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BACKGROUND: Climate change, in particular the exposure to heat, impacts on human health and can trigger diseases. Pregnant people are considered a vulnerable group given the physiological changes during pregnancy and the potentially long-lasting consequences for the offspring. Evidence published to date on higher risk of pregnancy complications upon heat stress exposure are from geographical areas with high ambient temperatures. Studies from geographic regions with temperate climates are sparse; however, these areas are critical since individuals may be less equipped to adapt to heat stress. This study addresses a significant gap in knowledge due to the temperature increase documented globally. METHODS: Birth data of singleton pregnancies (n = 42,905) from a tertiary care centre in Hamburg, Germany, between 1999 and 2021 were retrospectively obtained and matched with climate data from the warmer season (March to September) provided by the adjacent federal meteorological station of the German National Meteorological Service to calculate the relative risk of heat-associated preterm birth. Heat events were defined by ascending temperature percentiles in combination with humidity over exposure periods of up to 5 days. Further, ultrasound data documented in a longitudinal prospective pregnancy cohort study (n = 612) since 2012 were used to identify pathophysiological causes of heat-induced preterm birth. FINDINGS: Both extreme heat and prolonged periods of heat exposure increased the relative risk of preterm birth (RR: 1.59; 95% CI: 1.01-2.43; p = 0.045; RR: 1.20; 95% CI: 1.02-1.40; p = 0.025). We identified a critical period of heat exposure during gestational ages 34-37 weeks that resulted in increased risk of late preterm birth (RR: 1.67; 95% CI: 1.14-1.43; p = 0.009). Pregnancies with a female fetus were more prone to heat stress-associated preterm birth. We found heat exposure was associated with altered vascular resistance within the uterine artery. INTERPRETATION: Heat stress caused by high ambient temperatures increases the risk of preterm birth in a geographical region with temperate climate. Prenatal routine care should be revised in such regions to provide active surveillance for women at risk. FUNDING: Found in acknowledgements.

Background: Women developing preeclampsia (PE) or fetal growth restriction (FGR) during pregnancy are at higher risk for cardiovascular diseases (CVD) later in life. We aimed to analyse cardiovascular health of women 10–20 years after affected pregnancies in comparison to women after uneventful pregnancies. In addition, we assessed a potential long-term effect of the NO-donor pentaerythrityl tetranitrate (PETN). Methods: Women 10–20 years after severe PE, including women receiving PETN during pregnancy and matched controls were recruited and assessed for baseline clinical data and cardiovascular function by transthoracic echocardiography, VICORDER and USCOM. SPSS was used for statistical analysis. Results: 53 participants after PE/FGR (13 with former PETN intake) and 51 controls were recruited for follow-up at an average of 14 years after index pregnancies. Compared to controls, women after PE/FGR had a significantly higher incidence of arterial hypertension (13.7% vs. 41.5%, p<0.001), and were more likely to be hypertensive (41.2% vs. 67.30%, p = 0.008). There were no differences in cardiovascular function observed. Affected women with PETN intake during pregnancy showed lower mean values for right atrial area and ventricle in comparison to controls and also to affected women without former medication. Conclusions: In conclusion, our study results confirm that the risk of CVD is increased in women after PE/FGR compared to women after uneventful pregnancies. Contrary to our expectations, no major cardiovascular changes were observed in our cohort 10–20 years post pregnancy. The observed differences found in right heart dimensions were within reference ranges, and should be interpreted with caution. [ABSTRACT FROM AUTHOR]

Introduction: Prenatal exposure to supraphysiological glucocorticoid (GC) levels may lead to long‐lasting developmental changes in numerous biological systems. Our prior study identified an association between prenatal GC prophylaxis and reduced cognitive performance, electrocortical changes, and altered autonomic nervous system (ANS) activity in children aged 8–9 years. This follow‐up study aimed to examine whether these findings persisted into adolescence. Material and Methods: Prospective observational follow‐up study involving twenty‐one 14‐ to 15‐year‐old adolescents born to mothers who received betamethasone for induction of fetal lung maturation in threatened preterm birth, but who were born with a normal weight appropriate for their gestational age (median 37+4 gestational weeks). Thirty‐five children not exposed to betamethasone served as the reference group (median 37+6 gestational weeks). The primary endpoint was cognitive performance, measured by intelligence quotient (IQ). Key secondary endpoints included symptoms of attention‐deficit/hyperactivity disorder (ADHD) and metabolic markers. Additionally, we determined electrocortical (electroencephalogram), hypothalamus–pituitary–adrenal axis (HPAA), and ANS activity in response to a standardized stress paradigm. Results: No statistically significant group difference was observed in global IQ (adjusted mean: betamethasone 103.9 vs references 105.9, mean difference −2.0, 95% confidence interval [CI]: −7.12 to 3.12, p = 0.44). Similarly, ADHD symptoms, metabolic markers, the overall and stress‐induced activity of the HPAA and the ANS did not differ significantly between groups. However, the betamethasone group exhibited reduced electrocortical activity in the frontal brain region (spectral edge frequency–adjusted means: 16.0 Hz vs 17.8 Hz, mean difference −1.83 Hz, 95% CI: −3.21 to −0.45, p = 0.01). Conclusions: In 14‐ to 15‐year‐old adolescents, prenatal GC exposure was not associated with differences in IQ scores or ANS activity compared to unexposed controls. However, decelerated electrocortical activity in the frontal region potentially reflects disturbances in the maturation of cortical and/or subcortical brain structures. The clinical significance of these changes remains unknown. Given the small sample size, selective participation/loss of follow‐up and potential residual confounding, these findings should be interpreted cautiously. Further research is required to replicate these results in larger cohorts before drawing firm clinical conclusions. [ABSTRACT FROM AUTHOR]