Faculty Bibliography

Background: In ED patients who present with acute drug overdose, severe QTc prolongation (>500 ms) has been shown to be a predictor of adverse cardiovascular events (ACVE). However, it is unclear what clinical factors are associated with delayed severe QTc prolongation (dsQTp), and it is unknown whether dsQTp can predict ACVE. This study aims to: (1) Define clinical factors associated with dsQTp, and (2) test whether dsQTp is an independent predictor for ACVE.
Method(s): This was a prospective cohort study at 2 urban tertiary care EDs. Data was collected by trained research assistants, and included demographics, drug exposure, medication administration, initial and repeat ECG data, lab data, and outcome measures. dsQTp was defined as presence of initial QTc 499. The primary study outcome was the composite of ACVE defined as in-hospital occurrence of any of the following: MI, shock, ventricular dysrhythmia, and cardiac arrest. Univariate statistics and multivariable logistic regression calculations were made using SPSS version 24. With a fixed sample size of 1670, we calculated that we would have 99% power to show a 3-fold increase in risk with 0.05 alpha.
Result(s): Out of 2311 patients screened, 641 were excluded (age 500) leaving 1670 patients for analysis. The dsQTp group (N = 27) was found to be older than the control group (N = 1643)(40.1 vs 51.6, P
Conclusion(s): This cohort study reveals a subset of ED patients who are at greater risk of overdose-related ACVE but not immediately apparent by the initial ECG. Further study is needed to identify which patients are at risk for dsQTp, as they may require prolonged observation and repeated ECGs. Limitations include missing repeat QTc measurements, and inability to control for overdose severity as a surrogate for repeat ECGs. Future study is warranted to further characterize patients at risk for dsQTp to evaluate other exposure-related factors as yet undiscovered

Learning, memory, and emotional regulation are all modulated by sleep. Sleep influences on neural circuit function and plasticity occur in all mammalian brain regions examined to date, including the noncanonical olfactory system, suggesting sleep disruption could have wide-ranging consequences on behavior and cognition. New evidence suggests that sleep disturbances during early development can have particularly insidious and long-lasting consequences. In particular, work from our lab and others suggests that early-life adverse events can disrupt sleep across the life span, thus contributing to a variety of negative cognitive and behavioral outcomes. These findings raise the possibility that interventions targeting sleep may have therapeutic value for children or adults exposed to early-life adverse events. Here, we describe sleep and sleep ontogeny and then describe the role of sleep in normal and pathological brain function. Finally, we explore how early-life adverse events and sleep disturbances may reciprocally interact to produce a range of psychopathological outcomes.
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[This corrects the article DOI: 10.3389/fnins.2019.00117.].