scholarly journals Nocturnal ventricular repolarization lability predicts cardiovascular mortality in the Sleep Heart Health Study

2019 ◽  
Vol 316 (3) ◽  
pp. H495-H505 ◽  
Author(s):  
Martin Schmidt ◽  
Mathias Baumert ◽  
Thomas Penzel ◽  
Hagen Malberg ◽  
Sebastian Zaunseder

The objective of the present study was to quantify repolarization lability and its association with sex, sleep stage, and cardiovascular mortality. We analyzed polysomnographic recordings of 2,263 participants enrolled in the Sleep Heart Health Study (SHHS-2). Beat-to-beat QT interval variability (QTV) was quantified for consecutive epochs of 5 min according to the dominant sleep stage [wakefulness, nonrapid eye movement stage 2 (NREM2), nonrapid eye movement stage 3 (NREM3), and rapid eye movement (REM)]. To explore the effect of sleep stage and apnea-hypopnea index (AHI) on QT interval parameters, we used a general linear mixed model and mixed ANOVA. The Cox proportional hazards model was used for cardiovascular disease (CVD) death prediction. Sex-related differences in T wave amplitude ( P < 0.001) resulted in artificial QTV differences. Hence, we corrected QTV parameters by T wave amplitude for further analysis. Sleep stages showed a significant effect ( P < 0.001) on QTV. QTV was decreased in deep sleep compared with wakefulness, was higher in REM than in NREM, and showed a distinct relation to AHI in all sleep stages. The T wave amplitude-corrected QTV index (cQTVi) in REM sleep was predictive of CVD death (hazard ratio: 2.067, 95% confidence interval: 1.105–3.867, P < 0.05) in a proportional hazards model. We demonstrated a significant impact of sleep stages on ventricular repolarization variability. Sex differences in QTV are due to differences in T wave amplitude, which should be corrected for. Independent characteristics of QTV measures to sleep stages and AHI showed different behaviors of heart rate variability and QTV expressed as cQTVi. cQTVi during REM sleep predicts CVD death. NEW & NOTEWORTHY We demonstrate here, for the first time, a significant impact of sleep stages on ventricular repolarization variability, quantified as QT interval variability (QTV). We showed that QTV is increased in rapid eye movement sleep, reflective of high sympathetic drive, and predicts death from cardiovascular disease. Sex-related differences in QTV are shown to be owing to differences in T wave amplitude, which should be corrected for.

SLEEP ◽  
2021 ◽  
Author(s):  
Brian Geuther ◽  
Mandy Chen ◽  
Raymond J Galante ◽  
Owen Han ◽  
Jie Lian ◽  
...  

Abstract Study Objectives Sleep is an important biological process that is perturbed in numerous diseases, and assessment its substages currently requires implantation of electrodes to carry out electroencephalogram/electromyogram (EEG/EMG) analysis. Although accurate, this method comes at a high cost of invasive surgery and experts trained to score EEG/EMG data. Here, we leverage modern computer vision methods to directly classify sleep substages from video data. This bypasses the need for surgery and expert scoring, provides a path to high-throughput studies of sleep in mice. Methods We collected synchronized high-resolution video and EEG/EMG data in 16 male C57BL/6J mice. We extracted features from the video that are time and frequency-based and used the human expert-scored EEG/EMG data to train a visual classifier. We investigated several classifiers and data augmentation methods. Results Our visual sleep classifier proved to be highly accurate in classifying wake, non-rapid eye movement sleep (NREM), and rapid eye movement sleep (REM) states, and achieves an overall accuracy of 0.92 +/- 0.05 (mean +/- SD). We discover and genetically validate video features that correlate with breathing rates, and show low and high variability in NREM and REM sleep, respectively. Finally, we apply our methods to non-invasively detect that sleep stage disturbances induced by amphetamine administration. Conclusions We conclude that machine learning based visual classification of sleep is a viable alternative to EEG/EMG based scoring. Our results will enable non-invasive high-throughput sleep studies and will greatly reduce the barrier to screening mutant mice for abnormalities in sleep.


1991 ◽  
Vol 70 (6) ◽  
pp. 2574-2581 ◽  
Author(s):  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White

We propose that a sleep-induced decrement in the activity of the tensor palatini (TP) muscle could induce airway narrowing in the area posterior to the soft palate and therefore lead to an increase in upper airway resistance in normal subjects. We investigated the TP to determine the influence of sleep on TP muscle activity and the relationship between changing TP activity and upper airway resistance over the entire night and during short sleep-awake transitions. Seven normal male subjects were studied on a single night with wire electrodes placed in both TP muscles. Sleep stage, inspiratory airflow, transpalatal pressure, and TP moving time average electromyogram (EMG) were continuously recorded. In addition, in two of the seven subjects the activity (EMG) of both the TP and the genioglossus muscle simultaneously was recorded throughout the night. Upper airway resistance increased progressively from wakefulness through the various non-rapid-eye-movement sleep stages, as has been previously described. The TP EMG did not commonly demonstrate phasic activity during wakefulness or sleep. However, the tonic EMG decreased progressively and significantly (P less than 0.05) from wakefulness through the non-rapid-eye-movement sleep stages [awake, 4.6 +/- 0.3 (SE) arbitrary units; stage 1, 2.6 +/- 0.3; stage 2, 1.7 +/- 0.5; stage 3/4, 1.5 +/- 0.8]. The mean correlation coefficient between TP EMG and upper airway resistance across all sleep states was (-0.46). This mean correlation improved over discrete sleep-awake transitions (-0.76). No sleep-induced decrement in the genioglossus activity was observed in the two subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)


Neurology ◽  
2017 ◽  
Vol 90 (2) ◽  
pp. e135-e141 ◽  
Author(s):  
Yinge Li ◽  
Yanping Li ◽  
John W. Winkelman ◽  
Arthur S. Walters ◽  
Jiali Han ◽  
...  

ObjectiveWe prospectively examined whether women with physician-diagnosed restless legs syndrome (RLS) had a higher risk of total and cardiovascular disease (CVD) mortality relative to those without RLS.MethodsThe current study included 57,417 women (mean age 67 years) from the Nurses' Health Study without cancer, renal failure, and CVD at baseline (2002). Main outcomes were total and CVD mortality. We used the Cox proportional hazards model to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and CVD-specific mortality based on RLS status, adjusting for age, presence of major chronic diseases, and other potential confounders.ResultsWe documented 6,448 deaths during 10 years of follow-up. We did not observe a significant association between presence of physician-diagnosed RLS and high risk of total mortality (adjusted HR 1.15, 95% CI 0.98–1.34). When cause-specific mortality was studied, participants with RLS had a significantly higher risk of CVD mortality (adjusted HR 1.43, 95% CI 1.02–2.00) relative to those without RLS after adjustment for potential confounders. Longer duration of RLS diagnosis was significantly associated with a higher risk of CVD mortality (p for trend = 0.04). Excluding participants with common RLS comorbidities strengthened the association between RLS and total (adjusted HR 1.43, 95% CI 1.03–1.97) and CVD mortality (adjusted HR 2.27, 95% CI 1.21–4.28). However, we did not find a significant association between RLS and mortality due to cancer and other causes.ConclusionsWomen with RLS had a higher CVD mortality rate, which may not be fully explained by common co-occurring disorders of RLS.


1985 ◽  
Vol 59 (2) ◽  
pp. 384-391 ◽  
Author(s):  
D. P. White ◽  
J. V. Weil ◽  
C. W. Zwillich

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Marcus Ng ◽  
Milena Pavlova

Since the formal characterization of sleep stages, there have been reports that seizures may preferentially occur in certain phases of sleep. Through ascending cholinergic connections from the brainstem, rapid eye movement (REM) sleep is physiologically characterized by low voltage fast activity on the electroencephalogram, REMs, and muscle atonia. Multiple independent studies confirm that, in REM sleep, there is a strikingly low proportion of seizures (~1% or less). We review a total of 42 distinct conventional and intracranial studies in the literature which comprised a net of 1458 patients. Indexed to duration, we found that REM sleep was the most protective stage of sleep against focal seizures, generalized seizures, focal interictal discharges, and two particular epilepsy syndromes. REM sleep had an additional protective effect compared to wakefulness with an average 7.83 times fewer focal seizures, 3.25 times fewer generalized seizures, and 1.11 times fewer focal interictal discharges. In further studies REM sleep has also demonstrated utility in localizing epileptogenic foci with potential translation into postsurgical seizure freedom. Based on emerging connectivity data in sleep, we hypothesize that the influence of REM sleep on seizures is due to a desynchronized EEG pattern which reflects important connectivity differences unique to this sleep stage.


2003 ◽  
Vol 94 (3) ◽  
pp. 883-890 ◽  
Author(s):  
Michael F. Fitzpatrick ◽  
Helen S. Driver ◽  
Neela Chatha ◽  
Nha Voduc ◽  
Alison M. Girard

The oral and nasal contributions to inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 ± 5 yr, with normal nasal resistance (mean 2.0 ± 0.3 cmH2O · l−1 · s−1) by use of a divided oral and nasal mask. Minute ventilation awake (5.9 ± 0.3 l/min) was higher than that during sleep (5.2 ± 0.3 l/min; P < 0.0001), but there was no significant difference in minute ventilation between different sleep stages ( P = 0.44): stage 2 5.3 ± 0.3, slow-wave 5.2 ± 0.2, and rapid-eye-movement sleep 5.2 ± 0.2 l/min. The oral fraction of inhaled ventilation during wakefulness (7.6 ± 4%) was not significantly different from that during sleep (4.3 ± 2%; mean difference 3.3%, 95% confidence interval −2.1–8.8%, P = 0.19), and no significant difference ( P = 0.14) in oral fraction was observed between different sleep stages: stage two 5.1 ± 2.8, slow-wave 4.2 ± 1.8, rapid-eye-movement 3.1 ± 1.7%. Thus the inhaled oral fraction in normal subjects is small and does not change significantly with sleep stage.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A188-A189
Author(s):  
Salma Patel ◽  
Wojciech Zareba ◽  
Bonnie LaFleur ◽  
Jean-Philippe Couderc ◽  
Xiaojuan Xia ◽  
...  

Abstract Introduction Sleep disordered breathing (SDB) is associated with increased mortality. Obstructive apneas/hypopneas have been associated with an increase in both QTc duration and QT variability. These markers of ventricular repolarization are associated with arrhythmias and death. It is unknown whether SDB-related QTc changes are responsible for the relationship between QTc/QT variability and cardiovascular death (CVD). Methods From the Sleep Heart Health Study, we randomly selected 200 subjects in each of four groups based on overall apnea/hypopnea index: those with no SDB and those in either, mild, moderate or severe SDB at baseline, matched for gender, age and BMI. Respiratory-related channels and electrocardiograms (ECG) from each polysomnography were analyzed. QTc was calculated using Bazett’s heart rate correction. The following measures of QT variability were obtained: i) standard deviation of QT intervals (SDQT) at 1- and 5-minute intervals and ii) short-term interval QT variability (STVQT) at 5-minute intervals. Cox proportional hazards regression models were used to evaluate potential predictors of CVD. Results Twenty-nine subjects were excluded either due to missing data or low quality ECG. The 771 subjects included were 68±10 years of age, half were female. During follow-up, 220 subjects (28.5%) died of CVD among whom, 67 (30.5%) had comorbid severe SDB, 45 (20.5%) had no SDB, and the remaining CVD deaths had mild (47, 21.4%) and moderate 61 (27.7%) SDB. The CVD patients were more likely to be older(p&lt;0.001), hypertensive (p&lt;0.001), diabetic(p&lt;0.001), and had increased SDQT(p&lt;0.001), STVQT(p&lt;0.001) and QTc (0.017). After adjusting for covariates, the presence of mild (p=0.562), moderate(p=0.439) and severe SDB (p=0.912) did not moderate the association between QTc prolongation and CVD. Additionally, mild (p=0.486), moderate(p=0.478) and severe SDB (p=0.849) did not moderate the association between SDQT and CVD. Similarly, mild (p=0.144), moderate(p=0.594) and severe SDB (p=0.508) did not moderate the association between STVQT and CVD. However, QTc, SDQT, STVQT, mild and severe SDB were individually associated with CVD (p=0.004, 0.000, 0.000, 0.014, 0.022, respectively). Conclusion SDB was not a factor in the relationship between QTc prolongation/QT variability and CVD. Support (if any) American Academy of Sleep Medicine Foundation (203-JF-18), National Institutes of Health (HL126140), University of Arizona Health Sciences Career and Development Award (5299903)


1984 ◽  
Vol 56 (3) ◽  
pp. 671-677 ◽  
Author(s):  
C. M. Shapiro ◽  
C. C. Goll ◽  
G. R. Cohen ◽  
I. Oswald

Heat production during sleep was studied by continuous indirect calorimetry with simultaneous electroencephalographic monitoring. Controlling for gross influences on heat production, comparisons of heat production during different sleep stages showed heat production in stage 4 sleep to be significantly lower than in other sleep stages. There appeared to be a gradation in heat production in non-rapid-eye-movement stages of sleep with stage 2 higher and stage 4 lower than stage 3. Heat production in stage 4 was less variable than in any other sleep stage. Both the level and variability of heat production was similar in stage 2 and rapid-eye-movement sleep. Heat production during the night was 9% lower than during resting wakefulness. The average heat production in stage 4 sleep was 14.4% lower than resting wakeful values.


2020 ◽  
Vol 10 (6) ◽  
pp. 1274-1280
Author(s):  
Yung-Ming Chung ◽  
Shyh-Liang Lou ◽  
Peng-Zhe Tsai ◽  
Ming-Chen Wang ◽  
Liang-Wen Hang

Sleep apnea has increasingly become a public health issue. To further elucidate the physiological changes in different sleep apnea severity levels, we analyzed the autonomic nervous system (ANS) activity in each sleep stage by heart rate variability (HRV), moreover, we clarified how sleep apnea severity affects hypnogram and sleep quality. Subjects used in this study was obtained from PhysioNet, and the patient data were grouped into mild, moderate, and severe levels of sleep apnea according to apnea–hypopnea index (AHI). The electrocardiogram readings during the period of free apnea were extracted and evaluated by HRV and represented to the sleep stages as follows: Awake, rapid eye movement (REM), and nonrapid eye movement (NREM) in different sleep apnea levels, respectively. The results indicated that the severe group (AHI ≥ 30 events per hour) has higher sympathetic nervous system (SNS) activity and lower parasympathetic nervous system (PNS) activity in NREM. This elevates the ANS tone in NREM similar to Awake, making the ANS activity between NREM and Awake indistinguishable. Furthermore, we evaluated the effects both with (w/) and without (w/o) apnea events in REM and NREM separately. Apnea events that occurred in REM (w/) were not different compared to those in REM (w/o). On the other hand, apnea events occurring in NREM (w/) activated SNS and suppressed PNS activity. This altered the ANS tone, which suggested an early sleep stage transition to REM or Awake. This study indicates how sleep apnea severity correlates to the imbalance of ANS activity and it might disrupt the normal hypnogram. Consequently, from the ANS point of view that patients with severe apnea do not get appropriate rest from sleeping, these patients need some medical interventions or treatment to prevent the development of chronic diseases.


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