# Cumulative burden of maternal vascular malperfusion and its association with early cerebral oxygenation in neonates

**Authors:** Yao Zhang, Tong Yang, Jiaxi Wu, Yanxia Mao, Jingxian Shi, Haoran Dou, Jinhui Li, Jun Tang, Tao Xiong

PMC · DOI: 10.3389/fcell.2026.1756278 · Frontiers in Cell and Developmental Biology · 2026-02-11

## TL;DR

This study shows that a higher number of maternal vascular malperfusion lesions in the placenta is linked to changes in early neonatal brain oxygenation patterns.

## Contribution

The study introduces a novel analysis of cumulative MVM lesion burden and its specific impact on neonatal cerebral oxygenation.

## Key findings

- Neonates with 3–5 MVM lesion types had significantly higher cerebral oxygen saturation (crSO2) in the first postnatal week.
- These neonates also showed lower cerebral fractional tissue oxygen extraction (cFTOE) compared to those without MVM.
- Early differences in cerebral oxygenation between groups diminished over time as postnatal age increased.

## Abstract

Maternal vascular malperfusion (MVM) represents a major cause of chronic fetal hypoxia and is associated with adverse neonatal outcomes. However, whether the cumulative burden of MVM lesions influences early cerebral oxygenation in neonates remains unclear. This study aimed to evaluate the association between the number of placental MVM lesion types and neonatal cerebral regional oxygen saturation (crSO2) and cerebral fractional tissue oxygen extraction (cFTOE).

In this retrospective observational study, 508 neonates admitted between January 2021 and March 2024 were included. Based on placental histopathology, infants were categorized into three groups according to the number of MVM lesion types: no MVM, 1–2 MVM types, and 3–5 MVM types. Cerebral oxygenation was monitored weekly from birth to postnatal day 28 using near-infrared spectroscopy. Multivariable linear regression models were used to assess associations between MVM burden and crSO2/cFTOE during the first postnatal week, adjusting for relevant maternal and neonatal covariates.

Compared with neonates without MVM, those with placental findings of 3–5 types of MVM had significantly higher crSO2 (β = 1.65; 95% CI, 0.05–3.24; P = 0.044) and lower cFTOE (β = −0.02; 95% CI, −0.04 to −0.01; P = 0.029) during the first postnatal week. No significant differences were observed in the 1–2 MVM group. Longitudinal analyses demonstrated decreasing crSO2 and increasing cFTOE with advancing postnatal age across all groups, with the early differences between groups attenuating over time.

A cumulative burden of 3–5 MVM types is independently associated with altered cerebral oxygenation patterns in the early neonatal period, characterized by higher crSO2 and lower cFTOE. These findings suggest that the cumulative burden of maternal vascular malperfusion lesions identified on postpartum placental examination may provide clinically relevant contextual information for interpreting early neonatal cerebral oxygenation patterns and underscore the need for enhanced physiological monitoring during the first postnatal week.

## Full-text entities

- **Genes:** CTSK (cathepsin K) [NCBI Gene 1513] {aka CTS02, CTSO, CTSO1, CTSO2, PKND, PYCD}
- **Diseases:** motor dysfunction (MESH:D000068079), sepsis (MESH:D018805), pregnancy (MESH:D011254), cognitive deficits (MESH:D003072), gastrointestinal bleeding (MESH:D006471), neurodevelopmental disorders (MESH:D002658), MVM (MESH:D000079262), dysfunction (MESH:D006331), necrotizing enterocolitis (MESH:D020345), Neonatal morbidities (MESH:D007232), Fetal distress (MESH:D005316), villous hypoplasia (MESH:D018253), infarction (MESH:D007238), ICP (MESH:C535932), stillbirth (MESH:D050497), bronchopulmonary dysplasia (MESH:D001997), vascular malperfusion (MESH:D057772), Endocrine disorders (MESH:D004700), inflammatory placental lesions (MESH:D010922), patent ductus arteriosus (MESH:D004374), HDP (MESH:D046110), preterm birth (MESH:D047928), Apnea (MESH:D001049), Pregnancy complications (MESH:D011248), Hypothyroidism (MESH:D007037), hypertensive disorders (MESH:D006973), brain injury (MESH:D001930), placental insufficiency (MESH:D010927), hypoproteinemia (MESH:D007019), placental abruption (MESH:D000037), cFTOE (MESH:D000860), fetal hypoxia (MESH:D005311), respiratory distress syndrome (MESH:D012128), genetic or metabolic diseases (MESH:D008659), FVM (MESH:D005315), bleeding (MESH:D006470), GDM (MESH:D016640), intraventricular hemorrhage (MESH:D000074042), retinopathy of prematurity (MESH:D012178), weight gain (MESH:D015430), white matter injury (MESH:D056784), neonatal respiratory distress syndrome (MESH:D012127), intracranial hemorrhage (MESH:D020300), neurological complications (MESH:D002493), neurodevelopmental abnormalities (MESH:D063647), preeclampsia (MESH:D011225), MVM lesion (MESH:D014652), Decidual vasculopathy (MESH:C564818), gestational hyperthyroidism (MESH:C566384), Intrahepatic cholestasis (MESH:D002780), placenta previa (MESH:D010923), FGR (MESH:D005317), hematoma (MESH:D006406), anomalies (MESH:D000013), inflammation (MESH:D007249), hypoplasia (MESH:D000080344)
- **Chemicals:** formalin (MESH:D005557), caffeine (MESH:D002110), MVM (-), oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12932476/full.md

## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932476/full.md

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Source: https://tomesphere.com/paper/PMC12932476