Ukachi N. Emeruwa

BACKGROUND: The placenta is known to be critical in the etiology of preeclampsia. However, there is a subset of preeclampsia cases without identifiable placental pathology. We evaluated which clinical preeclampsia classification system best distinguishes preeclampsia with placental pathology from preeclampsia without placental pathology. METHODS: We evaluated 5 placental pathological features in 197 placentas from patients with preeclampsia grouped by 3 clinical preeclampsia subclasses: (1) preeclampsia with calculated infant birthweight P <0.0001). SGA preeclampsia and SGA normotensive placentas were abnormal and shared alterations in hypoxia, TNFα (tumor necrosis factor alpha), glycolysis, unfolded protein response, estrogen response, ultraviolet response, p53, TGFβ (transforming growth factor beta), and mTORC1 (mammalian target of rapamycin complex 1) signaling pathways. CONCLUSIONS: Classifying preeclampsia based on birthweight percentile for gestational age is the most useful system for consistently identifying preeclampsia associated with placental pathology.

Obstetrics and gynecology journal impact factor trends during the COVID-19 pandemic were similar to those seen among other medical specialties, and our findings further highlight the ongoing need to implement a metric of research impact that is not as easily manipulated by selective publication.

Introduction: De novo postpartum hypertension (dnPPHTN), defined as new‐onset high blood pressure (BP) after delivery in individuals who were normotensive through pregnancy and delivery, accounts for up to two‐thirds of postpartum hypertension cases. Despite its prevalence, there is limited knowledge of BP trends in the postpartum period, hindering opportunities for early detection and timely intervention for dnPPHTN. This study aimed to characterize longitudinal postpartum BP patterns in patients at high risk for dnPPHTN. Methods: This secondary analysis utilized data from a negative randomized controlled trial (PMID: 38641089) involving 82 normotensive patients at high risk for dnPPHTN, who were randomized to receive either a 5‐day course of 20 mg oral furosemide or placebo starting from postpartum day 1. BPs were monitored every 4‐8 h from delivery to discharge, and subsequently via Bluetooth‐enabled remote monitoring twice daily for 6 weeks. The primary goal of this secondary analysis was to characterize distinct patterns of longitudinal BP trajectories in the placebo group. Secondary goals included exploring differences in early postpartum BP trends between those who developed dnPPHTN and those who remained normotensive, as well as identifying the timing of peak BPs. Trends were assessed graphically using local polynomial regression fitting. Linear mixed‐effects models were used to examine temporal BP trajectories, including random intercepts and slopes, with an interaction term for the time trend and dnPPHTN diagnosis to explore differential impacts. Results: A total of 40 participants from the placebo arm of the parent trial were included, contributing a total of 2235 postpartum BP measurements. Both systolic BP (SBP) and diastolic BP (DBP) increased until postpartum days 9 and 12, respectively, before subsequently declining. Significant differences in BP trajectories were observed between participants who developed dnPPHTN ( n = 3; 167 BP readings) and those who remained normotensive ( n = 37; 2068 BP measurements). Those with dnPPHTN had a significantly steeper rise in SBP preceding the diagnosis, which occurred at a median of 5 days (IQR 5–5.5 days). SBP rose by 1.6 mmHg more per day until its peak at postpartum day 9 in those with dnPPHTN, compared to normotensive participants ( p < 0.001). DBP rose by 0.3 mmHg more per day and peaked later (postpartum day 14 in those with dnPPHTN vs. day 12 in those who remained normotensive; p < 0.001). Conclusion: Using remote monitoring technology, we characterized distinct postpartum BP trajectories in patients at risk for dnPPHTN, revealing a prolonged rise into the second postpartum week and trends that distinguish physiologic from pathophysiologic BP changes. These findings suggest that extended postpartum BP monitoring may be important for timely identification and intervention in patients developing dnPPHTN.