The assessment of fetal growth and well-being remains a central focus of prenatal care [1]. In the last years, studies have investigated maternal breathing disorders and pregnancy compliance [2]. The sleep disorder also impacts fetal growth. One such condition is obstructive sleep apnea (OSA), with recurrent apneic episodes during sleep due to upper airway collapse, with consequently intermittent hypoxia and sleep alteration [3].

Management of temporomandibular joint (TMJ) disorders in patients with OSA typically involves conservative treatment approaches aimed at symptom relief and functional improvement [4]. Among these, oral appliances—particularly mandibular advancement devices—are commonly used and have shown efficacy in addressing both TMJ disorders and OSA-related symptoms [5].

OSA is more commonly associated with maternal complications—such as excessive daytime sleepiness, gestational hypertension, pre-eclampsia, and gestational diabetes [6]. Its role in intermittent fetal hypoxia is of growing concern. Prolonged or repeated hypoxic episodes may impair placental function, ultimately compromising fetal growth and development [3].

Different studies showed an increased prevalence of OSA during pregnancy [7]. Common symptoms of OSA include snoring, nocturia, personality changes, and excessive daytime sleepiness [3]. The symptoms worsen during the last pregnancy period due to the hormonal modification, increased body mass index (BMI), reduced lung volume, and trachea restriction [3]. Women with no previous history of sleep disorders may show symptoms during the third trimester [6]. OSA increased the risk of preterm delivery, gestational hypertension and preeclampsia and gestational diabetes [8].

Fetal well-being is evaluated through antenatal ultrasound test and cardiotocography (CTG) [9, 10]. Antepartum CTG is a primary method for evaluating fetal cardiac status [11]. This test permits the evaluation of the fetal heart rate (FHR) compensation due to fetal hypoxia [11]. Since CTG is not routinely performed during maternal sleep, episodes of OSA may impact fetal oxygenation and alter FHR variability without detection [9]. The impact of maternal OSA on fetal well-being, particularly in relation to CTG-detected FHR changes, remains under-researched and poorly understood.

We aimed to evidence the maternal OSA impact on the fetal heart rate. This represents a gap in the current research and should improve our understanding of the OSA influence on adverse prenatal outcomes.

Our systematic review included six studies published between 1991 and 2023 that analysed the effects of maternal obstructive sleep apnea (OSA) on fetal heart rate (FHR), assessed using cardiotocography (CTG) and fetal electrocardiography (fECG) [13, 14, 15, 16, 17, 18, 19]. Except for Pitts et al. [16], which diagnosed the maternal sleep disorders with the home sleep test, all the studies diagnosed sleep disorders with polysomnography [13, 14, 15, 17, 18].

Half of the studies included in our review did not provide evidence of an impact of maternal OSA on fetal heart rate [13, 15, 18]. Three studies evidenced the association between maternal OSA and fetal heart distress, despite the limited sample [14, 16, 17]. Skrzypek et al. [17] investigated OSA in pregnant women with preterm fetal growth restriction (FGR) comorbidity. The results indicated that fetuses with this condition have more acute FHR events compared to the controls [17]. Moreover, FGR is a fetal condition that predisposes to hypoxia and adversely affects fetal outcomes [20, 21].

Olivarez et al. [15] and DiPietro et al. [18] did not evidence a direct correlation between OSA and fetal abnormalities. The predictive value of the Berlin screening questionnaire during pregnancy was explored by Olivarez et al. [15]. They included 100 pregnant women with gestational ages ranging from 26 to 39 weeks, and the authors concluded that the mechanism by which OSA may affect the fetus during maternal apneic episodes remains unclear [15]. DiPietro et al. [18] included 84 obese pregnant women at term of gestation. They observed only a modest compensatory increase in fetal heart rate variability in response to apneic and hypopneic episodes, without any pathological fetal heart response [18].

The case report by Charbonneau et al. [13] described a 32-year-old pregnant woman at 36 weeks of gestation, affected by severe obesity (155 kg), gestational diabetes, and fetal growth restriction. Despite an apnea–hypopnea index of 159 events per hour and maternal oxygen desaturation, CTG monitoring showed normal fetal heart rate reactivity in this patient [13].

Sahin et al. [14] analysed 35 term pregnant women, among whom only four were diagnosed with OSA. In these four cases, a strong correlation (75%) was observed between fetal heart rate decelerations and maternal oxygen desaturation [14]. Furthermore, neonates of women affected by OSA showed lower Apgar scores and birth weights [14]. Similarly, Pitts et al. [16] reported a strong correlation between maternal respiratory events and the occurrence of late and prolonged fetal heart rate decelerations. In their cohort of 40 women, 17 were diagnosed with sleep-disordered breathing during the third trimester; among them, 37 late decelerations were recorded, 84% of which were associated with maternal respiratory events [16].

Other studies evidenced the relation between the maternal hypoxic episodes and the fetal growth restriction, preterm delivery, and other adverse perinatal outcomes [22, 23, 24]. Apneic phase is associated with maternal desaturation, with an impact on the fetal circulation and fetal heart rate [25]. This association is not well recognised in pregnant populations. Fetal and placental circulatory systems may be well adapted, allowing the fetus to tolerate brief episodes of maternal desaturation without adverse effects [26, 27, 28].

Other risk factors—such as elevated body mass index (BMI), gestational hypertension, and gestational diabetes—may worsen fetal outcomes, predisposing affected individuals to increased susceptibility to the effects of maternal sleep disorders [29, 30, 31]. According to DiPietro et al. [18], maternal apneic episodes may cause fetal compensatory mechanisms.

Based on our systematic review, the studies included showed contradictory findings. This difference may originate from different study designs and different outcomes. Even studies that employed overnight polysomnography with continuous fetal ECG monitoring during maternal respiratory events reported contrasting findings [16, 18]. The presence of comorbid conditions may directly influence fetal heart rate patterns and confound the study’s results [13, 17].

Obesity remains the most significant confounding factor, as the majority of patients with maternal sleep disorders associated with fetal heart abnormalities were also affected by severe obesity [32]. Most studies were conducted in obese pregnant women, which represent an independent risk factor [13, 14, 16, 17, 18].

Other limitations are related to the geographic variability among the study settings [33]. Main studies were conducted in high-resource settings, North America and Australia [13, 15, 16, 17, 18], and could not represent the low-resource setting. The high-resource study predominance limits our generalizability [33, 34, 35].

Biases were evaluated with the modified Newcastle-Ottawa scale, to a rigorous systematic review.

OSA represents a possible risk factor for the fetal well-being and fetal heart modification. The current evidence are not unanimous about the OSA impact on the fetal heart modification. Despite these unclear findings, early diagnosis and management of maternal sleep disorders remain a significant point of prenatal care. Further standardized studies are needed to understand the complete relationship between OSA and fetal heart adaptation.

• We conducted a systematic review of the literature on the influence of maternal OSA on FHR.

• Six studies were included in our analysis, with three showing no significant effect on FHR and the other three demonstrating fetal distress in OSA pregnant women, characterised by FHR decelerations and changes.

• These discrepancies could be related to differences in study settings, sample size, diagnostic criteria for OSA, and methods of fetal monitoring.

• Despite those limitations, for the first time, this review has focused on the possible relationship between maternal OSA and FHR, which is significant for maternal sleep disorder management during pregnancy in order to optimize prenatal care and minimize the impacts of associated risks.

All the data of this study are included in this article.

Conceptualization, MLV, MMM and GM; methodology, MDB, RM and MC; formal analysis, AP; investigation, MLV; data curation, AP and RM; writing—original draft preparation, AP and RM; writing—review and editing, MDB and GM; visualization, HU and MMM; supervision, MDB and GM; All authors contributed to the important editorial changes in the manuscript. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

Not applicable.

Not applicable.

This research received no external funding.

GM was serving as one of the Editorial Board Members of this journal. We declare that GM had no involvement in the review of this article and has no access to information regarding its review. Full responsibility for the editorial process for this article was delegated to John Alcolado. Other authors declared no conflict of interest.

Supplementary material associated with this article can be found, in the online version, at https://doi.org/10.31083/BJHM53217.