Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_41_библиотеки_им_акад_М_И_Перельмана

With regard to maternal health, few studies have specically investigated the relationships between sleep duration and blood pressure in pregnancy. In a self­report study, Williams etal. found that both maternally reported short sleep duration (dened as ≤6hours) and long sleep duration (dened as at least 9hours) in early pregnancy were both associated with increases in systolic and diastolic blood pres­sure in the third trimester [15]. In particular, a report of <5hours’ sleep was found to have a particularly high odds of preeclampsia (aOR 9.5, 95%CI 1.8–49.4), although sleeping more than 10hours did not show an increase in preeclampsia: aOR 2.5 (95%CI 0.7–8.2) [15]. Conversely, results from an actigraphy-based study in over 700 women found no relationship between short sleep duration (dened as <7hours) and a diagnosis of hypertension [16]. Recently, Tang etal. have demon­strated that in the rst trimester, both systolic and diastolic blood pressure was lower in women who slept longer; in longitudinal analyses across pregnancy, women with longer sleep durations had lower systolic blood pressure [17].

Associations between sleep duration and gestational diabetes (GDM) have been studied more than maternal blood pressure. A large study of >1200 women found that GDM risk was increased among those who slept ≤4hours per night when com­pared to those sleeping at least 9hours per night, with a relative risk (RR) of 5.6 (95%CI 1.3–23.7) [18]. Sleep duration has been reported to have a “J”-shaped asso­ciation with GDM; in over 900 women, with sleep durations of ≥9 hours and <7hours, the odds for GDM were 1.2 (95%CI 1.0–1.4) and 1.4 (95%CI 0.9–2.1), respectively, although the proportion of women in the short sleep category was

small [19]. In a cohort of over 600 multiethnic Asian women, those who reported sleeping less than 6hours per night had the highest frequency of GDM compared to those who slept 7–8hours per night (27.3% vs. 16.8%), and fasting glucose levels were observed to decrease linearly with increasing sleep duration [20]. However, after accounting for other covariates, no relationship with sleep duration and glu­cose levels was evident. Associations between sleep duration and GDM have been reported to differ by prepregnancy obesity status. Findings from the multi-site Fetal Growth Study of approximately 2500 women [21] found that the association between maternal sleep duration and GDM was only signicant among nonobese women, with a twofold higher increased risk of GDM in women who reported more or less than 8–9hours. The highest adjusted relative risk for GDM (aRR 2.5, 95%CI

1.27–5.0) was observed among nonobese women who slept 5–6hours in the second trimester. Specically, in women who slept <7hours, the risk for GDM was more than twice that of women who slept 8–9 (aRR 2.5, 95%CI 1.2–5.1), with long sleep­ers (at least 10hours) who rarely or never napped having the highest risk of GDM (aRR 3.1, 95%CI 1.0–9.2) [21]. Napping appears to modify the sleep-GDM asso­ciation with a signicant association among women who rarely or never napped in the second trimester. Recent work in Chinese pregnant women supports these nd­ings; the inuence of shorter nighttime sleep duration on GDM was found to be weaker in women with more napping, and midday napping reduced the risk of GDM among women with insufcient sleep [22].

Objective data from 782 women with actigraphy also supports that sleep dura­tion <7 hours per night is associated with an increased risk of GDM (aOR 2.2, 95%CI 1.1–4.5) [16]. Furthermore, an individual patient data (IPD) meta-analysis has demonstrated that pregnant women who slept <6–7hours were at higher odds of GDM compared to those without short sleep: aOR 1.7 (95%CI, 1.2–2.3) [23]. In addition, compared to sleeping >6.25 hours, women who slept ≤6.25 hours had higher 1-hour glucose levels and an increased odds of GDM, aOR 2.8 (95%CI

of sleep at 30weeks’ gestation that had smaller babies than women who reported more than 9hours’ sleep [13].

Nonetheless, it should be noted that cross-sectional studies have limitations when measuring fetal outcomes. Insults in early pregnancy may inuence subse­quent fetal growth, which is not captured with cross-sectional designs. Longitudinal studies are therefore critical to investigate the impacts of maternal sleep on fetal health. For example, in 1500 women who were assessed at several times across pregnancy, those sleeping at least 9hours per night hours before the 17- and 28-week assessments had mean birth weights 74g and 60g higher, respectively, compared to other women, and a linear trend was evident at 17weeks [28]. In contrast, cross­sectional studies of those sleeping more than 9hours per night nd no association with a single measure of birth weight [25]. In a large cohort of over 3500 women, those who slept <7hours in early pregnancy, compared to those who slept 8–9hours, had a shorter birth length by 2.4mm and a 42.7g reduction in birth weight. The risk of low birth weight increased 83% and the risk of SGA increased 56% in women sleeping <7 hours [29]. More recently, a Brazilian study reported rst-trimester 24-hour sleep duration and its change throughout pregnancy were inversely associ­ated with birth weight such that women with greater decreases in sleep duration gave birth to infants with lower birth weight z-scores [30]. These ndings were only in nulliparous women and no associations were detected in multiparous women. In a large study of women who had delivered at full term, no association between sleep durations in the second trimester was found with SGA [31]. A recent study in which subjective and objective sleep measures were collected in 166 low-risk women found that shorter self-reported sleep duration (but not actigraphy-assessed dura­tion) was associated with shorter gestational age [32]. The authors posited that in otherwise healthy women, there appears to be minimal evidence that sleep measures in early gestation impact pregnancy outcomes. Despite this, ndings of recent meta­analyses suggest that women with the shortest sleep duration have an increased rela­tive risk of preterm birth compared to women with the longest sleep durations (RR1.23, 95%CI 1.01–1.50) [33] although ndings are unclear in regard to whether short– or long– sleep duration impacts fetal growth as the adjusted odds ratios for SGA and large for gestational age (LGA) were found to be 1.3 “(95%CI 0.9–2.0) and 1.5 (95%CI 0.7–2.8) [34]. However, it should be noted that both of the latter meta- analyses included cross-sectional studies as well as longitudinal ones.

The National Women’s Sleep Poll (www.sleepfoundation.org) found that 30% of pregnant women rarely/never get a good night’s sleep, which is twice as many as nonpregnant women who endorsed the same question. Reasons for this include increased need to urinate, difculty nding comfortable sleeping positions, and body aches [35]. Prevalence estimates of poor sleep quality in pregnancy, as mea­sured by the Pittsburgh Sleep Quality Index (PSQI) [36] with a score of at least 5,

3.6, 95%CI 1.1–11.7), but isolated insomnia had no association [68]. The same study also demonstrated that isolated insomnia increased the odds for babies being born large for gestational age even after adjustment for confounders. An observa­tional study of approximately three million women reported that a diagnosis of insomnia was associated with a 30% in the odds of preterm birth [69]. Furthermore, women with a recorded insomnia diagnosis were almost twice as likely to deliver before 34weeks’ gestation (OR 1.7, 95% CI 1.1–2.6) compared to women without a sleep disorder diagnosis, and the risk was highest for preterm premature rupture of membranes at less than 34weeks (OR 4.1, 95% CI 2.0–8.3). It should be noted insomnia is often discussed in the context of poor sleep quality and insufcient sleep, both of which have been associated with poor pregnancy outcomes [9], but studies focused on insomnia and pregnancy outcomes are lacking.

1.3–1.6 [34]. While these ndings may appear counterintuitive, it is plausible that the underlying mechanisms of SDB may differentially affect fetal growth such that hypertension and its associated sympathetic activation may be associated with fetal growth restriction, while a poor metabolic environment may be more likely to be related to macrosomia.

Symptoms of restless leg syndrome (RLS) increase as pregnancy progresses, peak­ing in third trimester and resolving a few days before delivery [115–118]. A recent meta-analysis [119] reported that the frequency of RLS increases across the rst, second, and third trimesters of pregnancy, with 8%, 16%, and 22% of women, respectively, reporting RLS symptoms, with a large decrease in frequency to 4% after delivery. RLS symptoms are associated with shorter total sleep time, more dif­culty initiating and maintaining sleep, and more daytime sleepiness compared to pregnant women without RLS [115, 116, 118, 120]. In extreme cases, symptoms are so disturbing that evening relaxation and falling asleep is almost impossible and creates a high risk for depression [120, 121]. The prevalence of RLS is approxi­mately two- to threefold higher in pregnant women compared to nonpregnant women [116], at about 3–36% [115, 116, 122]. In a prospective study of 1428 women, prepregnancy RLS was found to be a risk factor for both prenatal and post­natal depression, while no added risk was seen in those with new-onset RLS during pregnancy [121]. Moreover, RLS has been linked with poor sleep quality, poor day­time function, and excessive daytime sleepiness although it should be noted that despite the high frequency of RLS in pregnancy, there is little evidence to suggest an association with birth outcomes [122–124]. However, in a study that used a sur­rogate measure of RLS (“jumpy or jerky leg movements”), having such movements “always” was associated with an increased incidence of preterm birth and a lower birth weight [125].

The mechanisms of sleep disruption– especially SDB– that affect cardiovascular morbidity in nonpregnant adults are remarkably similar to the biological pathways for preeclampsia and include sympathetic activation, oxidative stress, inammation, and endothelial dysfunction [126, 127]. In SDB, increased sympathetic activation is propagated by frequent arousals and repetitive apneas; the surges in sympathetic activity ultimately result in elevated nocturnal and daytime blood pressures, a key