Although parents of very preterm infants have higher rates of maternal mental health challenges, mothers of full-term infants at high social risk are also impacted.

Altered brain development is a common feature of the neurological sequelae of complex congenital heart disease (CHD). These alterations include abnormalities in brain size and growth that begin prenatally and persist postnatally. However, the longitudinal trajectory of changes in brain volume from the prenatal to postnatal environment have not been investigated. We aimed to evaluate the trajectory of brain growth in a cohort of patients with complex CHD (n = 16) and healthy controls (n = 15) to test the hypothesis that patients with complex CHD would have smaller total brain volume (TBV) prenatally, which would become increasingly prominent by three months of age. Participants underwent fetal magnetic resonance imaging (MRI) at a mean of 32 weeks gestation, a preoperative/neonatal MRI shortly after birth, a postoperative MRI (CHD only), and a 3-month MRI to evaluate the trajectory of brain growth. Three-dimensional volumetric analysis was applied to the MRI data to measure TBV, as well as tissue-specific volumes of the cortical gray matter (CGM), white matter (WM), subcortical (deep nuclear) gray matter (SCGM), cerebellum, and cerebrospinal fluid (CSF). A random coefficients model was used to investigate longitudinal changes in TBV and demonstrated an altered trajectory of brain growth in the CHD population. The estimated slope for TBV from fetal to 3-month MRI was 11.5 cm3 per week for CHD infants compared to 16.7 cm3 per week for controls (p = 0.0002). Brain growth followed a similar trajectory for the CGM (p < 0.0001), SCGM (p = 0.002), and cerebellum (p = 0.005). There was no difference in growth of the WM (p = 0.30) or CSF (p = 0.085). Brain injury was associated with reduced TBV at 3-month MRI (p = 0.02). After removing infants with brain injury from the model, an altered trajectory of brain growth persisted in CHD infants (p = 0.006). These findings extend the existing literature by demonstrating longitudinal impairments in brain development in the CHD population and emphasize the global nature of disrupted brain growth from the prenatal environment through early infancy.

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Objective The aim of this study was to compare trajectories of maternal and paternal psychological distress after prenatal diagnosis of fetal moderate–severe congenital heart disease (CHD), from pregnancy through early-mid infancy. Methods Pregnant women who received a prenatal diagnosis of fetal moderate–severe CHD, and their partners, were enrolled in a prospective, longitudinal study. Symptoms of psychological distress were measured twice during pregnancy and twice after birth, using the Depression Anxiety Stress Scales (DASS-42). Patterns and predictors of psychological distress were examined using generalized hierarchical linear modeling. Results Psychological distress was present in 42% (18/43) of mothers and 22% (8/36) of fathers at least once during the study. The rates of distress did not differ between mothers and fathers. There was also no change in probability of distress over time or difference in distress trajectories between mothers and fathers. However, individual trajectories demonstrated considerable variability in symptoms for both mothers and fathers. Predictors of psychological distress included low social support for mothers and a history of mental health conditions for fathers. Conclusions Parents who receive a prenatal diagnosis of fetal CHD commonly report symptoms of psychological distress from the time of diagnosis through early-mid infancy and display highly variable trajectories. These data suggest that early and repeated psychological screening is important once a fetal CHD diagnosis is made and that providing mental health and social support to parents may be an important component of their ongoing care.