Why the study?
Does acute sleep deprivation increase QT dispersion and QTmax in healthy young adults?
Does acute sleep deprivation increase QT dispersion and QTmax in healthy young adults?
Even a single night of sleep deprivation significantly increases QT maximum and QT dispersion in healthy young adults, suggesting a potential mechanism for increased arrhythmia risk.
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May indicate heightened arrhythmia vulnerability after sleep loss; hypothesis-generating in healthy adults and requires validation in prospective studies.
BACKGROUND: Sleep deprivation (SD) is known to be associated with worse cardiovascular outcome including mortality. We investigated the association between acute SD and electrocardiographic maximum QT interval (QTmax), QT, and corrected QT dispersion (QTd/cQTd), which are known to be among predictors of ventricular arrhythmias and sudden death. METHODS: We obtained electrocardiograms of 37 healthy young volunteers (age: 28.45 +/- 7.97 years; 11 women) after a night with regular sleep and repeated after a night with sleep debt. We measured minimum QT interval (QTmin), QTmax, QTd, and cQTd in milliseconds. RESULTS: Average sleep time of the subjects were 7.7 +/- 0.8 hours during regular sleep and 1.7 +/- 1.6 hours during a night with sleep debt (P < 0.001). Subjects had similar values of QTmin in milliseconds after a night of sleep debt when compared to after regular sleep (347.56 +/- 29.75 vs 344.59 +/- 20.89; P = 0.51), whereas they had significantly higher values of QTmax, QTd, and cQTd (396.48 +/- 30.11 vs 378.10 +/- 23.90; P = 0.001, 49.45 +/- 9.11 vs 33.51 +/- 10.05; P < 0.001 and 54.92 +/- 10.42 vs 37.23 +/- 10.81; P < 0.001, respectively). In Pearson's correlation analysis, QTmax, QTd, and cQTd were inversely correlated with sleep time (P = 0.012, r =-0.291; P < 0.001, r =-0.625 and P < 0.001, r =-0.616, respectively) CONCLUSIONS: In conclusion, we clearly demonstrated that even one night of SD is associated with significant increase in QTmax, QTd, and cQTd in healthy young adults despite remaining within normal limits. These electrocardiographic changes in acute SD might contribute to development and/or recurrence of arrhythmias. This implication deserves further studies for clarifying the possible linkage between SD and arrhythmias.
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Özer et al. (2008) studied this question.
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