy, have elevated mean arterial pressure (MAP), increased neuroinflammation, inflammation‐induced impairment of homeostatic plasticity in the respiratory control system, and gut dysbiosis. Specifically, adult male GIH offspring have decreased relative abundance of gut bacteria that produce butyrate, a short‐chain fatty acid that has potent anti‐inflammatory properties and regulates immune function in the central nervous system. Since literature suggests that gut dysbiosis, neuroinflammation, and hypertension exist in a complicated vicious cycle, we treated male GIH offspring with tributyrin, a butyrate prodrug. Prior to tributyrin treatment, MAP in male GIH offspring was 96±3 mmHg, versus 76±1 mmHg in control rats receiving gestational intermittent normoxia (GNX). Similarly, male GIH offspring exhibited deficits in respiratory plasticity in response to recurrent central apneas (3.6±6.8% plasticity), when compared to GNX offspring (59.3±4.8% plasticity). GIH offspring exhibited evidence of elevated neuroinflammation in brain regions underlying cardiorespiratory control (e.g., IL‐1β expression 1.6±0.2‐fold higher than GNX controls (1.0±0.2)). Following three weeks of tributyrin treatment, MAP had normalized (80±2 mmHg), neuroinflammation was reduced to control levels, and the ability to express respiratory neuroplasticity was rescued (78±30%). These data indicate that gut dysbiosis may contribute to sex‐specific impairments induced by maternal exposure to intermittent hypoxia during gestation that can be rescued in adulthood by supplementing with butyrate.

Sleep quality and sleep disturbances in Chinese pregnant women: a multicenter cross-sectional study

Objective: This study aims to investigate the sleep quality of pregnant women in Xuhui District, Shanghai, and the related factors of sleep disturbances during pregnancy. Methods: From February 2019 to February 2021, we used online integrated sleep questionnaire (including PSQI, BQ, ESS, AIS) in Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, The International Peace Maternity and Child Health Hospitals of China Welfare Institution, and Shanghai Eighth People's Hospital, to investigate the sleep quality across pregnancy. We also collected maternal physical examination results, childbearing history, sociodemographic, and other clinical data. The prevalences and related factors of various sleep disturbances in pregnant women were analyzed, including insufficient/excessive nighttime sleep, low sleep efficiency, difficulty falling asleep, poor sleep quality, insomnia, daytime sleepiness, and high risk of sleep-disordered breathing (SDB). Results: This study includes 1 898 cases in the first trimester (T1), 3 099 cases in the second trimester (T2), and 1 539 cases in the third trimester (T3). Poor sleep quality (38.6%), daytime sleepiness (mild 41.9%, moderate 17.7%, severe 2.1%), and suspicious insomnia (32.3%) are most prevalent among women in T1 (P<0.01). In comparison, short sleep time (2.7%), long sleep time (8.6%), difficulty falling asleep (12.2%), poor sleep efficiency (35.4%), very poor sleep quality (6.7%), clinical insomnia (21.8%), and high-risk SDB (6.4%) are most prevalent among women in T3 (P<0.05). During pregnancy, late gestation (OR=1.016, 95%CI: 1.006-1.025) and multiple induced/drug abortions (OR=1.329, 95%CI: 1.043-1.692) are risk factors for poor sleep quality (PSQI>5), while multiple full-term deliveries (OR=0.800, 95%CI: 0.675-0.949) is its protective factor. Advanced maternal age (OR=0.976, 95%CI: 0.956-0.997), multiple full-term deliveries (OR=0.808, 95%CI: 0.680-0.959), late gestation (OR=0.983, 95%CI: 0.974-0.992) and hypertension (OR=0.572, 95%CI: 0.401-0.814) are protective factors for daytime sleepiness (ESS>6). The high-risk pregnancy category (OR=9.312, 95%CI: 1.156-74.978) is a risk factor for insomnia (AIS≥4), while multiple full-term deliveries (OR=0.815, 95%CI: 0.691-0.961) is its protective factor. High BMI (OR=1.334, 95%CI: 1.270-1.402) and hypertension (OR=4.427, 95%CI: 2.539-7.719) are risk factors for high-risk SDB in pregnant women. Conclusions: The prevalences of various sleep disturbances are high throughout pregnancy. Noticeably, symptoms of maternal SDB develop along with pregnancy. Different types of sleep disturbances are associated with different factors. Women of high-risk pregnancy category, in late gestation, with high BMI, hypertension, a history of induced/drug abortion, or without a history of full-term delivery can be at high risk of sleep disturbances during pregnancy.

Fetal Heart Rate Decelerations in Women with Sleep-Disordered Breathing.

Emerging literature has shown that women with sleep-disordered breathing (SDB) have increased risk for gestational hypertension/preeclampsia and gestational diabetes. Case reports suggest an association between maternal apnea and fetal heart rate deceleration but data are lacking on how maternal sleep impacts fetal health. Since decelerations may be associated with adverse outcomes, we sought to determine whether fetal heart rate decelerations were associated with SDB. A cohort study of third trimester pregnant women with a singleton fetus was conducted. Participants underwent a home sleep test with continuous portable electronic fetal monitoring. SDB was defined as a respiratory disturbance index (RDI)≥10 events/hour. The temporality between a respiratory event and fetal heart rate decelerations was determined to be present if a deceleration occurred < 30 s after a respiratory event. Forty women were included with mean (±SD) age, BMI, and gestational age of 32.0±5.5 years, 37.1±8.0 kg/m2, and 34.6±2.4 weeks respectively. Overall, n=23 (57.5%) women had SDB. Thirty-seven late decelerations were observed in 18 women; of these, 84% were temporally associated with a respiratory event. Nine of the 18 women (50%) had SDB. Ten prolonged decelerations were observed in 6 women of which nine (90%) were temporally associated with a respiratory event. Five of the six women (83%) had an RDI≥10. These initial data suggest that, in this population, the majority of both late and prolonged fetal heart rate decelerations occur with a maternal respiratory event. Since respiratory events are characteristic of maternal SDB, this raises the possibility that SDB may influence fetal well-being.

Perinatal Hypoxemia and Oxygen Sensing.

The development of the control of breathing begins in utero and continues postnatally. Fetal breathing movements are needed for establishing connectivity between the lungs and central mechanisms controlling breathing. Maturation of the control of breathing, including the increase of hypoxia chemosensitivity, continues postnatally. Insufficient oxygenation, or hypoxia, is a major stressor that can manifest for different reasons in the fetus and neonate. Though the fetus and neonate have different hypoxia sensing mechanisms and respond differently to acute hypoxia, both responses prevent deviations to respiratory and other developmental processes. Intermittent and chronic hypoxia pose much greater threats to the normal developmental respiratory processes. Gestational intermittent hypoxia, due to maternal sleep-disordered breathing and sleep apnea, increases eupneic breathing and decreases the hypoxic ventilatory response associated with impaired gasping and autoresuscitation postnatally. Chronic fetal hypoxia, due to biologic or environmental (i.e. high-altitude) factors, is implicated in fetal growth restriction and preterm birth causing a decrease in the postnatal hypoxic ventilatory responses with increases in irregular eupneic breathing. Mechanisms driving these changes include delayed chemoreceptor development, catecholaminergic activity, abnormal myelination, increased astrocyte proliferation in the dorsal respiratory group, among others. Long-term high-altitude residents demonstrate favorable adaptations to chronic hypoxia as do their offspring. Neonatal intermittent hypoxia is common among preterm infants due to immature respiratory systems and thus, display a reduced drive to breathe and apneas due to insufficient hypoxic sensitivity. However, ongoing intermittent hypoxia can enhance hypoxic sensitivity causing ventilatory overshoots followed by apnea; the number of apneas is positively correlated with degree of hypoxic sensitivity in preterm infants. Chronic neonatal hypoxia may arise from fetal complications like maternal smoking or from postnatal cardiovascular problems, causing blunting of the hypoxic ventilatory responses throughout at least adolescence due to attenuation of carotid body fibers responses to hypoxia with potential roles of brainstem serotonin, microglia, and inflammation, though these effects depend on the age in which chronic hypoxia initiates. Fetal and neonatal intermittent and chronic hypoxia are implicated in preterm birth and complicate the respiratory system through their direct effects on hypoxia sensing mechanisms and interruptions to the normal developmental processes. Thus, precise regulation of oxygen homeostasis is crucial for normal development of the respiratory control network. © 2021 American Physiological Society. Compr Physiol 11:1653-1677, 2021.

Mild maternal sleep-disordered breathing during pregnancy and offspring growth and adiposity in the first 3 years of life

Sleep-disordered breathing (SDB) during pregnancy has been linked to adverse fetal outcomes. Since the intrauterine milieu plays a critical role in childhood growth, we explored the interactions between maternal SDB and offspring growth and adiposity patterns during infancy. Fifty-eight healthy women with uncomplicated pregnancies underwent an objective sleep study and laboratory evaluation during the third trimester, their offspring underwent a 3-year growth surveillance. The 14 (24.1%) women with SDB had a higher body mass index (BMI) (P = 0.003), elevated C-reactive protein levels (P = 0.003), and decreased HDL-cholesterol levels (P = 0.009) than the women without SDB. A general linear model evaluated the interactions between maternal SDB and offspring growth and adiposity measurements after controlling for gestational age and maternal and paternal BMIs. The offspring of mothers with SDB had a significantly smaller head circumference at birth (P = 0.004), with a distinctive pattern of catchup growth by the end of the first year of life (P = 0.018). Their growth pattern was distinguished by compromised birth weight-to-length, rapid catch-up growth, and an increase in both weight-to-length and triceps thickness by the age of three (P < 0.001 and P = 0.001, respectively). Our findings suggest that maternal SDB during pregnancy affects head circumference growth and adiposity acquisition from birth through infancy.

Maternal Sleep-Disordered Breathing in Pregnancy and Increased Nocturnal Glucose Levels in Women with Gestational Diabetes Mellitus

Women with hyperglycemia during pregnancy are at high risk for adverse perinatal outcomes. Maternal sleep-disordered breathing (SDB) during pregnancy is common and is a risk factor for gestational diabetes mellitus (GDM). However, the relationship between SDB severity and glucose control is unknown. Is there an association between SDB severity and glucose levels as assessed by continuous glucose monitoring in GDM? Women with GDM underwent sleep recordings and 72-hour continuous glucose monitoring. Linear mixed models were used to estimate the association of the apnea-hypopnea index (AHI), rapid eye movement (REM)-AHI, and non-REM-AHI with mean glucose levels during nighttime (two periods: 11 pm to 3 am and 3 am to 6 am), daytime (8 am to 9 pm), and 24-hours. Models were adjusted for BMI and antihyperglycemic medications. In 65 participants who were 35 ± 5 (mean ± SD) years of age with BMI of 33 ± 7kg/m2, 31%were undergoing insulin and/or metformin therapy. A ten-unit increase in AHI was associated with elevated nocturnal glucose levels (11 pm to 3 am: 0.20mmol/L [95%CI, 0.04-0.40]) with persistent elevations into the morning (8 am: 0.26mmol/L [95%CI, 0.08-0.4]) when adjusted for BMI and medications. REM-AHI was also associated with higher nocturnal and morning glucose levels, whereas non-REM was not. AHI was not associated with either mean daytime or 24-hour glucose levels. Greater severity of SDB was associated with higher nocturnal and morning glucose levels in women with GDM.

OR10-01 Mild Maternal Sleep Disordered Breathing in Pregnant Women Affects Growth Patterns of Head Circumference and Adiposity During the First Three Years of Life

BackgroundThe intrauterine environment affects growth and adiposity acquisition from the fetal period until adulthood. Mild sleep disordered breathing (SDB) during pregnancy is a common underdiagnosed medical condition in healthy women. We aimed to investigate the interaction between maternal isolated SDB during the third trimester of pregnancy and the offspring’s growth and adiposity during the first three years of life.MethodsHealthy pregnant women in the third trimester of an uncomplicated singleton pregnancy who were followed at the low-risk obstetric surveillance clinic of our hospital were recruited between 4/2013 and 5/2016. They were followed from enrollment until their offspring was three years old. During their third trimester of pregnancy, they underwent an ambulatory overnight sleep study by means of a validated sleep technology [SDB defined as apnea hypopnea index (AHI) ≥5]. Fasting blood samples were drawn on the following morning for glucose, insulin, HbA1c, lipid profile and C-reactive protein (CRP) levels. The offspring’s growth (length, weight and head circumference) and adiposity (subscapular and triceps skinfolds) parameters were measured at birth, 1 and 4 months, and 1, 2, and 3 years of age. Growth parameters were presented as standard deviation scores using the CDC growth charts. A general linear model was used to evaluate the interaction between maternal SDB and her offspring’s growth and adiposity measurements, after controlling for gestational week at delivery and maternal and paternal body mass index (BMI).ResultsFourteen of 58 women (24.1%) were diagnosed with SDB (AHI range 5.3–14.7). They had a significantly higher mean BMI during the third trimester of pregnancy (30.1 ± 3.9 vs 27.2 ± 3.5, P = 0.011), elevated CRP levels, and decreased HDL-cholesterol levels (6.39 ± 2.29 mg/L vs 4.28 ± 2.15 mg/L, P = 0.003 and 67 ± 14 mg/dl vs 82 ± 19 mg/dl, P = 0.009, respectively) compared to women with normal sleep study results. Offspring of mothers with SDB had a smaller mean head circumference SDS at birth (-0.95 ± 0.70 vs -0.30 ± 0.71, P = 0.004), with a distinctive pattern of catchup growth by the end of the first year of life (P = 0.018). They also had increased mean adiposity at birth measured by triceps and subscapular skinfolds (6.8 ± 1.8 mm vs 5.4 ± 1.2 mm, P =0.002 and 5.8 ± 1.3 mm vs 5.0 ± 1.0 mm, P =0.019, respectively), with a distinctive pattern of increased triceps thickness at age 3 years (P = 0.001). There was no significant difference in offspring length or weight between groups.ConclusionsOur findings suggest that isolated maternal SDB during pregnancy affected longitudinal head circumference growth and adiposity acquisition in the fetus and during the first three years of life.

Maternal sleep disordered breathing during pregnancy as a cause of autism relevant neuronal and behavioral aberrations in the offspring.

Sleep disordered breathing (SDB) is characterized by recurring breathing cessations during sleep, causing intermittent hypoxia (oxygen deprivation) often several hundred times per night. SDB is present in ~15% of pregnant women as compared to ~2–4% of non‐pregnant women of childbearing age. Risk factors for gestational SDB development bear striking similarities to the collection of maternal risk factors for autism spectrum disorders (ASD), including advanced maternal age and maternal obesity. Maternal immune activation/inflammation is both a consequence of SDB, and an independent risk factor for, ASD. We posit that an overlooked, yet increasingly common inflammatory stimulus, maternal SDB, contributes to ASD etiology. We recently developed a rat model in which to study the consequences of maternal SDB on the offspring by exposing pregnant rats to nightly intermittent hypoxia from gestational days 10–21. Our findings indicate that offspring of mothers subjected to intermittent hypoxia during pregnancy exhibit deficits in several autism‐relevant behaviors, including a constellation of cognitive impairments, reduced interest in social interaction, and heightened anxiety. In most instances, the magnitude of behavioral disruption was more severe in male than female offspring. To begin to understand the mechanisms contributing to these behavioral aberrations, we examined the density of dendritic spines in the prefrontal cortex (PFC) and CA3 region of the hippocampus. Our data suggest that the offspring of mothers subjected to nightly intermittent hypoxia exhibited a striking increase in dendritic spine density in the PFC when compared to control offspring. However, the dendritic spine density in the CA3 region showed no significant differences between groups. Similar to our behavioral observations, dendritic spine aberrations were more prominent in male vs. female offspring. Additionally, these male offspring showed significant differences in spine morphology when compared to control offspring. Taken together, these findings indicate that maternal sleep disordered breathing not only induces autism‐relevant behavioral impairments, but also mimics the heightened cortical synaptic connectivity phenotypes recently uncovered in autism. Future studies are aimed at identifying a role for microglial inflammation and concomitant reduction in microglial‐mediated synaptic pruning in the behavioral and synaptic structural alterations that we have revealed in this model.Support or Funding InformationR25 Team‐ScienceUW2020 Pilot Award

Sleep Disordered Breathing, a Novel, Modifiable Risk Factor for Hypertensive Disorders of Pregnancy.

Pathophysiology of hypertensive disorders of pregnancy (HDP), especially preeclampsia, has not been fully elucidated. Most trials aimed at the prevention of preeclampsia have failed to show significant benefit and investigation of novel, modifiable risk factors is sorely needed. Sleep disordered breathing (SDB), a group of disorders for which treatments are available, meets these criteria. SDB impacts about a third of all pregnancies and is associated with hypertension in the general non-pregnant population. Recent studies have shown a high prevalence of SDB, especially in complicated pregnancies. Several studies have shown that pregnant women with SDB have a higher risk for developing HDP, and these two disorders are associated with similar maternal long-term cardiovascular outcomes. Based on limited animal models of gestational intermittent hypoxia and human studies, SDB and HDP share similar risk factors and some pathophysiological mechanisms. However, there is paucity of studies addressing causality of this association and identifying therapeutic targets for intervention. Maternal SDB represents a novel and modifiable risk factor of HDP. Further studies are needed in order to establish the exact mechanisms underlying this association and to identify specific areas for clinical interventions.

Sleep disordered breathing in pregnancy: A review of the pathophysiology of adverse pregnancy outcomes.

Sleep disordered breathing (SDB) is a common obesity-related co-morbidity with strong associations to cardiometabolic disease. The risk of SDB is increased during pregnancy, particularly among obese pregnant women. Accumulating evidence suggests that an association exists between maternal SDB and the development of adverse pregnancy outcomes, particularly gestational diabetes and hypertensive disorders of pregnancy. Intermittent hypoxia, a central characteristic of SDB, has been shown in animal and clinical studies to dysregulate several biological pathways. This includes the promotion of oxidative stress, increased inflammation, activation of the hypothalamic-pituitary-adrenal axis, increased sympathetic activity and impaired glucose and insulin metabolism. This review considers how, during pregnancy, these pathophysiological processes are plausible mechanisms through which SDB may contribute to an increased risk of adverse outcomes, for the mother and perhaps also the offspring. However, a lack of robust evidence specific to the pregnant population, including limited evaluation of the placental function in affected pregnancies, limits our ability to draw definite conclusions on mechanisms contributing to adverse pregnancy outcomes and, indeed, the strength of association between SDB and certain pregnancy complications.

An Epworth Sleep Score ≥11 is associated with emergency operative birth and poor neonatal composite outcome at term.

During pregnancy, the Epworth Sleepiness Scale can be used as a surrogate marker for maternal sleep-disordered breathing, a condition that is becoming increasingly prevalent in obstetric populations and is associated with a multitude of pregnancy complications. The aim of this observational study was to investigate the relationship between the Epworth Sleepiness Scale score and indication and mode of delivery during pregnancy. The Epworth Sleepiness Scale was completed by 178 women at Mater Mothers' Hospital, Brisbane, Australia. Women with a score ≥11 were less likely to achieve a spontaneous vaginal delivery (aOR 0.43, 95% CI 0.21-0.88, P=0.02), and were more likely to have an instrumental (aOR 2.81, 95% CI 1.30-6.08, P=0.01) or any operative birth (instrumental and caesarean section aOR 2.32, 95% CI 1.14-4.71, P=0.02). These women were also more likely to have an operative birth for intrapartum fetal compromise (aOR 2.62, 95% CI 1.21-5.69, P=0.015), as well as an infant with poor neonatal outcomes (aOR 2.77, 95% CI 1.09-7.03, P=0.03). These results show that symptoms of sleep-disordered breathing are associated with emergency operative birth, particularly when the indication for operative birth was intrapartum fetal compromise.

0781 Patterns of Fetal Heart Rate Response to Maternal Sleep-Disordered Breathing Events

0781 Patterns of Fetal Heart Rate Response to Maternal Sleep-Disordered Breathing Events

Sleep-Disordered Breathing in Pregnancy

Sleep-disordered breathing (SDB) during pregnancy has emerged as a predictor of both maternal and fetal adverse outcomes. Data suggest that SDB during pregnancy is associated with maternal gestational hypertension and preeclampsia as well as gestational diabetes. Furthermore, there are increasing reports that SDB may play a role in fetal growth restriction, preterm birth, increased cesarean sections, and increased neonatal intensive care unit (NICU) admissions. The public health impact of unrecognized maternal SDB is therefore immense. Treatment of SDB in the general population has been shown to improve cardiovascular outcomes and daytime functioning, and although no large intervention trial has been conducted in pregnant women, small pilot studies demonstrate promising results.

Maternal sleep-disordered breathing and the risk of delivering small for gestational age infants: a prospective cohort study

ObjectiveIt is unclear whether objectively measured maternal sleep-disordered breathing (SDB) leads to poor fetal outcomes. In this study, we prospectively assessed whether polysomnography-based diagnosis of SDB in the third trimester...

Association between maternal symptoms of sleep disordered breathing and fetal telomere length.

Our investigation aims to assess the impact of symptoms of maternal sleep-disordered breathing, specifically sleep apnea risk and daytime sleepiness, on fetal leukocyte telomere length. Pregnant women were recruited upon hospital delivery admission. Sleep exposure outcomes were measured using the Berlin Questionnaire to quantify sleep apnea and the Epworth Sleepiness Scale to measure daytime sleepiness. Participants were classified as "High Risk" or "Low Risk" for sleep apnea based on responses to the Berlin, while "Normal" or "Abnormal" daytime sleepiness was determined based on responses to the Epworth. Neonatal umbilical cord blood samples (N = 67) were collected and genomic DNA was isolated from cord blood leukocytes using Quantitative PCR. A ratio of relative telomere length was derived by telomere repeat copy number and single copy gene copy number (T/S ratio) and used to compare telomere lengths. Bootstrap and ANOVA statistical procedures were employed. On the Berlin, 68.7% of participants were classified as Low Risk while 31.3% were classified as High Risk for sleep apnea. According to the Epworth scale, 80.6% were determined to have Normal daytime sleepiness, and 19.4% were found to have Abnormal daytime sleepiness. The T/S ratio among pregnant women at High Risk for sleep apnea was significantly shorter than for those at Low Risk (P value < 0.05), and the T/S ratio among habitual snorers was significantly shorter than among non-habitual snorers (P value < 0.05). Although those with Normal Sleepiness had a longer T/S ratio than those with Abnormal Sleepiness, the difference was not statistically significant. Our results provide the first evidence demonstrating shortened telomere length among fetuses exposed to maternal symptoms of sleep disordered breathing during pregnancy, and suggest sleep disordered breathing as a possible mechanism of accelerated chromosomal aging.

Maternal Sleep-disordered Breathing and Adverse Pregnancy Outcomes

Maternal Sleep-disordered Breathing and Adverse Pregnancy Outcomes

The effect of maternal sleep-disordered breathing on the infant’s neurodevelopment

We sought to examine the effect of maternal sleep-disordered breathing (SDB) on infant general movements (GMs) and neurodevelopment. Pregnant women with uncomplicated full-term pregnancies and their offspring were prospectively recruited from a community and hospital low-risk obstetric surveillance. All participants completed a sleep questionnaire on second trimester and underwent ambulatory sleep evaluation (WatchPAT; Itamar Medical, Caesarea, Israel). They were categorized as SDB (apnea hypopnea index>5) and controls. Infant GMs were assessed in the first 48 hours and at 8-11 and 14-16 weeks of age. At 12 months of age the Infant Developmental Inventory and the Brief Infant Sleep Questionnaire were administered. In all, 74 women and their full-term infants were studied. Eighteen (24%) women had SDB. Mean birthweight was 3347.1±423.9 g. Median Apgar score at 5 minutes was 10 (range, 8-10). In adjusted comparisons, no differences were found between infants born to mothers with SDB and controls in GM scores in all 3 evaluations. Low social developmental score was detected at 12 months in 64% of infants born to SDB mothers compared to 25% of infants born to controls (adjusted P=.036; odds ratio, 16.7). Infant snoring was reported by 41.7% of mothers with SDB compared to 7.5% of controls (P=.004). Our preliminary results suggest that maternal SDB during pregnancy has no adverse effect on neonatal and infant neuromotor development but may affect social development at 1 year.