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Background <p>Critical congenital heart disease (CHD) is associated with poor neurodevelopmental outcomes and long-term psychosocial morbidity. The pre-natal environment is increasingly recognized as a critical effector. However, the association of specific placental lesions with fetal brain volume in CHD remains unexamined.</p> Methods <p>This was a multi-site prospective, nested case-control study, that&#xa0;recruited pregnant women with typical fetal&#xa0;development and prenatally diagnosed fetal CHD. Fetal brain MRI was performed at 32.8 ± 3.0 weeks gestation. Placentas were examined pathologically after delivery. Clinical characteristics were gathered from self-reports and medical charts. Multiple linear regression modeling was performed in R with <i>p</i> &lt; 0.05 considered significant.</p> Results <p>Placental hypoplasia (weight &lt;10th %ile) was associated with lower total fetal intracranial volume in CHD (<i>p</i> = 0.006) and combined (CHD + non-CHD) cohorts (<i>p</i> = 0.001). Maternal and/or fetal vascular malperfusion was also associated with lower total fetal intracranial volume in combined (<i>p</i> = 0.026), and non-CHD cohorts (<i>p</i> = 0.020). Presence of any placental pathology was associated with reduced total fetal intracranial volume (<i>p</i> = 0.047), an effect moderated by the presence of CHD (interaction term <i>p</i> = 0.037).</p> Conclusion <p>Placental hypoplasia, vascular malperfusion, and the presence of any placental pathology are associated with decreased total intracranial volumes in-utero. Fetuses with CHD and concomitant placental lesions appear particularly susceptible.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Placental vascular malperfusion is associated with reduced fetal intracranial volume.</p> </ItemContent> <ItemContent> <p>Placental hypoplasia (weight &lt;10th %ile) is associated with smaller intracranial volumes in fetal congenital heart disease.</p> </ItemContent> <ItemContent> <p>Placental pathologies uniquely affect in-utero brain development in congenital heart disease.</p> </ItemContent> <ItemContent> <p>This study is the first to link fetal brain development to specific placental pathologies using standardized, reproducible criteria (Amsterdam) with comparative inclusion of a non-congenital heart disease cohort.</p> </ItemContent> <ItemContent> <p>Evidence builds that the in-utero environment impacts neurodevelopment in congenital heart disease; this study points to specific placental lesions that may mediate the pathophysiology underlying these observations.</p> </ItemContent> </UnorderedList></p>

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Placental hypoplasia and vascular malperfusion are associated with reduced brain volumes in fetal congenital heart disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月7日

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  • Claire Baldauf,
  • Valeria Rosas,
  • Paul Zamiara,
  • William T. Reynolds,
  • Shuo Wang,
  • Nhu Tran,
  • Rafael Ceschin,
  • Melissa L. Wilson,
  • Jodie K. Votava-Smith,
  • Jessica L. Wisnowski,
  • Vidya Rajagopalan

摘要

Background

Critical congenital heart disease (CHD) is associated with poor neurodevelopmental outcomes and long-term psychosocial morbidity. The pre-natal environment is increasingly recognized as a critical effector. However, the association of specific placental lesions with fetal brain volume in CHD remains unexamined.

Methods

This was a multi-site prospective, nested case-control study, that recruited pregnant women with typical fetal development and prenatally diagnosed fetal CHD. Fetal brain MRI was performed at 32.8 ± 3.0 weeks gestation. Placentas were examined pathologically after delivery. Clinical characteristics were gathered from self-reports and medical charts. Multiple linear regression modeling was performed in R with p < 0.05 considered significant.

Results

Placental hypoplasia (weight <10th %ile) was associated with lower total fetal intracranial volume in CHD (p = 0.006) and combined (CHD + non-CHD) cohorts (p = 0.001). Maternal and/or fetal vascular malperfusion was also associated with lower total fetal intracranial volume in combined (p = 0.026), and non-CHD cohorts (p = 0.020). Presence of any placental pathology was associated with reduced total fetal intracranial volume (p = 0.047), an effect moderated by the presence of CHD (interaction term p = 0.037).

Conclusion

Placental hypoplasia, vascular malperfusion, and the presence of any placental pathology are associated with decreased total intracranial volumes in-utero. Fetuses with CHD and concomitant placental lesions appear particularly susceptible.

Impact

Placental vascular malperfusion is associated with reduced fetal intracranial volume.

Placental hypoplasia (weight <10th %ile) is associated with smaller intracranial volumes in fetal congenital heart disease.

Placental pathologies uniquely affect in-utero brain development in congenital heart disease.

This study is the first to link fetal brain development to specific placental pathologies using standardized, reproducible criteria (Amsterdam) with comparative inclusion of a non-congenital heart disease cohort.

Evidence builds that the in-utero environment impacts neurodevelopment in congenital heart disease; this study points to specific placental lesions that may mediate the pathophysiology underlying these observations.