Early human development
October 7, 2026 · via Europe PMC
The fetal heart-brain axis as a new frontier for long-term outcomes in children with congenital heart disease.
Hou S, Wang J, Mao B, Zhou Y, Wang J
AI summary — for doctors, generated from the abstract only
Brain development in congenital heart disease is already altered before birth, so neuroprotection should start prenatally.
What was studied
Narrative review of fetal heart-brain axis physiology, mechanisms of disruption in CHD, links to long-term outcomes, prenatal assessment tools and possible interventions.
Key findings
- Fetal MRI, CMR, Doppler and placental studies suggest CHD-related brain changes exist before surgery.
- Disrupted blood streaming, placental dysfunction, genetics, inflammation and oxidative stress may reduce brain volume and delay white-matter maturation.
- Gaps remain, including the need for multicentre longitudinal cohorts and multimodal prediction models.
Clinical relevance
Neurodevelopmental outcomes now drive morbidity in CHD survivors, so prenatal and perinatal care should look beyond cardiac repair.
Who should care
Limitations
A narrative review, so the evidence is not systematically graded and prenatal interventions remain largely theoretical.
Emphasise neurodevelopmental surveillance and continuous neuroprotection from the fetal period in CHD care.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Survival among children with congenital heart disease (CHD) has improved substantially with advances in prenatal screening, perioperative care and cardiac surgery. However, neurodevelopmental, cognitive-behavioural and health-related quality-of-life outcomes remain major determinants of long-term morbidity. Recent work using fetal magnetic resonance imaging (MRI), fetal cardiovascular magnetic resonance (CMR), Doppler haemodynamic assessment and placental studies suggests that CHD-related alterations in brain development do not arise solely after postnatal surgery or intensive care, but may already be present before birth. In normal fetal circulation, finely tuned coupling between the placenta, heart and brain preferentially directs oxygen-rich blood towards the cerebral and coronary circulations. Complex CHD can disrupt this streaming physiology, leading to reduced cerebral perfusion, oxygenation and metabolism. Placental dysfunction, genetic variation, inflammation and oxidative stress may further amplify heart-brain imbalance, making reduced brain volume, delayed white-matter maturation and abnormal brain-network development important intermediate phenotypes for later neurodevelopmental risk. This review discusses the normal physiology of the fetal heart-brain axis, mechanisms of fetal heart-brain-axis disruption in CHD, links with long-term outcomes, prenatal assessment tools and potential intervention strategies. We also identify key knowledge gaps and emphasise the need for multicentre longitudinal cohorts and multimodal prediction models, with the aim of shifting CHD care from cardiac repair alone towards continuous neuroprotection before and after birth.
DOI
10.1016/j.earlhumdev.2026.106693
PMID
42858691
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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