Lack of Association Between Race and Ethnicity and Timely Treatment of Severe Peripartum Hypertension.

Background: Hypertensive disorders of pregnancy are a leading cause of severe maternal morbidity and mortality. National guidelines recommend treatment within 30 to 60 minutes of confirmed severe hypertension to reduce the risk of maternal stroke. The objectives of this study were to quantify the number of patients who did not receive timely treatment of severe hypertension, identify barriers to timely treatment, and evaluate if race/ethnicity was associated with timeliness of treatment.

Impact of labor and delivery unit policy modifications on maternal and neonatal outcomes during the coronavirus disease 2019 pandemic.

Background: In response to the coronavirus disease 2019 pandemic, hospitals nationwide have implemented modifications to labor and delivery unit practices designed to protect delivering patients and healthcare providers from infection with severe acute respiratory syndrome coronavirus 2. Beginning in March 2020, our hospital instituted labor, and delivery unit modifications targeting visitor policy, use of personal protective equipment, designation of rooms for triage and delivery of persons suspected or infected with coronavirus disease 2019, delivery management, and newborn care. Little is known about the ramifications of these modifications in terms of maternal and neonatal outcomes.

Routine Multidisciplinary Review of Severe Maternal Morbidity Is Associated with a Reduction in Preventable Cases of Severe Maternal Morbidity.

Objective: Severe maternal morbidity (SMM) has increased by 45% in the United States and is estimated to affect up to 1.5% of all deliveries. Research has not yet been conducted that demonstrates a benefit to multidisciplinary review of SMM.

Maternal Mortality in the Twenty-First Century.

Maternal mortality plagues much of the world. There were 303,000 maternal deaths in 2015 representing an overall global maternal mortality ratio of 216 maternal deaths per 100,000 live births. In the United States, the maternal mortality ratio had been decreasing until 1987, remained stable until 1999, and then began to increase.

Opportunities for improvement in care among women with severe maternal morbidity.

Background: Severe maternal morbidity is increasing in the United States and has been estimated to occur in up to 1.3% of all deliveries. A standardized, multidisciplinary approach has been recommended to identify and review cases of severe maternal morbidity to identify opportunities for improvement in maternal care.

Impact of fertility treatment on severe maternal morbidity.

Objective: To determine if fertility treatment is associated with increased risk of severe maternal morbidity (SMM) compared with spontaneous pregnancies.

Design: Retrospective cohort study.

Setting: Academic medical center.

Pulmonary hypertension in transgenic mice expressing a dominant-negative BMPRII gene in smooth muscle.

Bone morphogenetic peptides (BMPs), a family of cytokines critical to normal development, were recently implicated in the pathogenesis of familial pulmonary arterial hypertension. The type-II receptor (BMPRII) is required for recognition of all BMPs, and targeted deletion of BMPRII in mice results in fetal lethality before gastrulation. To overcome this limitation and study the role of BMP signaling in postnatal vascular disease, we constructed a smooth muscle-specific transgenic mouse expressing a dominant-negative BMPRII under control of the tetracycline gene switch (SM22-tet-BMPRII(delx4+) mice).

Endothelin B receptor deficiency predisposes to pulmonary edema formation via increased lung vascular endothelial cell growth factor expression.

Endothelin (ET) may contribute to pulmonary edema formation, particularly under hypoxic conditions, and decreases in ET-B receptor expression can lead to reduced ET clearance. ET increases vascular endothelial cell growth factor (VEGF) production in vitro, and VEGF overexpression in the lung causes pulmonary edema in vivo. We hypothesized that pulmonary vascular ET-B receptor deficiency leads to increased lung ET, that excess ET increases lung VEGF levels, promoting pulmonary edema formation, and that hypoxia exaggerates these effects.