What is the clinical evidence from this study?

Study design: Observational. Population: Congenital Heart Disease (CHD) in fetuses (n=44). Intervention: Maternal hyperoxia vs. Controls (fetuses without CHD). Primary outcome: T2* decay time (fetal cerebral oxygenation) (beta -14.4, 95% CI -23.3 to -5.6, p=0.002).

What does this research mean for the field?

Fetuses with congenital heart disease have lower cerebral tissue oxygenation compared to controls and exhibit variable responses to maternal hyperoxia depending on their specific cardiac physiology. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

December 21, 2020Journal of the American Heart AssociationOpen Access

Fetal Cerebral Oxygenation Is Impaired in Congenital Heart Disease and Shows Variable Response to Maternal Hyperoxia

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Key result

Fetal CHD is linked to faster T2* decay times, indicating lower cerebral tissue oxygenation.

beta -14.4
95% CI -23.3 to -5.6
P=0.002
n=44

Why the study?

Impairments in fetal oxygen delivery are implicated in brain dysmaturation in CHD, suggesting a role for in utero transplacental oxygen therapy, but fetal cerebral oxygenation and its response to maternal hyperoxia remained to be quantified.

Does brief maternal hyperoxia improve fetal cerebral oxygenation in fetuses with congenital heart disease?

Comparison

Fetuses with CHD vs controls before and after maternal hyperoxia

Design

Prospective observational study

Authors

SPShabnam PeyvandiPediatric / Congenital Cardiology DXDuan XuUniversity of California, San Francisco YWYan WangChildren's Hospital of Philadelphia

Discussion

Member takes

Implication

Lower cerebral oxygenation in CHD fetuses warrants attention; leaves open consistent maternal hyperoxia benefit by lesion physiology.

Study Design

Type

Observational (n=44)

Structured PICO

Does brief maternal hyperoxia improve fetal cerebral oxygenation in fetuses with congenital heart disease?

Population

44 pregnant mothers in the third trimester with a prenatal diagnosis of fetal congenital heart disease (CHD=24, focusing on transposition or left-sided obstruction) and controls (n=20).

Intervention

Brief administration of maternal hyperoxia

Comparator

Control fetuses without CHD, and baseline measurements before hyperoxia

Outcome

Fetal cerebral oxygenation quantified by measuring T2* decay on fetal brain MRIsurrogate

Main Result

Effect estimate: beta -14.4 (95% CI -23.3 to -5.6)

p-value: p=0.002

Fetal cerebral tissue oxygenation is lower in complex CHD, but shows variable improvement in response to maternal hyperoxia depending on the specific cardiovascular physiology.

Cite This Study

Peyvandi et al. (2020) conducted an observational in Congenital Heart Disease (CHD) in fetuses (n=44). Maternal hyperoxia vs. Controls (fetuses without CHD) was evaluated on T2* decay time (fetal cerebral oxygenation) (beta -14.4, 95% CI -23.3 to -5.6, p=0.002). Fetuses with congenital heart disease had faster T2* decay times compared with controls (beta=-14.4; 95% CI, -23.3 to -5.6; P=0.002), indicating lower cerebral tissue oxygenation.

synapsesocial.com/papers/6a17868e8d470cd99253606f https://doi.org/10.1161/jaha.120.018777

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Fetal Cerebral Oxygenation Is Impaired in Congenital Heart Disease and Shows Variable Response to Maternal Hyperoxia

Discussion

Member takes

Implication

Study Design

Structured PICO

Main Result

Cite This Study

Fetal Cerebral Oxygenation Is Impaired in Congenital Heart Disease and Shows Variable Response to Maternal Hyperoxia

Discussion

Member takes

Implication

Study Design

Structured PICO

Main Result

Cite This Study

Also Consider

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