Compelling evidence indicates that psychiatric and developmental disorders are generally caused by disruptions in the functional connectivity (FC) of brain networks. Events occurring during development, and in particular during fetal life, have been implicated in the genesis of such disorders. However, the developmental timetable for the emergence of neural FC during human fetal life is unknown. We present the results of resting-state functional magnetic resonance imaging performed in 25 healthy human fetuses in the second and third trimesters of pregnancy (24 to 38 weeks of gestation). We report the presence of bilateral fetal brain FC and regional and age-related variation in FC. Significant bilateral connectivity was evident in half of the 42 areas tested, and the strength of FC between homologous cortical brain regions increased with advancing gestational age. We also observed medial to lateral gradients in fetal functional brain connectivity. These findings improve understanding of human fetal central nervous system development and provide a basis for examining the role of insults during fetal life in the subsequent development of disorders in neural FC.

The human brain undergoes dramatic maturational changes during late stages of fetal and early postnatal life. The importance of this period to the establishment of healthy neural connectivity is apparent in the high incidence of neural injury in preterm infants, in whom untimely exposure to ex-uterine factors interrupts neural connectivity. Though the relevance of this period to human neuroscience is apparent, little is known about functional neural networks in human fetal life. Here, we apply graph theoretical analysis to examine human fetal brain connectivity. Utilizing resting state functional magnetic resonance imaging (fMRI) data from 33 healthy human fetuses, 19 to 39 weeks gestational age (GA), our analyses reveal that the human fetal brain has modular organization and modules overlap functional systems observed postnatally. Age-related differences between younger (GA <31 weeks) and older (GA≥31 weeks) fetuses demonstrate that brain modularity decreases, and connectivity of the posterior cingulate to other brain networks becomes more negative, with advancing GA. By mimicking functional principles observed postnatally, these results support early emerging capacity for information processing in the human fetal brain. Current technical limitations, as well as the potential for fetal fMRI to one day produce major discoveries about fetal origins or antecedents of neural injury or disease are discussed.

Pregnancy is a time of significant hemodynamic, metabolic, and hormonal stress that can unmask underlying subclinical cardiovascular abnormalities, and pregnancy-related complications may serve as early warning signs for future risk of cardiovascular disease. The increased recognition of these sex-specific risk factors could identify women who may benefit from more intensive risk factor modification to reduce morbidity and mortality later in life. In this review, we describe several pregnancy-related complications that have been associated with the risk of cardiovascular disease, including hypertensive disorders of pregnancy, gestational diabetes mellitus, preterm delivery, and pregnancy loss. Pregnancy-associated risk factors must be identified to fully assess a woman’s future cardiovascular risk and may influence strategies for risk reduction.

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Background: Atrial fibrillation and atrial flutter (AF) during pregnancy may confer increased risk of perinatal complications, particularly since pregnancy is a known hypercoagulable and arrhythmogenic state. However, few studies of outcomes among this population exist, and the optimal management strategy is unclear. We sought to determine the risk of adverse outcomes among pregnant women with AF. Methods: In this single-center study, patients with documented AF in pregnancy (1/1998-9/2018) were retrospectively analyzed. Charts were manually reviewed for demographics, comorbidities, underlying cardiac disease, and medications. Outcomes included arrhythmias, need for cardioversion, and thromboembolic events. Results: Of 66 pregnant women with documented AF, 20 (30.3%) had a diagnosis of AF prior to pregnancy and 46 (69.6%) had new onset AF during pregnancy or immediately postpartum (within six weeks of delivery). Nine women (13.6%) had persistent AF. Thirty women (45.4%) had valve disease and/or congenital heart disease and/or preexisting cardiomyopathy, and eight (12.1%) had AF precipitated by active infection or severe nausea/vomiting. Comorbidities included diabetes mellitus (3%), hypertension (9%), thyroid disease (13.6%), and obesity (32.6%). Electrical cardioversion was performed in 10 women before or after pregnancy, and five women underwent electrical cardioversion during their first or second trimesters of pregnancy. Rate-controlling medications were prescribed in 75.7%, with the most common medication being metoprolol (39.3%). Anticoagulation strategies varied from no intervention (53%), low-dose aspirin monotherapy (18.2%), enoxaparin (13.6%), warfarin (13.6%), or warfarin plus aspirin (3%). AF with rapid rate occurred during labor/delivery in 6/44 (13.6%) women with available telemetry data. One woman had a stroke during pregnancy related to vertebral artery dissection; she was in sinus rhythm at presentation. No other thromboembolic complications occurred. Conclusion: Pregnant women with AF may require rate-controlling medication and/or cardioversion during pregnancy, but appear to be at low risk for thromboembolic complications when appropriately anticoagulated. Larger studies of pregnant women both with and without underlying structural heart disease are needed to further assess complications and thromboembolic risk to optimize management of AF in pregnancy.