0821 Maternal Sleep in Pregnancies Complicated by Fetal Congenital Heart Disease

Abstract Introduction Declining morbidity for children with congenital heart disease (CHD) has shifted efforts to understanding causes and improving long-term outcomes. While a genetic etiology is identified in ~25%, and other factors such as teratogens contribute a small percentage, the etiology is unknown for most patients. Fetuses with CHD have a 2-3-fold increased risk of prematurity and maternal sleep disruption has been shown to be associated with adverse fetal outcomes including preterm birth and fetal growth restriction. Emerging data raise the possibility that maternal sleep may play a role in birth defects. We sought to investigate sleep during pregnancy in women whose fetuses were diagnosed with CHD, a common anatomical malformation impacting ~40,000 births/year in the United States. Methods Pregnant participants were recruited from an academic medical center and queried about their sleep including snoring, sleep duration, sleep quality and sleep midpoint. Sleep midpoint later than 04:00am was considered as circadian misalignment. Demographic and clinical information was abstracted from medical records. Results Fifty-one pregnancies with fetal CHD were compared to 1361 pregnancies without fetal CHD, with a mean gestational age of 33.9±4.2 weeks at the time of survey administration. Women with a CHD pregnancy had a non-significant increase in Type 2 diabetes mellitus (6.3% vs. 3.4%; p=0.29) and gestational diabetes (15.7% vs. 8.3%; p=0.29), with no difference in pre-eclampsia (4.2% vs. 6.1%; p=0.67). There were no differences in the proportion of women with CHD fetuses who reported habitual snoring (35% vs. 35%; p=0.89) or poor sleep quality (63% vs. 71%; p=0.2) compared to women with non-CHD fetuses. However, women whose pregnancies were complicated by CHD had sleep midpoints that were later (~34 minutes) than women with typically developing fetuses (04:06am vs. 03:32am; p=0.04), despite the same sleep duration (8.5hrs vs. 8.5hrs). Notably, 40% of CHD pregnancies had delayed sleep midpoint compared to 29% of non-CHD pregnancies (p=0.1). Conclusion We hypothesize that delayed sleep timing, even when sleep duration is within normal limits, may be a risk factor for CHD. Mechanistic studies are required to investigate how altered circadian rhythms during development could trigger systemic changes that increase vulnerability to cardiac defects. Support (if any) R21HL089918