The implications of maternal sleep disruption on cardiovascular adaptations and cardiometabolic outcomes

Abstract

Pregnancy involves profound physiological changes that, although necessary for gestation, might promote maladaptive systemic responses, an important consideration given rising maternal morbidity and mortality in the USA, and the role of cardiovascular disease as a leading cause of pregnancy-related death. This Personal View examines the link between disrupted peripartum sleep and adverse cardiometabolic outcomes. Sleep quality and duration often decline during pregnancy because of many factors, including hormonal changes, physical discomfort, and behavioural influences. Sleep pathologies, such as insomnia and sleep-disordered breathing, also become more common as pregnancy progresses. The transition from pregnancy to postpartum introduces a unique set of stressors, including newborn care and novel social demands and restrictions, which frequently compromise sleep quality. Persistent sleep disruption, during pregnancy or otherwise, should not be overlooked, as emerging evidence links poor sleep with increased inflammation, altered autonomic regulation, and impaired metabolic function. In the context of pregnancy, such processes are closely linked to the development of hypertensive disorders of pregnancy, gestational diabetes, and increased cardiovascular risk across the lifespan. Although the number of studies assessing the role of sleep are increasing, important gaps remain in defining optimal perinatal sleep and identifying effective interventions to improve maternal sleep. Greater attention to sleep health within routine perinatal care, along with continued research in this area, is an important step towards improving maternal cardiovascular outcomes.

Introduction

Pregnancy has the potential to be one of the most dangerous periods of a woman’s life, particularly with respect to cardiovascular health. The peripartum period is a time of unparalleled haemodynamic and metabolic change that is necessary to support a healthy pregnancy but can exacerbate underlying vulnerabilities or introduce novel factors contributing to the development of heart disease.^1,2 Pregnancy-induced physiological changes include increased cardiac output, blood volume expansion, and decreased systemic vascular resistance, any of which can reveal or worsen pre-existing cardiovascular conditions.¹ Furthermore, adverse pregnancy outcomes, including gestational hypertension, pre-eclampsia, gestational diabetes, and peripartum cardiomyopathy, confer increased long-term risks for persistent maternal hypertension, chronic kidney disease, cardiovascular disease, and, in some cases, death.³

A growing body of research suggests that sleep disruption is an under-recognised contributor to adverse pregnancy outcomes.⁴ Poor sleep is one of the most common complaints in pregnant women, particularly from the second half of pregnancy until the first year after birth.⁵ Numerous disturbances contribute to poor sleep quality in this population, including pre-existing sleep disorders, fragmented sleep, insomnia, circadian rhythm disruption (eg, shift work), and sleep-disordered breathing (SDB).^6,7 In non-pregnant individuals, such disturbances are associated with increased risk of developing cardiovascular disease, including hypertension, arrhythmias, and ischaemic heart disease.⁷

Although emerging evidence links poor sleep during pregnancy to adverse outcomes,⁸ comprehensive, multidisciplinary reviews are needed to clarify the extent to which sleep disruption contributes to maternal cardiovascular pathology in the pregnant and postpartum settings. The primary goal of this Personal View is to discuss existing literature on typical sleep changes during pregnancy and the role of sleep disruption in the development of cardiovascular disease during pregnancy and the postpartum period, and to highlight key areas for future investigation.

Maternal mortality in the USA

To appreciate the significance of pregnancy-related cardiovascular stress, it is necessary to first consider the current trends in maternal morbidity and mortality in the USA. Throughout the 20th century, maternal mortality rates declined because of improvements in living conditions, surgical safety, anaesthesia, blood transfusions, hospital-based deliveries, and the use of antibiotics.⁹ However, since the early 21st century this progress has reversed. In the USA pregnancy-related deaths increased from 25·3 per 100 000 livebirths in 2015 to 32·6 per 100 000 livebirths in 2022—the highest rate among high-income countries and a global ranking of 55th.^9,10 Up to a fifth of maternal deaths occur after the traditional 6-week postpartum visit, when many individuals are no longer receiving routine obstetric follow-up. Late maternal deaths, defined as those occurring between 42 days and 1 year after delivery, rose from 7·3 per 100 000 livebirths in 2018 to 11·1 per 100 000 livebirths in 2022.⁹ Cardiovascular disease is now the leading cause of maternal morbidity and mortality during this period.^9,11

Women with a history of hypertensive disorders of pregnancy—including chronic hypertension, gestational hypertension, pre-eclampsia, eclampsia, and hypertension with superimposed pre-eclampsia—are recognised to have a higher long-term risk of developing hypertension, cardiovascular disease, stroke, diabetes, and chronic kidney disease.¹² Hypertensive disorders are also strong predictors of cardiovascular-related maternal mortality both at delivery and within the first postpartum year.^12–14 Additional contributors to cardiovascular-related maternal mortality include the rising prevalence of pre-existing heart disease, such as adults with congenital heart disease who survive to reproductive age, and an ageing maternal population.^1,15 Sleep disruption might compound cardiovascular risk, particularly in the postpartum period, when most maternal deaths now occur. Sleep deficiencies—defined by insufficient duration, poor quality, or irregular timing—are associated with perturbations in metabolism, inflammatory status, and normal cardiovascular regulation that are directly relevant to cardiometabolic disease.^15,16 Such changes might plausibly worsen blood pressure control and systemic inflammation, which are both central to hypertensive disorders of pregnancy and postpartum cardiovascular complications.^15,17 Furthermore, inadequate sleep is more common among populations in the USA that already have disparities in health and health-care access.¹⁶ Current evidence suggests that sleep health disparities arise from the same structural conditions that shape broader health inequities, including systemic racism, income inequality, residential segregation, and disproportionate exposure to environmental stressors.^16,18,19 In this sense, sleep functions as one pathway through which upstream socioeconomic factors influence physiological risk. The relationship is also bidirectional: sleep deficiencies are linked to higher risks of cardiovascular disease, diabetes, depression, and mortality, which might in turn widen existing health gaps.¹⁸ To better appreciate these relationships, we must first consider how the maternal cardiovascular system adapts to stress during the perinatal period.

Search strategy and selection criteria

Between Sept 15, 2025, and Feb 25, 2026, a three-phase literature search was conducted via PubMed to identify English-language, peer-reviewed human studies published from Jan 1, 2000 to Feb 25, 2026. We cross-referenced our search using the Web of Science database. Because of the high amount of overlap with our search terms and criteria (appendix pp 1–2) and the inclusion and exclusion criteria, we focused on the output of PubMed, which provided a larger number of publications to review than Web of Science. The search used structured Boolean strategies and keyword filtering focused on the intersection of maternal sleep (disruption, apnoea, insomnia, and circadian rhythms) and cardiometabolic health (cardiovascular physiology, hypertensive disorders, pre-eclampsia, and gestational diabetes). Specific attention was given to maternal mortality trends in the USA, health-care disparities (stratified by race and ethnicity), inflammatory biomarkers (eg, C-reactive protein [CRP] and IL-6), and lifestyle moderators (eg, shift work and diet). Abstracts were independently screened for clinical relevance, prioritising studies that detailed biological mechanisms and variation across populations while excluding all non-human research.

Changes in cardiovascular physiology during pregnancy

During pregnancy, the maternal body undergoes many physiological adaptations to support both the mother and the baby. From a haemodynamic perspective, plasma volume doubles due to water and sodium retention.²⁰ Although not inherently harmful, this process can trigger the development of functional (flow) murmurs, which might alarm health-care providers outside the obstetrics and cardiology specialties.²¹ Additionally, cardiac output increases, initially via increased stroke volume, then with the addition of increased heart rate as the pregnancy progresses.^3,20 Finally, systemic vascular resistance decreases in the maternal body due to the vasodilatory effects of hormones, such as relaxin, nitric oxide, prostaglandins, and progesterone. This causes maternal blood pressure to decrease in the first half of pregnancy, reaching a nadir around 20–24 weeks, before increasing again in the third trimester, approaching pre-pregnancy values.^3,9,20

As the uterus enlarges, mechanical effects influence maternal circulation. Compression of abdominal veins can lead to lower extremity oedema, and pressure on the inferior vena cava reduces venous return and can cause sharp drops in blood pressure.³ However, labour, delivery, and the immediate postpartum period represent times of maximal haemodynamic stress. Oxygen consumption increases three-fold during labour, and blood pressure rises with contractions.¹⁴ Giving birth is the point of most abrupt stress, via intrapartum and postpartum blood loss. The most common complication of delivery is postpartum haemorrhage, which accounts for 27% of maternal deaths worldwide.^22,23 Immediately after delivery, relief of caval compression and autotransfusion from the contracting uterus can also cause a temporary surge in intracardiac pressures.¹⁴

In response to the increased blood volume observed during pregnancy, the heart undergoes structural changes—namely cardiac hypertrophy.^2,13 This hypertrophy is marked by an overall increase in heart mass and ventricular chamber dimensions.^2,24 Unlike pathological hypertrophy, this remodelling occurs without fibrosis or functional impairment and typically resolves within 6 months postpartum or upon lactation cessation.^2,13,24 These structural changes are supported by clinical imaging data: intrapartum echocardiography studies show increases in left ventricular thickness and mass of 28% and 52%, respectively, and cardiac MRI data indicate that right ventricular mass can increase by up to 40% during gestation.^13,20,24,25 Structural changes are more pronounced in multiparous women, who show lower ejection fraction, worse cardiac mechanics, and higher postmenopausal systolic blood pressure compared with nulliparous women.²⁶ These findings suggest that repeated exposure to pregnancy-related cardiac stress might have lasting effects on the maternal heart, with changes during the reproductive years shaping future cardiovascular disease risk in women.²⁷

Given the profound cardiovascular changes that occur during pregnancy, it is important to consider how external factors might influence the cardiac and vascular remodelling necessary to support both the mother and the baby. Substantial evidence from non-gravid populations suggests that poor sleep health adversely affects cardiovascular haemodynamics and structural remodelling. Chronic insomnia, short sleep duration, and obstructive sleep apnoea have been associated with autonomic and inflammatory dysregulation and endothelial dysfunction, processes that impair blood pressure control and increase myocardial workload.^28,29 Evidence from both prospective studies and meta-analyses links poor sleep to atrial fibrillation, hypertension, coronary heart disease, stroke, heart failure, and cardiovascular death.^29–31 In recognition of these data, sleep was recently incorporated into the American Heart Association’s Life’s Essential 8.³² Emerging evidence suggests that sleep disturbances during pregnancy might adversely influence the cardiovascular adaptations essential for healthy gestation.^7,33–35

Sleep in the perinatal and postpartum periods

Sleep is a fundamental physiological process for physical and mental wellbeing.^36,37 During pregnancy and the postpartum period, sleep becomes even more important amid hormonal shifts, metabolic changes, and new psychosocial challenges associated with pregnancy and parenthood. Most women report declining sleep quality throughout gestation, with common problems including difficulty falling asleep, frequent night-time waking, and daytime fatigue.^4–6,15 These issues are often related to physical discomfort (eg, fetal growth, reflux, nocturia, and difficulty finding a comfortable sleeping position), hormonal changes, and mood fluctuations that accompany the many physiological and emotional adjustments of pregnancy^5,6 (figure 1).

Figure 1: Factors affecting sleep in the perinatal period.

Key factors contributing to sleep changes across all trimesters in a typical pregnancy and within the postpartum period in women. GORD=gastro-oesophageal reflux disease.

Pregnancy also changes sleep architecture and efficiency. Rising oestrogen and progesterone concentrations affect respiratory function and vascular tone, which causes increased airway resistance and the risk of obstructive events during sleep.³³ In addition, weight gain, fluid retention, and changes in the anterior–posterior diameter of the thorax and upper airway anatomy (tracheal shortening) from the growing uterus reduce lung capacity and oxygen reserve. Together, these physical changes create an environment that is uniquely susceptible to SDB and associated cardiovascular strain.^33,38 Furthermore, some sleep disorders become more common in pregnancy. These include obstructive sleep apnoea, insomnia—especially when total sleep drops below 6 h—and restless leg syndrome.^33,38 Objective evidence reinforces these findings. For example, a study using level 3 home sleep apnoea testing showed that SDB prevalence increased from 3·6% early in pregnancy to 8·3% by mid-gestation; SDB was also independently associated with pre-eclampsia, gestational hypertension, and gestational diabetes.³⁹ Poly somno graphic studies have also shown that both the quantity and quality of sleep decline during pregnancy, with the greatest disruptions occurring in late gestation.³⁴ Subjective reports from pregnant individuals confirm this pattern, citing progressive declines in total sleep time as pregnancy progresses.^6,40

Sleep often becomes even more fragmented in the early postpartum period, especially during the first 3 months after delivery, when infant care frequently interrupts maternal rest.^6,41 For many individuals, night-time sleep does not return to pre-pregnancy patterns for several months; reduced sleep duration has been documented beyond 1 year postpartum.^5,6 In addition, national policy differences might shape the postpartum experience in ways that affect sleep, as the USA remains the only high-income country without a federally mandated paid maternity leave policy.⁴² At the same time, workforce participation among mothers of young children is high, and many women resume employment soon after giving birth—approximately 23% of US-based first-time mothers return to work within 2 weeks, and 43% return within 1 month.⁴² For many families, the prompt return to work occurs during a period marked by fragmented sleep, ongoing physical recovery, and the challenges of caring for a newborn, all of which might influence cardiovascular risk.

Cardiovascular implications of sleep disruption during pregnancy

SDB, particularly obstructive sleep apnoea, is well established as a risk factor for hypertension, type 2 diabetes, coronary disease, and stroke in non-pregnant populations.^28,34,35 During pregnancy, women with both pre-eclampsia and obstructive sleep apnoea have a substantially higher risk of severe maternal and cardiovascular morbidity compared with women who have either condition alone, suggesting shared pathophysiological pathways (figure 2).^33,38 Obstructive sleep apnoea imposes physiological stress during pregnancy via recurrent airway obstruction and intermittent hypoxia, which can trigger frequent arousals from sleep and oxygen desaturations. In turn, these induce sympathetic activation and hypothalamic–pituitary–adrenal axis dysregulation, along with oxidative stress, hypercoagulability, endothelial inflammation, and vascular dysfunction.^29,43,44 Loss of typical nocturnal blood pressure dipping is also observed, which is a more sensitive marker for adverse cardiovascular events than either daytime blood pressure or 24 h averages.⁴⁵ These disturbances can exacerbate endothelial vulnerability and interfere with the vascular remodelling necessary for normal placentation, thereby increasing susceptibility to hypertensive disorders and long-term cardiovascular disease risk.^38,44,45 Population-level studies support these mechanisms. In the cohort study by Facco and colleagues,³⁴ they measured that SDB in mid-gestation was associated with increased odds of gestational hypertension and pre-eclampsia, independent of age and BMI.³⁴ Similar associations with hypertensive complications and preterm delivery have been reported in other studies.^7,34,46 Clinically, these findings underscore the importance of screening for SDB in at-risk pregnant patients and implementing early interventions to mitigate cardiovascular stress.

Figure 2: Cardiometabolic consequences of sleep disruption during pregnancy.

Key risk factors (left side) and the clinical manifestations (right side) arising from sleep disruption during pregnancy in women and contributing to heightened cardiometabolic disease risk.

Beyond SDB, sleep disruption also contributes to cardiometabolic dysfunction. Short sleep duration and poor sleep quality are associated with insulin resistance and impaired glucose tolerance, both of which increase the risk of gestational diabetes.^7,34,46,47 Even modest sleep restriction in pregnant women has been linked to elevated fasting glucose and insulin concentrations.^15,34 These findings parallel those in non-pregnant populations, where insufficient sleep predicts obesity, type 2 diabetes, and metabolic syndrome.⁴⁸ Mechanistically, sleep loss increases cortisol secretion, reduces insulin sensitivity, and alters leptin–ghrelin signalling; additionally, intermittent hypoxia exacerbates sympathetic and metabolic stress.^7,46 From a clinical perspective, promoting sufficient sleep duration and quality during pregnancy might help prevent early metabolic dysregulation and reduce the risk of developing gestational diabetes.

Elevated markers of systemic inflammation, particularly IL-6 and CRP, provide objective biological links between sleep disruption and adverse maternal cardiovascular outcomes. At baseline, pregnant women have higher serum CRP concentrations than non-pregnant women.⁴⁹ However, exaggerated elevations of IL-6 and ultra-high-sensitivity CRP are observed in pre-eclampsia, where they probably contribute to endothelial dysfunction and disease pathogenesis.⁵⁰ Elevated first-trimester CRP is independently associated with an increased risk of gestational diabetes⁵¹, which is a cardiovascular disease risk factor; additionally, higher maternal IL-6 and CRP concentrations are linked to spontaneous preterm birth before 32 weeks.⁵² These associations implicate inflammation in serious maternal and fetal morbidity. IL-6 and high-sensitivity CRP are not merely correlates of pregnancy complications—they are well established predictors of major adverse cardiovascular events and all-cause mortality in non-pregnant populations.^53,54 These findings suggest that sleep disruption during pregnancy might amplify a pro-inflammatory state that accelerates endothelial injury, cardiometabolic dysfunction, and vascular remodelling, thereby increasing both short-term maternal morbidity and long-term cardiovascular disease risk. These observations suggest that targeting systemic inflammation through lifestyle, pharmacological, or sleep-based interventions could offer a strategy to protect maternal vascular health.

Dietary behaviour represents another pathway linking sleep and cardiometabolic risk. Short and poor-quality sleep are associated with an increased risk of obesity.⁵⁵ Suboptimal sleep is linked with increased total energy intake, increased snacking, irregular meal timing, reduced fibre and vegetable intake, and stronger preferences for energy-dense, salty, and sweet foods.^55,56 Sleep disruption also promotes reward-driven eating, dietary disinhibition, and impaired control over intake, patterns that favour overconsumption and weight gain.⁵⁶ Therefore, pregnancy might present a context that favours poor nutrition, predisposing an individual to the development of gestational diabetes, which increases a woman’s risk of developing type 2 diabetes—a well established contributor to cardiometabolic disease—later in life.^57,58 Encouraging structured meal timing, mindful eating, and healthy snacking strategies alongside sleep optimisation could help reduce these risks during pregnancy.

Shift work, defined as employment outside conventional daytime hours—including fixed night, rotating, and irregular schedules—disrupts the internal circadian timing system, leading to misalignment between behavioural cycles (eg, sleep, eating, and activity) and endogenous biological rhythms.^59,60 Most shift workers fail to fully adapt to circadian disruption, resulting in persistent desynchrony that impairs insulin sensitivity, elevates blood pressure, increases postprandial glucose and lipid concentrations, and disrupts autonomic regulation.^59,60 Over time, these physiological alterations contribute to the development of cardiometabolic disease, with disproportionately greater risk observed in women than men.⁶¹ During pregnancy, these effects might be amplified. Actigraphy studies show higher rates of gestational diabetes among pregnant women working evening or night shifts.^47,62 A late sleep midpoint (after 0500 h) is also associated with increased rates of gestational diabetes, independent of sleep quality or duration, which reinforces the hypothesis that shift work impairs metabolism during pregnancy.⁴⁷ Meta-analyses show that rotating shift work increases the odds of preterm delivery, small-for-gestational-age birth, pre-eclampsia, and gestational hypertension,⁶³ highlighting an association with maternal vascular complications. For pregnant shift workers, these findings emphasise the need for personalised strategies, such as schedule adjustments, circadian-aligned sleep interventions, and close metabolic monitoring, to reduce maternal and fetal risk. In addition, because of a partial understanding of how shift work affects normal maternal cardiometabolic adaptations, more studies are needed to assess sleep health and examine the effectiveness of these potential interventional strategies.

Knowledge gaps and directions for future research

Despite evidence linking perinatal sleep disturbance to adverse maternal outcomes, substantial gaps remain. To date, there are no pregnancy-specific guidelines for the diagnosis or treatment of SDB. There are no guidelines that indicate what constitutes optimal sleep during the perinatal period. Future research should prioritise exploration of the complex, multidirectional relationships between sleep, inflammation, obesity, and metabolic dysfunction to clarify causal mechanisms (figure 3). Foundational data in these areas are crucial for better characterisation of the physiological mechanisms underpinning normal sleep health during an uncomplicated pregnancy and for determining which pathways are disrupted in disease states, thereby identifying actionable targets to reduce maternal cardiometabolic risk. Preclinical studies will also be invaluable for assessing the mechanistic effects of sleep disruption and shift work during critical reproductive windows, with a specific emphasis on dietary patterns and circadian involvement. These studies cannot always be ethically conducted in women or accurately modelled in vitro. The long-term effects of SDB breathing in pregnancy, even if sleep normalises after pregnancy, require evaluation.

Figure 3: Gaps in knowledge regarding the implication of sleep on pregnancy outcomes and areas for future research.

CVD=cardiovascular disease. CHD=coronary heart disease.

Finally, we echo the sentiments of other researchers in the field, calling for rigorous clinical studies in pregnant and lactating women to better define normative maternal cardiovascular physiology and identify pathological adaptations during the perinatal period. A more refined understanding of these processes is essential to inform targeted prevention and treatment strategies. In parallel, interventional studies are needed to test the efficacy and feasibility of behavioural, pharmacological, and device-based therapies across diverse perinatal populations, with particular attention to ease of accessibility in the spirit of health equity. Although research of this nature is occurring in Europe, interventional research should be prioritised in the USA. Future studies should investigate the cardiovascular benefits of cognitive behavioural interventions, sleep health education, and relaxation interventions during pregnancy and the postpartum period to minimise sleep disruption—especially among female shift workers.³⁶ The history of perturbed sleep quality during previous pregnancies should also be routinely documented in the clinic to assess and reduce future disease risk. The goal, ultimately, should be to reduce the burden of perinatal sleep disruption on maternal and offspring health.

Conclusion

Over the past century, substantial progress has been made in reducing obstetric complications that were once common worldwide. In regions with ready access to modern medical advances—such as sterile technique, antibiotics, and caesarean delivery—maternal deaths from sepsis, obstructed labour, and eclampsia have declined dramatically.⁶⁴ Yet the risks of pregnancy have not been eliminated: cardiovascular disease now represents a leading cause of maternal morbidity and mortality in high-income countries, such as the USA. The reasons for this shift are likely complex, owing to a combination of factors. However, one contributor that has been largely neglected from a research and clinical perspective is disrupted sleep, whether stemming from pregnancy-related discomfort, caring for a newborn, working non-traditional hours, or other causes.

Sleep disruption is common throughout pregnancy and the postpartum period. Because of this prevalence, poor sleep during this time has historically been considered an unavoidable inconvenience of reproductive life rather than a clinical concern.⁶² However, new research challenges this perception, as ever-increasing data now suggest that sleep disruption negatively affects complex pathways involving inflammation, autonomic dysregulation, and oxidative stress. In turn, these disruptions increase the incidence and prevalence of adverse cardiovascular outcomes. These effects are not limited to pregnancy or the newborn phase—the sequelae of sleep disruption continue throughout a woman’s life.

In addition, the populations most likely to have adverse maternal–fetal outcomes—those with poorer health-care access and greater reliance on shift work—are also those most likely to experience sleep disruption due to socioeconomic, behavioural, environmental, and professional factors.^16,19 Therefore, for many reasons, sleep disruption should be reconsidered as a clinically meaningful and potentially modifiable health issue, rather than an inevitable consequence of pregnancy. This reconsideration allows perinatal sleep support to be integrated into broader strategies to protect women’s cardiovascular health.