Abstract P417: Relationship Between Blood Pressure Variability and Sleep Architecture

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Xiaoyue Liu ◽  
Jeongok G Logan ◽  
Younghoon Kwon ◽  
Jennifer Lobo ◽  
Hyojung Kang ◽  
...  

Introduction: Blood pressure (BP) variability (BPV) is a novel marker for cardiovascular disease (CVD) independent of high BP. Sleep architecture represents the structured pattern of sleep stages consisting of rapid eye movement (REM) and non-rapid eye movement (NREM), and it is an important element in the homeostatic regulation of sleep. Currently, little is known regarding whether BPV is linked to sleep stages. Our study aimed to examine the relationship between sleep architecture and BPV. Methods: We analyzed in-lab polysomnographic studies collected from individuals who underwent diagnostic sleep studies at a university hospital from 2010 to 2017. BP measures obtained during one year prior to the sleep studies were included. BPV was computed using the coefficient of variation for all individuals who had three or more systolic and diastolic BP data. We conducted linear regression analysis to assess the relationship of systolic BPV (SBPV) and diastolic BPV (DBPV) with the sleep stage distribution (REM and NREM sleep time), respectively. Covariates that can potentially confound the relationships were adjusted in the models, including age, sex, race/ethnicity, body mass index, total sleep time, apnea-hypopnea index, mean BP, and history of medication use (antipsychotics, antidepressants, and antihypertensives) during the past two years before the sleep studies. Results: Our sample (N=3,565; male = 1,353) was racially and ethnically diverse, with a mean age 54 ± 15 years and a mean BP of 131/76 ± 13.9/8.4 mmHg. Among the sleep architecture measures examined, SBPV showed an inverse relationship with REM sleep time after controlling for all covariates ( p = .033). We subsequently categorized SBPV into four quartiles and found that the 3 rd quartile (mean SBP SD = 14.9 ± 2.1 mmHg) had 3.3 fewer minutes in REM sleep compared to the 1 st quartile ( p = .02). However, we did not observe any relationship between DBPV and sleep architecture. Conclusion: Greater SBPV was associated with lower REM sleep time. This finding suggests a possible interplay between BPV and sleep architecture. Future investigation is warranted to clarify the directionality, mechanism, and therapeutic implications.

1994 ◽  
Vol 77 (4) ◽  
pp. 1811-1818 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.


Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 289-296 ◽  
Author(s):  
Sebastian Zaremba ◽  
Dagny Holle ◽  
Thomas E Wessendorf ◽  
Hans C Diener ◽  
Zaza Katsarava ◽  
...  

Background: The connection of cluster headache (CH) attacks with rapid eye movement (REM) sleep has been suggested by various studies, while other authors challenge this assumption. We performed serial polysomnography to determine the association of nocturnal CH attacks and sleep. Methods: Five patients diagnosed with CH (two with the episodic and three with the chronic subtype) were included and studied over four consecutive nights to evaluate connections between attacks onset and sleep stage. Results: Twenty typical CH attacks were reported. Thirteen of these attacks arose from sleep. Seven attacks were reported after waking in the morning or shortly before going to sleep. The beginnings of sleep-related attacks were distributed arbitrarily between different non-REM sleep stages. No association of CH attacks with REM or sleep disordered breathing was observed. Increased heart rate temporally associated with transition from one sleep state to another was observed before patients awoke with headache. Total sleep time, total wake time, arousal index and distribution of non-REM sleep stages were different between chronic and episodic CH. Conclusion: CH attacks are not associated with REM sleep. Brain regions involved in sleep stage transition might be involved in pathophysiology of CH. Differences in sleep characteristics between subgroups might indicate adaptation processes or underlying pathophysiology.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 159-159
Author(s):  
Tiana Broen ◽  
Tomiko Yoneda ◽  
Jonathan Rush ◽  
Jamie Knight ◽  
Nathan Lewis ◽  
...  

Abstract Previous cross-sectional research suggests that age-related decreases in Rapid-Eye Movement (REM) sleep may contribute to poorer cognitive functioning (CF); however, few studies have examined the relationship at the intraindividual level by measuring habitual sleep over multiple days. Applying a 14-day daily diary design, the current study examines the dynamic relationship between REM sleep and CF in 69 healthy older adults (M age=70.8 years, SD=3.37; 73.9% female; 66.6% completed at least an undergraduate degree). A Fitbit device provided actigraphy indices of REM sleep (minutes and percentage of total sleep time), while CF was measured four times daily on a smartphone via ambulatory cognitive tests that captured processing speed and working memory. This research addressed the following questions: At the within-person level, are fluctuations in quantity of REM sleep associated with fluctuations in next day cognitive measures across days? Do individuals who spend more time in REM sleep on average, perform better on cognitive tests than adults who spend less time in REM sleep? A series of multilevel models were fit to examine the extent to which each index of sleep accounted for daily fluctuations in performance on next day cognitive tests. Results indicated that during nights when individuals had more REM sleep minutes than was typical, they performed better on the working memory task the next morning (estimate = -.003, SE = .002, p = .02). These results highlight the impact of REM sleep on CF, and further research may allow for targeted interventions for earlier treatment of sleep-related cognitive impairment.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.


SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Sarah L Appleton ◽  
Andrew Vakulin ◽  
Angela D’Rozario ◽  
Andrew D Vincent ◽  
Alison Teare ◽  
...  

AbstractStudy ObjectivesQuantitative electroencephalography (EEG) measures of sleep may identify vulnerability to obstructive sleep apnea (OSA) sequelae, however, small clinical studies of sleep microarchitecture in OSA show inconsistent alterations. We examined relationships between quantitative EEG measures during rapid eye movement (REM) and non-REM (NREM) sleep and OSA severity among a large population-based sample of men while accounting for insomnia.MethodsAll-night EEG (F4-M1) recordings from full in-home polysomnography (Embletta X100) in 664 men with no prior OSA diagnosis (age ≥ 40) were processed following exclusion of artifacts. Power spectral analysis included non-REM and REM sleep computed absolute EEG power for delta, theta, alpha, sigma, and beta frequency ranges, total power (0.5–32 Hz) and EEG slowing ratio.ResultsApnea–hypopnea index (AHI) ≥10/h was present in 51.2% (severe OSA [AHI ≥ 30/h] 11.6%). In mixed effects regressions, AHI was positively associated with EEG slowing ratio and EEG power across all frequency bands in REM sleep (all p < 0.05); and with beta power during NREM sleep (p = 0.06). Similar associations were observed with oxygen desaturation index (3%). Percentage total sleep time with oxygen saturation <90% was only significantly associated with increased delta, theta, and alpha EEG power in REM sleep. No associations with subjective sleepiness were observed.ConclusionsIn a large sample of community-dwelling men, OSA was significantly associated with increased EEG power and EEG slowing predominantly in REM sleep, independent of insomnia. Further study is required to assess if REM EEG slowing related to nocturnal hypoxemia is more sensitive than standard PSG indices or sleepiness in predicting cognitive decline.


1998 ◽  
Vol 274 (4) ◽  
pp. R1136-R1141 ◽  
Author(s):  
Richard L. Verrier ◽  
T. Rern Lau ◽  
Umesha Wallooppillai ◽  
James Quattrochi ◽  
Bruce D. Nearing ◽  
...  

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg iv) and the β-adrenergic blocking agent atenolol (0.3 mg/kg iv) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.


2010 ◽  
Vol 109 (4) ◽  
pp. 1053-1063 ◽  
Author(s):  
H. Schwimmer ◽  
H. M. Stauss ◽  
F. Abboud ◽  
S. Nishino ◽  
E. Mignot ◽  
...  

Sleep influences the cardiovascular, endocrine, and thermoregulatory systems. Each of these systems may be affected by the activity of hypocretin (orexin)-producing neurons, which are involved in the etiology of narcolepsy. We examined sleep in male rats, either hypocretin neuron-ablated orexin/ataxin-3 transgenic (narcoleptic) rats or their wild-type littermates. We simultaneously monitored electroencephalographic and electromyographic activity, core body temperature, tail temperature, blood pressure, electrocardiographic activity, and locomotion. We analyzed the daily patterns of these variables, parsing sleep and circadian components and changes between states of sleep. We also analyzed the baroreceptor reflex. Our results show that while core temperature and heart rate are affected by both sleep and time of day, blood pressure is mostly affected by sleep. As expected, we found that both blood pressure and heart rate were acutely affected by sleep state transitions in both genotypes. Interestingly, hypocretin neuron-ablated rats have significantly lower systolic and diastolic blood pressure during all sleep stages (non-rapid eye movement, rapid eye movement) and while awake (quiet, active). Thus, while hypocretins are critical for the normal temporal structure of sleep and wakefulness, they also appear to be important in regulating baseline blood pressure and possibly in modulating the effects of sleep on blood pressure.


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.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Ian M Greenlund ◽  
Hannah A Cunningham ◽  
Anne L Tikkanen ◽  
John J Durocher ◽  
Carl A Smoot ◽  
...  

2020 ◽  
Author(s):  
Joseph A. Stucynski ◽  
Amanda L. Schott ◽  
Justin Baik ◽  
Shinjae Chung ◽  
Franz Weber

ABSTRACTThe two major stages of mammalian sleep – rapid eye movement sleep (REMs) and non-REM sleep (NREMs) – are characterized by distinct brain rhythms ranging from millisecond to minute-long (infraslow) oscillations. The mechanisms controlling transitions between sleep stages and how they are synchronized with infraslow rhythms remain poorly understood. Using opto- and chemogenetic manipulation, we show that GABAergic neurons in the dorsomedial medulla (dmM) promote the initiation and maintenance of REMs, in part through their projections to the dorsal and median raphe nuclei. Fiber photometry revealed that dmM GABAergic neurons are strongly activated during REMs. During NREMs, their activity fluctuated in close synchrony with infraslow oscillations in the spindle band of the electroencephalogram, and the phase of this rhythm modulated the latency of optogenetically induced REMs episodes. Thus, dmM inhibitory neurons powerfully promote REMs, and their slow activity fluctuations may coordinate transitions from NREMs to REMs with infraslow brain rhythms.


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