Charlotte Brennan-Richardson

University of Manchester

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Paul Brownbill

University of Manchester

Angelos Evangelinos

University of Manchester

Stefan R. Hansson

Lund University

Kurt Hecher

University Medical Center Hamburg-Eppendorf

J. Brodszki

Skåne University Hospital

Adam Brook

University of Manchester

Kasia Maksym

University College London

Rebecca Spencer

University College London

Neil Marlow

University College London

Anna L. David

University College London

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University of Manchester

Manchester Academic Health Science Centre

St Mary's Hospital

University College London

St Mary's Hospital

University College Hospital

St. Mary's Hospital

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Manchester University NHS Foundation Trust

London Women's Clinic

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Fetoplacental vascular effects of maternal adrenergic antihypertensive and cardioprotective medications in pregnancy

Journal of Hypertension (2023)

Teresa Tropea Weerawaroon Mavichak Angelos Evangelinos Charlotte Brennan‐Richardson Elizabeth Cottrell

Maternal cardiovascular diseases, including hypertension and cardiac conditions, are associated with poor fetal outcomes. A range of adrenergic antihypertensive and cardioprotective medications are often prescribed to pregnant women to reduce major maternal complications during pregnancy. Although these treatments are not considered teratogenic, they may have detrimental effects on fetal growth and development, as they cross the fetoplacental barrier, and may contribute to placental vascular dysregulation. Medication risk assessment sheets do not include specific advice to clinicians and women regarding the safety of these therapies for use in pregnancy and the potential off-target effects of adrenergic medications on fetal growth have not been rigorously conducted. Little is known of their effects on the fetoplacental vasculature. There is also a dearth of knowledge on adrenergic receptor activation and signalling within the endothelium and vascular smooth muscle cells of the human placenta, a vital organ in the maintenance of adequate blood flow to satisfy fetal growth and development. The fetoplacental circulation, absent of sympathetic innervation, and unique in its reliance on endocrine, paracrine and autocrine influence in the regulation of vascular tone, appears vulnerable to dysregulation by adrenergic antihypertensive and cardioprotective medications compared with the adult peripheral circulation. This semi-systematic review focuses on fetoplacental vascular expression of adrenergic receptors, associated cell signalling mechanisms and predictive consequences of receptor activation/deactivation by antihypertensive and cardioprotective medications.

10.1097/hjh.0000000000003532

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Free fetal haemoglobin in an early onset fetal growth restriction cohort (EVERREST) threatens placental function: A prospective multi-centre study Short version title: Free fetal haemoglobin in severe FGR

Authorea (Authorea) (2024)

Adam Brook Georgia C. Baynes Jonathan Scargill Angelos Evangelinos Charlotte Brennan‐Richardson

Fetal growth

10.22541/au.172620545.56168829/v1

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Free Foetal Haemoglobin in Severe Early‐Onset Foetal Growth Restriction: A Prospective Multi‐Centre Study

BJOG An International Journal of Obstetrics & Gynaecology (2025)

Adam Brook Georgia C. Baynes Jonathan Scargill Angelos Evangelinos Charlotte Brennan‐Richardson

ABSTRACT Objective To assess foetal circulating free foetal haemoglobin (fHbF) levels and heme defences, correlated to foetal circulatory biometry and foetal sex in severe early‐onset foetal growth restriction (FGR). Design, Setting and Population A prospective study severe early‐onset foetal growth restriction pregnancies with close clinical management (estimated foetal weight (EFW) < 3rd centile and < 600 g at 20–26 + 6 weeks; N = 20). Method & Main Outcome Measures Temporal foetal vascular obstetric biometry was recorded. Cord blood fHbF and key heme‐scavenger defences were measured and compared with normal term births ( N = 26) and births with late‐onset FGR ( N = 12). Results fHbF was elevated in early‐onset FGR compared with normal pregnancy: 0.437(0.337/0.753) mg/mL; and 0.098 (0.045/0.264) mg/mL, respectively ( p < 0.0001); whilst hemopexin was downregulated in early‐ ( p < 0.001) and late‐onset FGR ( p < 0.0001), compared to normal pregnancy: 36(14/81) μg/mL, 25(19/40) μg/mL, and 155(132/219) μg/mL, respectively; median (interquartile ranges). Early‐onset FGR male foetuses had higher HbF compared with the normal males: 0.710(0.433/0.857) mg/mL; ( p < 0.001); 0.099(0.043/0.246) mg/mL, respectively; median (interquartile ranges). In early‐onset FGR, ratios of mid‐cerebral artery and umbilical artery pulsatility indices correlated positively with heme‐scavenger levels (hemopexin and a heme‐handling composite measure: p < 0.05, r = 0.672; and p < 0.01, r = 0.620; respectively), indicating lower levels are associated with cerebral vascular redistribution. These heme handling measures also positively correlated with gestational age at delivery ( r = 0.713 and r = 0.642, respectively, p < 0.01, both) and birthweight ( r = 0.742, p < 0.001; and r = 0.523, p < 0.05; respectively). Conclusion Overproduction of fHbF and an inadequate heme defence may contribute to foetal distress and poor umbilical arterial Dopplers in early onset FGR due to elevated placental vascular resistance and vascular inflammation.

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10.1111/1471-0528.18104

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