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In this review, we summarize how an increasingly stressed and aging placenta contributes to the maternal clinical signs of preeclampsia, a potentially lethal pregnancy complication. The pathophysiology of preeclampsia has been conceptualized in the two‐stage model. Originally, highlighting the importance of poor placentation for early‐onset preeclampsia, the revised two‐stage model explains late‐onset preeclampsia as well, which is often preceded by normal placentation. We discuss how cellular senescence in the placenta may fit with the framework of the revised two‐stage model of preeclampsia pathophysiology and summarize potential cellular and molecular mechanisms, including effects on placental and maternal endothelial function. Cellular senescence may occur in response to inflammatory processes and oxidative, mitochondrial, or endoplasmic reticulum stress and chronic stress induce accelerated, premature placental senescence. In preeclampsia, both circulating and tissue‐based senescence markers are present. We suggest that aspirin prophylaxis, commonly recommended from the first trimester onward for women at risk of preeclampsia, may affect placentation and possibly mechanisms of placental senescence, thus attenuating the risk of preeclampsia developing clinically. We propose that biomarkers of placental dysfunction and senescence may contribute to altered preventive strategies, including discontinuation of aspirin at week 24–28 depending on placenta‐associated biomarker risk stratification. [ABSTRACT FROM AUTHOR]

Purpose: Women with hypertensive disorders of pregnancy (HDP) are at increased risk of developing premature cardiovascular disease (CVD). The mechanisms behind this are not fully understood, but microvascular alterations have been documented in retinal arterioles and venules. The aim of this study was to use non‐invasive retinal imaging to investigate the structural and functional properties of arterioles, venules and capillaries in this patient group. Methods: We examined 27 women with previous HDP and 23 controls at 3 years postpartum. The retinal microvasculature was assessed by vessel calibre measurements, retinal oximetry and optical coherence tomography angiography. Differences were analysed using non‐parametric tests and multiple regression analyses, adjusted for age and body mass index. Results: Median arteriolar oxygen saturation (SaO2; 94.2% vs. 93.0%), venular oxygen saturation (SvO2; 60.1% vs. 62.4%) and arteriovenous saturation difference (AV‐difference; 32.8% vs. 32.3%) were similar across groups. Capillary vessel density (VD; 46.2% vs. 46.3%), skeletonised VD (VSD; 21.3 vs. 21.1 mm/mm2) and vessel diameter index (21.65 vs. 21.86) were also comparable. In the HDP group, mean arterial pressure (MAP) was positively correlated with AV‐difference (R2 = 0.209) and negatively correlated with arteriolar diameter (CRAE; r2 = 0.382). Conclusions: Structural microvascular alterations appear not to be key biomarkers for CVD risk after HDP as early as 3 years postpartum in otherwise healthy women. Further studies are needed to evaluate whether such changes occur later in life. MAP was associated with AV‐difference only in the HDP group, suggesting specific mechanisms affecting functional microvascular properties in these women. [ABSTRACT FROM AUTHOR]

Preeclampsia is a pregnancy complication that can have severe health consequences for both the mother and baby. Screening algorithms for preeclampsia often include the categorization of "race" and ethnicity, but studies on the association between these factors and preeclampsia risk have contradictory findings. Additionally, social determinants of health, such as socioeconomic deprivation, can also influence the prevalence of placenta-mediated adverse pregnancy outcomes. Further research is needed to disentangle the effects of socioeconomic factors and ethnicity in screening algorithms and to better understand the impact of these factors on pregnancy outcomes. [Extracted from the article]

Objective: To explore the contribution of pregnancy‐related complications on the prevalence of extremely, very and late preterm births in singleton and twin pregnancies. To study the risk of spontaneous preterm birth in twin pregnancies compared with singleton pregnancies. Design: Population‐based registry study. Setting: Medical birth registry of Norway and Statistics Norway. Population: Nulliparous women with singleton (n = 472 449) or twin (n = 8727) births during 1999–2018. Methods: Prevalence rates of pregnancy‐related complications for extremely, very and late preterm birth in twin and singleton pregnancies were calculated with 95% confidence intervals. Multivariable logistic regression was applied to assess odds ratios for preterm birth, adjusted for obstetric and socio‐economic factors. Main outcome measures: Extremely preterm (<28+0 weeks of gestation), very preterm (28+0–33+6 weeks of gestation) and late preterm (34+0–36+6 weeks of geatation) birth. Results: Preterm birth was significantly more prevalent in twin pregnancies than in singleton pregnancies in all categories: all preterm (54.7% vs 6.1%), extremely preterm (3.6% vs 0.4%), very preterm (18.2% vs 1.4%) and late preterm (33.0% vs 4.3%) births. Stillbirth, congenital malformation and pre‐eclampsia were more prevalent in twin pregnancies than in singleton pregnancies, but the prevalence of complications differed in the three categories of preterm birth. Pre‐eclampsia was more prevalent in singleton than in twin pregnancies ending in extremely and very preterm birth. The adjusted odds of spontaneous preterm live birth were between 19‐ and 54‐fold greater in twin pregnancies than in singleton pregnancies. Conclusions: Singleton and twin pregnancies seem to have different pathways leading to extremely, very and late preterm birth. This article includes Author Insights, a video abstract available at: https://vimeo.com/manage/videos/775727344 [ABSTRACT FROM AUTHOR]