Andrea C. Hinton

TL;DR: Patterns of prenatal head growth and brain histopathology identify a spectrum of abnormal CNS development and/or injury in HLHS fetuses.

TL;DR: Placentas from pregnancies complicated by fetal HLHS are characterized by abnormal parenchymal morphology, suggesting immature structure may be due to vascular abnormalities, and increased leptin expression may indicate an attempt to compensate for these vascular abnormalities.

TL;DR: In term nonsyndromic HLHS, fetal and neonatal microcephaly are associated with early adverse neurologic outcomes but not mortality.

TL;DR: The majority of fetuses with HLHS demonstrate decreased growth velocity during later pregnancy, suggesting growth abnormalities manifest in utero, suggesting the potential relationship to future clinical outcomes warrants further study.

TL;DR: Despite common vascular disturbances in placentas from HLHAs and TGA, these do not account for the disparities in birthweights frequently seen between these CHD subtypes, in contrast transcriptomic and histologic analyses reveal differentially regulated mechanisms between the subtypes that may explain these disparities.