Altered Cardiovascular Variability in Obstructive Sleep Apnea

Narkiewicz, Krzysztof; Montano, Nicola; Cogliati, Chiara; Borne, Philippe J. H. van de; Dyken, Mark Eric; Somers, Virend K.

doi:10.1161/01.cir.98.11.1071

Cited by 509 publications

(390 citation statements)

References 49 publications

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“…Simultaneous assessment of BRS and HRV according to sleep microstructure could prove helpful in identifying patients at increased risk for nocturnal events (eg, early postmyocardial infarction, impaired left ventricular function, obstructive sleep apnea syndrome) 37 and in guiding therapy effectively during the nighttime. 1 This would be possible with a complete, noninvasive, minimally disturbing approach.…”

Section: Perspectivesmentioning

confidence: 99%

Baroreflex Buffering of Sympathetic Activation During Sleep

et al. 2004

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Abstract--We examined the effects of sleep microstructure, ie, the cyclic alternating pattern (CAP), on heart rate (HR)-and blood pressure (BP)-regulating mechanisms and on baroreflex control of HR in healthy humans and tested the hypothesis that sympathetic activation occurring in CAP epochs during non-rapid eye movement (non-REM) sleep periods is buffered by the arterial baroreflex. Ten healthy males underwent polysomnography and simultaneous recording of BP, ECG, and respiration. Baroreflex sensitivity (BRS) was calculated by the sequences method. Autoregressive power spectral analysis was used to investigate R-R interval (RRI) and BP variabilities. During overall non-REM sleep, BP decreased and RRI increased in comparison to wakefulness, with concomitant decreases in low-frequency RRI and BP oscillations and increases in high-frequency RRI oscillations. These changes were reversed during REM to wakefulness levels, with the exception of RRI. During CAP, BP increased significantly in comparison to non-CAP and did not differ from REM and wakefulness. The low-frequency component of BP variability was significantly higher during CAP than non-CAP. RRI and its low-frequency spectral component did not differ between CAP and non-CAP. BRS significantly increased during CAP in comparison to non-CAP. BRS was not different during CAP and REM and was greater during both in comparison with the awake state. Even during sleep stages, like non-REM sleep, characterized by an overall vagal predominance, phases of sustained sympathetic activation do occur that resemble that occurring during REM. Throughout the overnight sleep period, the arterial baroreflex acts to buffer surges of sympathetic activation by means of rapid changes in cardiac vagal circuits.

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Section: Perspectivesmentioning

confidence: 99%

Baroreflex Buffering of Sympathetic Activation During Sleep

et al. 2004

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“…Following obstructive apneas and hypopneas, there is an increase in sympathetic activity resulting in peripheral vasoconstriction and increased HR, which persists during the daytime (33). It has been hypothesized that the increased transmural gradients across the atria, ventricles and aorta, which may disrupt ventricular function and result from changes in intrathoracic pressure during obstructive events, lead to autonomic and hemodynamic instability (32).…”

Section: Repetitive Respiratory Events In Childrenmentioning

confidence: 99%

Augmented cardiovascular responses to episodes of repetitive compared with isolated respiratory events in preschool children with sleep-disordered breathing

et al. 2015

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Data presented as mean ± SEM or median (range). *P < 0.05; † P < 0.001. HR, heart rate; PTT, pulse transit time. Articles Walter et al. Cardiovascular Consequences of Repetitive vs. Isolated Respiratory EventsFor the episodes of repetitive events, the % change in HR from late to between events and from late event to postepisode were significantly higher when compared with the % change in HR from late to postevent in isolated respiratory events (P < 0.001 for both), as shown in Figure 2a. The % change in PTT from late event to postepisode was significantly greater (indicating a greater change in BP) for repetitive episodes when compared with the % change from late to postevents in isolated respiratory events (P < 0.05) (Figure 2b). There was no difference between % change in PTT from late to between events in repetitive episodes compared with % change from late to postevents in isolated respiratory events. The ratio of repetitive to isolated respiratory events for each child significantly predicted the mean HR, which increased with an increasing proportion of repetitive respiratory events compared with isolated events during N1, N2, REM, and total sleep (Figure 3). There were no relationships between mean PTT and the ratio of repetitive to isolated respiratory events during wake or any sleep stage. Determinants of Percentage Change in HR and PTT From Lateto Between-Event Phases in Episodes of Repetitive Respiratory EventsResults of the multiple linear regression analysis indicate that during total sleep, the repetitive to isolated events ratio, the number of individual respiratory events per episode, the number of arousals per episode, the ratio of the duration of the respiratory event to the duration of the subsequent between event period, and sleep stage were significantly, if weakly predictive of the % change in HR from the late event phase to between the respiratory events ( Table 3). The model predicted 44% of the % change in HR from the late event phase to between the respiratory events (P < 0.01). This suggests that the more repetitive events compared with isolated events, the more episodes, the more events and arousals per episode a child has, the higher the surge in HR. In contrast, there is a negative relationship between the surge in HR and sleep stage, suggesting that the HR surge is highest during N1 and decreases during N2, N3, and REM. There is also a weak negative relationship between the surge in HR and the ratio of the duration of an event to the duration of the between event period, suggesting that the closer together the events become the % change in HR is not as great.Further analyses separating the repetitive respiratory event episodes into the sleep stage in which they occurred demonstrated that when the episodes occurred during N1 sleep, the predictive variables remained the same as for total sleep. When the episodes occurred during N2 or REM sleep, only the number of arousals in the episode predicted the change in HR (r 2 = 0.3, P < 0.01; REM: r 2 = 0.5, P < 0.001). None of the variables ...

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“…This cycle may repeat itself hundreds of time during sleep, thus inducing an overall effect of nighttime sympathetic-excitation and surges of blood pressure, responsible for the "non-dipping" profile of blood pressure. However, one of the most remarkable characteristics of OSA is the presence of an heightened sympathetic activity also during wakefulness, as demonstrated by MSNA recordings (3,26) and spectral analysis of HRV (27). The mechanisms implicated in this phenomenon are still unclear.…”

Section: Sleep Breathing Disorders and Ansmentioning

confidence: 99%

“…Firstly, it has been hypothesized that the effect of sympathetic excitation induced by hypoxia might persist for a long time, also during normo-oxygenation conditions (28,29). Secondly, a potentiation of peripheral chemo-reflex responses has been detected in OSA subjects, possibly contributing to maintain a tonic sympathetic excitation during wakefulness (27,30). Lastly, a depressed baro-reflex sensitivity (BRS) was reported, although most studies assessed baroreceptor responses only during sleep (31)(32)(33)(34) while those reporting wakefulness data concluded that BRS was unchanged (35,36) (Figure 3).…”

Section: Sleep Breathing Disorders and Ansmentioning

confidence: 99%

Sympathovagal balance changes in sleep breathing disorders

Patruno¹

2014

sob

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SummaryThe autonomic nervous system (ANS) plays a leading role in controlling visceral functions and it is well known that the increase of sympathetic activity underlies most of cardiovascular diseases such as hypertension, heart failure, myocardial infarction and arrhythmias. On the other hand parasympathetic activity acts as protective factor against the above mentioned conditions. Sleep breathing disorders (SBD) are commonly divided in three syndromes: obstructive sleep apnoea syndrome, central sleep apnoea syndrome and Cheyne-Stokes breathing syndrome, the latter two both characterized by cyclic non-obstructive breathing patterns. Cheyne-Stokes Respiration is a form of periodic breathing characterized by a crescendo-decrescendo pattern of ventilation with (CSR-CSA) or without (CSR) central apnoea. Obstructive sleep apnea (OSA) is significantly associated with increased cardiovascular morbidity and mortality. OSA exerts strong modulatory effects on the autonomic nervous system through a number of mechanisms including central respiratory-cardiac coupling in the brain stem, chemo-reflex stimulation, baro-reflexes, and reflexes relating to lung inflation. EEG arousals, often related to apnea termination, also represent the final way of autonomic activation. CSR is common among patients with congestive heart failure, being present in 30-40% of the two largest reported. If CSR "per se" promotes an increase of sympathetic outflow during sleep is not really known.Several lines of argument would support the hypothesis that CSR may be a compensatory mechanism for severe HF.

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Altered Cardiovascular Variability in Obstructive Sleep Apnea

Cited by 509 publications

References 49 publications

Baroreflex Buffering of Sympathetic Activation During Sleep

Baroreflex Buffering of Sympathetic Activation During Sleep

Augmented cardiovascular responses to episodes of repetitive compared with isolated respiratory events in preschool children with sleep-disordered breathing

Sympathovagal balance changes in sleep breathing disorders

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