Maternal Obstructive Sleep Apnea Research Articles

Gestational intermittent hypoxia reduces mandibular growth with decreased Sox9 expression and increased Hif1a expression in male offspring rats.

Maternal obstructive sleep apnea (OSA) during pregnancy is the risk factor for impaired fetal growth with low birth weight in the offspring. However, it is unclear whether gestational intermittent hypoxia (IH, a hallmark of maternal OSA) has long-term detrimental consequences on the skeletal development of offspring. This study aimed to investigate postnatal maxillofacial bone growth and cartilage metabolism in male and female offspring that were exposed to gestational IH. Mother rats underwent IH at 20 cycles/h (nadir, 4% O2; peak, 21% O2; 0% CO2) for 8h per day during gestational days (GD) 7-20, and their male and female offspring were analyzed postnatally at 5 and 10weeks of age. All male and female offspring were born and raised under normoxic conditions. There was no significant difference in whole-body weight and tibial length between the IH male/female offspring and their control counterparts. In contrast, the mandibular condylar length was significantly shorter in the IH male offspring than in the control male offspring at 5 and 10weeks of age, while there was no significant difference in the female offspring. Real-time polymerase chain reaction (PCR) showed that gestational IH significantly downregulated the mRNA level of SOX9 (a chondrogenesis marker) and upregulated the mRNA level of HIF-1α (a hypoxia-inducible factor marker) in the mandibular condylar cartilage of male offspring, but not in female offspring. Gestational IH induced underdeveloped mandibular ramus/condyles and reduced mRNA expression of SOX9, while enhancing mRNA expression of HIF-1α in a sex-dependent manner.

Effect of Obstructive Sleep Apnea during Pregnancy on Fetal Development: Gene Expression Profile of Cord Blood.

Obstructive sleep apnea (OSA) is quite prevalent during pregnancy and is associated with adverse perinatal outcomes, but its potential influence on fetal development remains unclear. This study investigated maternal OSA impact on the fetus by analyzing gene expression profiles in whole cord blood (WCB). Ten women in the third trimester of pregnancy were included, five OSA and five non-OSA cases. WCB RNA expression was analyzed by microarray technology to identify differentially expressed genes (DEGs) under OSA conditions. After data normalization, 3238 genes showed significant differential expression under OSA conditions, with 2690 upregulated genes and 548 downregulated genes. Functional enrichment was conducted using gene set enrichment analysis (GSEA) applied to Gene Ontology annotations. Key biological processes involved in OSA were identified, including response to oxidative stress and hypoxia, apoptosis, insulin response and secretion, and placental development. Moreover, DEGs were confirmed through qPCR analyses in additional WCB samples (7 with OSA and 13 without OSA). This highlighted differential expression of several genes in OSA (EGR1, PFN1 and PRKAR1A), with distinct gene expression profiles observed during rapid eye movement (REM)-OSA in pregnancy (PFN1, UBA52, EGR1, STX4, MYC, JUNB, and MAPKAP). These findings suggest that OSA, particularly during REM sleep, may negatively impact various biological processes during fetal development.

Gestational Intermittent Hypoxia Impairs AT2R-Mediated Vascular Protection in Female Offspring on a High-Fat, High-Sucrose Diet.

Gestational intermittent hypoxia (GIH), a hallmark of maternal obstructive sleep apnea, sex-differentially causes hypertension and endothelial dysfunction in adult male offspring but not in females. This study investigated whether the GIH-exposed female offspring, a "protected" group against the hypertensive effects of maternal GIH exposure, exhibit increased susceptibility to hypertension and cardiovascular dysfunction when fed a high-fat high-sucrose (HFHS) diet and whether this effect could be reversed by pharmacological intervention activating the angiotensin II type 2 receptor (AT2R). Female offspring of control and GIH-exposed (10.5% O2, 8 h/d, E10-21) dams were assigned either an HFHS diet or a standard diet from 12 weeks of age. Blood pressure was monitored. At 28 weeks, a systemic CGP42112 (AT2R agonist) or saline infusion was administered through the osmotic pump. At 30 weeks, the heart was weighed and collected for H&E staining, mesenteric arteries for vascular reactivity assessment and protein analysis, and plasma for ELISA. The HFHS diet induced similar increases in body weight gain and blood pressure in control and GIH female offspring. HFHS feeding did not affect heart structure, but impaired endothelial-dependent vascular relaxation with associated decreased AT2R and eNOS expression and reduced plasma bradykinin levels in both control and GIH offspring. CGP42112 administration effectively mitigated HFHS-induced hypertension and endothelial dysfunction only in control offspring, accompanied by restored AT2R, eNOS, and bradykinin levels, but not in the GIH counterparts. These findings suggest that GIH induces endothelial dysfunction and AT2R insensitivity in female offspring exposed to an HFHS diet.

Maternal obstructive sleep apnea aggravates metabolic dysfunction-associated fatty liver disease via HMGB1-TLR4 signaling-mediated endoplasmic reticulum stress in male offspring rats

Aims/hypothesisMaternal obstructive sleep apnea (MOSA) may inflict long-term metabolic effects on offspring. We hypothesize that MOSA increases the propensity for metabolic dysregulation in offspring and thus facilitates the development of metabolic dysfunction-associated fatty liver disease (MAFLD). This study aims to test the hypothesis and explore the underlying mechanism. MethodsThe MOSA rat model of upper airway obstruction was established and fecundated. The postweaning male offspring (n = 171) from both the control group and MOSA group were randomly fed the normal chow diet (NCD, n = 89) or high-fat diet (HFD, n = 82) for the next 5 months. Liver function, lipid profile, glucose, and insulin levels were measured. Expression levels of fibrosis-related proteins and endoplasmic reticulum (ER) stress-related proteins in liver tissues were assessed using immunohistochemistry and western blotting. ResultsMOSA increased body and liver weight in male offspring, along with augmented liver organ coefficient. Serum levels of aminotransferases, low-density lipoprotein, high-density lipoprotein, triglycerides, total cholesterol, total bile acid, fasting glucose, and insulin increased significantly. MOSA exacerbated HFD-induced hepatic steatosis and fibrosis. These effects were driven by the overactivated double-stranded RNA-activated protein kinase (PKR)-like eukaryotic initiation factor 2(PERK)-activating transcription factor (ATF)4-C/EBP homologous protein (CHOP) signaling pathway-induced ER stress, and hyperacetylation and release of high mobility group box-1(HMGB1) elicited above signaling in a TLR4-dependent manner. ConclusionsThese findings indicate that MOSA can exert prolonged adverse effects manifested as metabolic dysfunction in male offspring. Therefore, surveillance and management of OSA during pregnancy may be necessary to prevent and alleviate MAFLD in offspring.

Epidemiological Study of Parental Obstructive Sleep Apnea and Subsequent Risk of ADHD in Their Children: A Nationwide Population-Based Study

Objective: Obstructive sleep apnea (OSA), with daytime drowsiness, nocturnal hypoxia, could result in systemic inflammation and oxidative damage. We hypothesize that parental OSA, with chronic systemic inflammation and oxidative stress, might contribute to children’s neurodevelopmental disorders, such as ADHD. Method: By linking National Birth Registry with the National Health Insurance Research Database, Taiwan, we identified 2006–2015 birth cohort, which comprised 1,723,873 singleton live births, and conducted a nested case-control study. We included children with ADHD and compared them with non-ADHD controls matched with ADHD case on index date. Conditional logistic regression was utilized to calculate adjusted odds ratio (aOR) when investigating the association between parental diseases with risk of ADHD in their offspring. Results: The aOR (95% CI) of offspring’s ADHD was 1.758 (1.458–2.119) with paternal OSA and 2.159 (1.442–3.233) with maternal OSA. The subgroup analysis revealed different effects of parental diseases among children’s gender. Conclusion: Our study demonstrates an association in parental OSA and offspring ADHD, which could inspire further research to clarify the mechanisms.

Early developmental outcome in children born to mothers with obstructive sleep apnea

Obstructive sleep apnea (OSA) during pregnancy leads to adverse maternal and perinatal outcomes. There have been limited studies evaluated the effect of intrauterine exposure to maternal OSA on childhood developmental outcomes. This study was aimed to evaluate the early development of children born to mothers with gestational OSA and the impact of continuous positive airway pressure (CPAP) treatment. MethodsChildren aged 6–36 months, born to high risk pregnant mothers who had overnight polysomnography performed, were invited to participate. The Ages and Stages Questionnaires, third edition (ASQ-3), age-specific parent-completed questionnaires determining five developmental domains (communication, gross motor, fine motor, problem-solving, and personal-social) were used for developmental screening. Children who had a score of at least one domain less than −1 SD of age cut-off were determined as having a risk of developmental delay (RDD). ResultsThere were 159 children (47% male, mean age 18 months) enrolled. The maternal PSG showed non-OSA, mild OSA, and moderate OSA in 14%, 46%, and 40%, respectively. Forty-two children (26%) had RDD, and the most affected domains were fine motor and problem-solving. Maternal moderate OSA was significantly associated with RDD (adjusted OR 5.39, 95%CI 1.11–26.12, P 0.037). Subgroup analysis showed that maternal moderate OSA with no CPAP treatment was significantly associated with RDD (OR 6.43, 95%CI 1.34–30.89, P = 0.020) ConclusionGestational moderate OSA in high-risk pregnancy mothers likely had a negative effect on early childhood developmental outcomes, particularly the mothers who did not have appropriate CPAP treatment.

Is OSA risk proportional to BMI or parentally mediated? A questionnaire-based study in a cohort of Egyptian children

IntroductionThere is an increased body of evidence that Obstructive Sleep apnea (OSA) in obese patients has familial tendencies. This familial predilection might be mediated through tendencies to atopy with subsequent nasal obstruction, tendencies to adenotonsillar enlargement by fat deposition, or through differential fatty deposits in the airway. The aim of this study was to study if paternal or maternal OSA might be predictive of OSA in offspring and to determine the relationship of OSA to Body Mass Index (BMI), gender, and waist circumference (WC). Methods100 obese patients retrieved from a consortium of Egyptian Schools were screened and their parents using sleep apnea clinical score (SACS), their gender, BMI, and WC were noted. For the performance of Receiver Operating Characteristic study, obese children were divided according to their SACS into high risk (1) (SACS>75) and low risk (0) (SACS≤75). The sensitivity of each of BMI, WC, gender, paternal and maternal SACS as predictors of OSA high risk was determined. Results: Paternal OSA risk was the single significant predictor of OSA risk in obese children (Sensitivity: 89%, Specificity: 97%), WC was the second-best predictor (Sensitivity: 78%, Specificity: 89%), female offsprings were at higher risk to be involved, BMI was a weak predictor of OSA risk with a cut off>34. Finally, yet importantly, maternal OSA risk was unrelated to OSA risk in obese children. ConclusionThis study confirms that genetic factors might play a much more important role than the degree of obesity in determining OSA risk in obese patients, these findings open the door to more in-depth studies to understand the genetic mechanisms involved in such a relationship.

Sex‐Specific Alterations in LPS‐Induced Peripheral and Central Inflammation in Adult Offspring Exposed to Gestational Intermittent Hypoxia: Potential Regulation by miR‐146

The prevalence of obstructive sleep apnea (OSA) and concomitant intermittent hypoxia (IH) in pregnant women is rising in parallel with the obesity epidemic. IH causes profound inflammation, and it is well‐established that maternal immune activation can lead to detrimental outcomes in her offspring. Although in recent years the acute consequences of maternal OSA on the health of both the mother and the newborn have become better appreciated, little remains known about the potential long‐lasting consequences to the offspring in adulthood. Given the effect of inflammation on the neural control of breathing, we studied the consequences of gestational intermittent hypoxia (GIH) on the central and peripheral immune responses of adult male and female offspring. We exposed rat dams to IH from gestational days 10–21 (8hrs/day, 2 min cycles alternating between 10.5% O2 and 21%O2, mimicking the desaturation and resaturation kinetics of human OSA). We challenged the adult offspring with a peripheral LPS injection (1 mg/kg i.p., 3 hrs) and assessed neural (whole brain homogenates) and peripheral (spleen) cytokine gene expression. We found that GIH gene‐specifically enhanced LPS‐induced neuroinflammation in adult offspring of both sexes. Conversely, while LPS‐induced peripheral inflammation was unchanged in GIH male offspring, it was strongly attenuated in GIH females, suggesting that the central and peripheral immune responses are differentially impacted by GIH, and that these effects differ by sex. Because microRNAs (miRNAs) are critical regulators of the immune response, we tested the hypothesis that miRNAs are differentially expressed in male and female GIH offspring. In spleens from adult GIH offspring, we screened the levels of several immunoregulatory miRNAs. Interestingly, miR‐146, a strongly immunosuppressive miRNA, was highly upregulated in female spleens. We suggest that augmented miR‐146 levels suppress peripheral immune responses to an inflammatory challenge in GIH offspring, and that miR‐146 levels will be reduced in the brain where neuroinflammation is enhanced in GIH offspring. Studies are underway using lentiviral‐mediated manipulation of miR‐146 activity to more directly test this hypothesis, and to understand how central and peripheral inflammation are ultimately regulated in the context of GIH. Regulating miR‐146 expression in adults exposed to maternal OSA in utero may represent a novel therapeutic target to control the detrimental consequences of aberrant inflammatory signaling.Support or Funding InformationSupported by NIH R01 NS085226 and HL105511, and a Wisconsin Alumni Research Foundation UW2020 grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The effect of maternal obstructive sleep apnea on the placenta.

Obstructive sleep apnea (OSA) during pregnancy has been associated with adverse maternal outcomes. However, the effect of maternal OSA on fetal growth is less clear. The placenta is a critical organ for fetal growth and development and the principal determinant of birthweight. We aimed to investigate the effect of maternal OSA on placental growth and function. Placentas of women recruited to a prospective longitudinal study were consecutively obtained immediately after delivery. Each placenta was measured for length, width, and thickness. Total RNA was isolated for gene expression analysis of VEGF, VEGF receptor, PIGF, and leptin. Histological and morphometric evaluations of the placenta were performed. A total of 53 placentas were investigated. Ten women (19%) had OSA, and the weight of their placentas was significantly higher compared with the placentas of the controls (526.1 ± 83.9 vs. 425.7 ± 95.5 g, p = 0.004). There was a significant positive correlation between placental weight and the log apnea-hypopnea index even after controlling for maternal body mass index (BMI; r = 0.31, p = 0.04). The birthweight/placental weight ratio was significantly lower in women with OSA compared with controls (p = 0.03). Placental weight and newborn triceps adiposity thickness correlated positively after controlling for maternal BMI (r = 0.29, p = 0.04). Leptin expression was 1.8-fold higher in placentas of women with OSA compared with controls (p = 0.02). No histological differences were found between the groups. Maternal OSA is associated with increased placental weight that correlated with OSA severity and neonatal adiposity independently of maternal BMI. Placental leptin overexpression may mediate/underlie the above findings.Trial Registration: Clinical Trials NCT00931099.

Maternal obstructive sleep apnea and neonatal birth outcomes in a population based sample

ObjectiveEvaluate the association of OSA with birth outcomes including the risk of congenital anomalies and the need for a higher level of clinical care at delivery. MethodsPopulation-based study that linked newborn records with maternal records. Data from 95 perinatal centers across all geographic census divisions of the U.S. of women with a delivery diagnosis from 2010 to 2014 whose records could be linked to the corresponding newborn record. An International Classification of Diseases, ninth Revision (ICD-9) code for sleep apnea was used to identify exposure and outcome variables. Univariate and multivariate logistic regression analyses were performed with a model that included substance use, obesity, diabetes, maternal co-morbidities, and pregnancy complications. ResultsIn this study, 1,423,099 maternal records were linked to live newborn records. OSA was associated with a higher risk for congenital anomalies in offspring (aOR 1.26, 1.11 to 1.43), with the highest risk being that of musculoskeletal anomalies (aOR 1.89, 1.16 to 3.07) after adjusting for comorbidities and potential teratogens. Neonates born to mothers with OSA were more likely to be admitted to the intensive care unit (25.3% vs. 8.1%, p < 0.001), require resuscitation (aOR 2.76, 1.35 to 5.64) and have a longer hospital stay (aOR 2.25, 1.85 to 2.65). ConclusionsAlthough our study does not establish causation, it is the first to demonstrate a higher risk of congenital anomalies and resuscitation at birth in neonates of mothers with OSA, emphasizing the importance of identifying OSA in pregnant women and women of reproductive age.

Mild Maternal Obstructive Sleep Apnea in Non-obese Pregnant Women and Accelerated Fetal Growth

The prevalence of obstructive sleep apnea (OSA) during pregnancy is rising. OSA during pregnancy has been associated with hypertensive disorders of pregnancy and gestational diabetes. The effect of maternal OSA on the fetus, particularly on fetal growth, is less apparent. Most of the currently available human data is based on non-objective assessment of OSA and includes heterogeneous populations with inadequate control on confounders, such as maternal obesity and pregnancy complications. Using objective tools in non-obese women with uncomplicated pregnancies, we aimed to investigate the association between maternal OSA and fetal growth. A total of 155 non-obese pregnant women were recruited. Birth-weight percentile of the newborns of women with mild OSA was significantly higher compared with the newborns of non-OSA controls (72% vs. 57%, respectively, P < 0.01). Birth-length and triceps thickness measurements were significantly higher among the newborns of women with OSA compared with controls (P = 0.02 for both). The proportion of large for gestational age (LGA) newborns was higher among women with OSA compared with controls (28% vs. 8%, respectively, P = 0.04). Our results suggest that maternal OSA during the third trimester of pregnancy - even in a mild form -is associated with accelerated fetal growth.

Effects of maternal obstructive sleep apnea on fetal growth: a case-control study.

ObjectiveTo investigate whether maternal obstructive sleep apnea (OSA) is associated with changes in fetal growth trajectory.Study DesignRetrospective review of pregnant women who underwent overnight polysomnography. Fetal growth was estimated using sonographic biometric measurements obtained during routine prenatal care. Customized estimated fetal weight and birth weight centiles were calculated and impaired fetal growth was defined as birth weight <10th centile or a slowing of fetal growth by >33% during the last trimester. Logistic regression models were used to determine the relationship between maternal OSA and altered fetal growth after adjusting for potential covariates.ResultsThere were 48 women without and 31 women with OSA. There were no differences in the proportion of infants with birth weight <10th centile between women with and without OSA (23% vs. 25%, p=1.0), However, the presence of maternal OSA was predictive of impaired fetal growth (aOR 3.9, 95% CI 1.2–12.6). Logistic regression models were repeated using only a slowing of fetal growth in the 3rd trimester (excluding birth weight <10th centile) and OSA predicted a slowing in fetal growth across the 3rd trimester (aOR 3.6, 95% CI 1.4–9.4). Fourteen additional women were treated with positive airway pressure during pregnancy; fetal growth was not significantly different in these women compared to controls.ConclusionObstructive sleep apnea is independently associated with altered fetal growth, which appears to be ameliorated with use of positive airway pressure.

Phenotypes of sleep-disordered breathing symptoms to two years of age based on age of onset and duration of symptoms

ObjectiveChildhood sleep-disordered breathing (SDB) symptoms may comprise multiple phenotypes depending on craniofacial anatomy, tonsil and adenoid growth, body habitus, and rhinitis symptoms. The primary objective of this study is to identify and characterize the different SDB phenotypes to two years of age. MethodsData from 770 infants in the Edmonton sub-cohort of the Canadian Healthy Infant Longitudinal Study (CHILD) were analyzed to identify SDB phenotypes based on age of onset and duration of symptoms. Parents completed the 22-item sleep-related breathing disorder (SRBD) scale. Children with a SRBD ratio greater than 0.33 were considered positive for SDB at each quarterly assessment between three months and two years. The STATA Proc trajectory extension identified SDB phenotypes based on their age of onset and duration of symptoms and attributed the percentage chance of a participant being assigned to each phenotype. Multivariate linear regression identified factors associated with increased risk of being assigned to each SDB phenotype. ResultsTrajectory analysis identified four phenotypes: no SDB (65.7%), early-onset SDB (15.7%) with peak symptoms at nine months, late-onset SDB (14.2%) with peak symptoms at 18 months, and persistent SDB (5.3%) with symptoms from 3 to 24 months. Rhinitis was associated with all three SDB symptom trajectories (p < 0.05). Children with gastroesophageal reflux disease presented with early (p = 0.03) and late SDB (p < 0.001). Maternal obstructive sleep apnea syndrome (OSAS) was associated with persistent (p = 0.01) and late SDB (p < 0.001). Atopy (positive skin prick test at one year) was associated with persistent SDB (p = 0.04). Infants born prior to 36.5 weeks gestational age were more likely to present with late SDB (p = 0.03). ConclusionChildhood SDB symptoms, rather than being a homogenous disorder, may comprise multiple overlapping phenotypes each with unique risk factors.

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats

Obstructive sleep apnea (OSA) is common in pregnancy and may compromise fetal and even postnatal development. We developed an animal model to determine if maternal OSA could have lasting effects in offspring. Pregnant Sprague-Dawley rats were exposed to reduced ambient O2 from 21 to 4-5%, approximately once per minute [chronic intermittent hypoxia (CIH)] for 8 h/day during gestation days 3-19. Similarly handled animals exposed to ambient air served as controls (HC). Offspring were studied for body growth and cardiovascular function for 8 postnatal weeks. Compared with HC, prenatal CIH led to growth restriction, indicated by smaller body weight and tibial length, and higher arterial blood pressure in both male and female offspring. Compared with same-sex HC, CIH males showed abdominal obesity (greater ratio of abdominal fat weight to body weight or tibial length), left ventricular (LV) hypertrophy (greater heart weight-to-tibial length ratio and LV posterior wall diastolic thickness), elevated LV contractility (increases in LV ejection fraction, end-systolic pressure-volume relations, and preload recruitable stroke work), elevated LV and arterial stiffness (increased end-diastolic pressure-volume relationship and arterial elasticity), and LV oxidative stress (greater lipid peroxide content). Compared with female CIH offspring, male CIH offspring had more profound changes in blood pressure (BP), cardiac function, myocardial lipid peroxidase (LPO) content, and abdominal adiposity. Rodent prenatal CIH exposure, mimicking human maternal OSA, exerts detrimental morphological and cardiovascular effects on developing offspring; the model may provide useful insights of OSA effects in humans. NEW & NOTEWORTHY Obstructive sleep apnea is common in human pregnancy. Following maternal exposure to chronic intermittent hypoxia, a hallmark of sleep apnea, both sexes of rat offspring showed growth retardation, with males being more vulnerable to hypertension and dysfunctional left ventricular changes. This model is useful to study detrimental effects of maternal obstructive sleep apnea on developing offspring in humans.

Rhinitis and pregnancy: literature review

IntroductionThere is a controversy concerning the terminology and definition of rhinitis in pregnancy. Gestational rhinitis is a relatively common condition, which has drawn increasing interest in recent years due to a possible association with maternal obstructive sleep apnea syndrome (OSAS) and unfavorable fetal outcomes. ObjectiveTo review the current knowledge on gestacional rhinitis, and to assess its evidence. MethodsStructured literature search. ResultsGestational rhinitis and rhinitis “during pregnancy” are somewhat similar conditions regarding their physiopathology and treatment, but differ regarding definition and prognosis. Hormonal changes have a presumed etiological role, but knowledge about the physiopathology of gestational rhinitis is still lacking. Management of rhinitis during pregnancy focuses on the minimal intervention required for symptom relief. ConclusionAs it has a great impact on maternal quality of life, both the otorhinolaryngologist and the obstetrician must be careful concerning the early diagnosis and treatment of gestational rhinitis, considering the safety of treatment measures and drugs and their current level of evidence.

Maternal obstructive sleep apnea and admissions to the neonatal intensive care unit

Snoring and excessive daytime sleepiness are classic symptoms of obstructive sleep apnea (OSA). This condition is associated with significant pathophysiologic sequelae, including intermittent hypoxemia and hypertension. Multiple factors present during pregnancy increase the risk for OSA, and the presence of OSA during pregnancy has been associated with untoward consequences to both the mother and fetus. We studied the impact of maternal OSA during pregnancy on a group of infants admitted to the neonatal intensive care unit (NICU). Our study group consisted of postpartum mothers who had delivered an infant admitted to the NICU within the previous 24 h. Data was collected between 6/09 and 3/12. Mothers were randomly selected and they were asked to complete two standardized questionnaires (Epworth Sleepiness Scale and Snoring Symptoms Inventory) to identify symptoms of OSA, specifically excessive daytime sleepiness and snoring. Maternal data regarding age, race, health status, pregnancy, labor, and delivery and infant data regarding gestational age, birthweight, and Apgar scores were collected. We enrolled 115 mothers. Their mean age was 34 ± 5 years. Seventy percent were Caucasian, 18% Hispanic, 6% African American, and 5% Asian. Smoking and alcohol use during pregnancy were reported in 2%. Most deliveries were via elective c-section (42%), followed by NSVD (32%), and emergency c-section in 24%. The relationship between the ESS and the SSI was analyzed using a Pearson Correlation Statistic ( r ). A high correlation between the two measures was seen ( r = 0.506; p < 0.0001). The relationships among ESS totals and SSI totals and pregnancy outcomes were analyzed. Elevated scores on the SSI were associated with adverse pregnancy outcomes, most significantly with preeclampsia. Lower infant Apgar scores were also noted. Pregnant women who demonstrate excessive daytime sleepiness are more likely to have sleep disturbances associated with snoring. Elevated scores on the SSI are associated with adverse prenancy outcomes. We found symptoms of maternal OSA in a high percentage of infants requiring admission to a NICU. The potential for treatment of OSA using CPAP underscores the importance of early diagnosis in pregnant women. NICU staff at The Valley Hospital for their support in completing this study.

Obstructive sleep apnea and pregnancy: the effect on perinatal outcomes

Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction, resulting in hypoxemia, hypercapnia and sleep fragmentation. Pathophysiological sequelae include sympathetic activation, increased oxidative stress and a generalized inflammatory response, culminating in endothelial dysfunction. These are the proposed mechanisms that mediate the increased risk of hypertension and cardiovascular disease among patients with OSA outside of pregnancy. It is intriguing to consider the consequences of these events on pregnancy outcomes. There is a growing literature on the impact of maternal OSA on hypertensive disorders of pregnancy, gestational diabetes and impaired fetal growth. The data, while promising, require confirmation with larger numbers to verify the findings. OSA may be an important mediator of the poor perinatal outcomes associated with maternal obesity; moreover, one which may be amenable to treatment. This review discusses OSA and summarizes the current literature linking OSA with adverse perinatal outcomes.

Optical coherence tomography captures rapid hemodynamic responses to acute hypoxia in the cardiovascular system of early embryos

The trajectory to heart defects may start in tubular and looping heart stages when detailed analysis of form and function is difficult by currently available methods. We used a novel method, Doppler optical coherence tomography (OCT), to follow changes in cardiovascular function in quail embryos during acute hypoxic stress. Chronic fetal hypoxia is a known risk factor for congenital heart diseases (CHDs). Decreased fetal heart rates during maternal obstructive sleep apnea suggest that studying fetal heart responses under acute hypoxia is warranted. We captured responses to hypoxia at the critical looping heart stages. Doppler OCT revealed detailed vitelline arterial pulsed Doppler waveforms. Embryos tolerated 1 hr of hypoxia (5%, 10%, or 15% O(2) ), but exhibited changes including decreased systolic and increased diastolic duration in 5 min. After 5 min, slower heart rates, arrhythmic events and an increase in retrograde blood flow were observed. These changes suggested slower filling of the heart, which was confirmed by four-dimensional Doppler imaging of the heart itself. Doppler OCT is well suited for rapid noninvasive screening for functional changes in avian embryos under near physiological conditions. Analysis of the accessible vitelline artery sensitively reflected changes in heart function and can be used for rapid screening. Acute hypoxia caused rapid hemodynamic changes in looping hearts and may be a concern for increased CHD risk.