Sleep Arousal-Related Ventricular Repolarization Lability Is Associated With Cardiovascular Mortality in Older Community-Dwelling Men

Shahrbabaki, Sobhan Salari; Linz, Dominik; Redline, Susan; Stone, Katie L.; Ensrud, Kristine E.; Baumert, Mathias

doi:10.1016/j.chest.2022.09.043

Cited by 8 publications

(4 citation statements)

References 40 publications

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“…In fact, data from an epidemiological study of older men showed that excessive QTVI during arousals predicted all-cause and cardiovascular mortality. 53 Such arousal-induced increases in QTVI appeared to be transient, as there were no associations between prearousal QTVI and mortality. Our results, however, suggest a cumulative impact of intermittent hypoxemia on cardiac repolarization.…”

Section: Discussionmentioning

confidence: 96%

“…Recurrent arousals from sleep increase sympathetic nervous system activity (54), which can increase ventricular repolarization lability and arrhythmogenicity. In fact, data from an epidemiological study of older men showed that excessive QTVI during arousals predicted all-cause and cardiovascular mortality (55). Such arousal-induced increases in QTVI appeared to be transient, as there were no associations between pre-arousal QTVI and mortality.…”

Section: Discussionmentioning

confidence: 99%

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Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

Solhjoo

Haigney

Siddharthan³

et al. 2023

Preprint

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BACKGROUND: Sleep-disordered breathing (SDB) is associated with an increased risk of cardiac arrhythmias, sudden cardiac death, and all-cause mortality. This study investigates the mechanisms underlying this association by examining the effects of prevalent and incident SDB and intermittent hypoxia on ventricular repolarization lability. METHODS: Electrocardiographic recordings from three cohorts were used for this study: (1) a cross-sectional sample of 61 participants with severe SDB and a matched group without SDB; (2) a longitudinal sample of 26 participants without SDB at baseline who developed SDB after a 5 year follow-up, and a matched group without SDB; and (3) a cohort of 19 healthy adults exposed to intermittent hypoxia or ambient air. Mean heart rate, heart rate variability (SDNN), and QT variability index (QTVI), a measure of ventricular repolarization lability, were calculated from one-lead ECG recordings. RESULTS: In the cross-sectional sample, participants with severe SDB had larger QTVI (P = 0.027), heart rate (P = 0.028), SDNN (P = 0.018), and hypoxemia burden as assessed by the total sleep time with oxygen saturation less than 90% (TST90; P < 0.001) than those without SDB. TST90, but not the frequency of arousals, was an independent predictor of QTVI (P = 0.017). Both heart rate and QTVI were predictive of all-cause mortality. In the longitudinal sample with incident SDB, QTVI increased from -1.23 ± 0.15 to 0.86 {plus minus} 0.14 (P = 0.017) over the 5-year follow-up period. Finally, in the cohort of healthy adults, 4 hours of exposure to intermittent hypoxia increased heart rate (P = 0.001) and QTVI (P = 0.016). CONCLUSIONS: Prevalent and incident SDB are associated with increased ventricular repolarization instability which predisposes to ventricular arrhythmias and sudden cardiac death. Intermittent hypoxemia can destabilize ventricular repolarization and is a likely mediator of increased mortality in SDB.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

Solhjoo

Haigney

Siddharthan³

et al. 2023

Preprint

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“…Their study provides information on the strength of predicting CVD-related outcomes even when accounting for confounding. Of note, some measures of sleep disturbance physiological burden, such as the sleep apnea–specific hypoxic burden in association with CVD, have been reported and in of itself does not represent a novel finding ( 6 – 8 ). Rather, the novelty of the present work resides in providing key insights into the interrelatedness of sleep-specific physiological burden metrics reflecting different pathophysiologic aspects.…”

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confidence: 98%

The Influence of Physiologic Burdens Related to Obstructive Sleep Apnea on Cardiovascular Outcomes

Araujo,

Mehra

2023

Am J Respir Crit Care Med

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“…10 Recently, it has been found that sleep fragmentation can increase QT interval variability during arousal, which is associated with an increased allcause and CV mortality. 11 The current issue to be dealt with is defining the cutoff value that leads to an increase in the CV risk. The task has been extremely difficult due to the lack of sufficient data until now.…”

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confidence: 99%

Sleep disorders and cardiovascular risk: Focusing on sleep fragmentation

Martynowicz,

Wichniak,

Wieckiewicz

2024

Dent. Med. Probl.

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In this comment, we explored the link between sleep fragmentation and the cardiovascular risk, considering various sleep disorders and methodologies for assessing sleep fragmentation.It is generally known that sleep deprivation increases the cardiovascular (CV) and metabolic risk. Additionally, some data indicates that prolonged sleep is also associated with such risk. 1 In addition to sleep duration, sleep quality is also essential in the assessment of the CV risk. The continuity of sleep is one of its crucial features that contributes to effective rest and refreshment. Sleep may be interrupted by arousals and awakenings, which can result in prolonged wakefulness after sleep onset (WASO). Therefore, it is important to deter mine the threshold for the number of arousals and awakenings during sleep to consider them a normal phenomenon. According to the American Academy of Sleep Medicine (AASM) definition, an arousal is an abrupt shift in electro encephalography (EEG) frequencies, including alpha, theta and/or frequencies greater than 16 Hz (but not spindles), that lasts at least 3 s, with at least 10 s of stable sleep preceding the change. 2 The scoring of arousals during rapid eye movement (REM) sleep requires a concurrent increase in the submental electro myography (EMG) lasting at least 1 s. 2 Arousals, which can be accompanied by respiratory events, periodic limb movements in sleep (PLMS) or sleep brux ism events, are usually followed by autonomic activation, resulting in increased heart rate and blood pressure. Nevertheless, they can also occur spontaneously or be elicited by pain, light, noise, or a change in temperature. The arousal index (ArI), counted as the number of arousals per sleep hour, is frequently considered to quantify sleep fragmentation. 3 Sleep fragmentation, character ized by repetitive interruptions of sleep, is one of the factors contributing to excessive daytime sleepiness.The apnea-hypopnea index (AHI) is generally considered an imperfect in dicator of obstructive sleep apnea (OSA) severity. It is strongly believed that oxygen saturation parameters (i.e., the mean oxygen saturation, the oxygen desaturation index (ODI), the nadir oxygen saturation, and the percentage of sleep with oxygen saturation <90%) are more effective predictors of CV complications than the index of respiratory events. 4 It is worth noting that Cite asMartynowicz H, Wichniak A, Więckiewicz M. Sleep disorders and cardiovascular risk: Focusing on sleep fragmentation [published online as ahead of print on March 22, 2024].

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Sleep Arousal-Related Ventricular Repolarization Lability Is Associated With Cardiovascular Mortality in Older Community-Dwelling Men

Cited by 8 publications

References 40 publications

Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

The Influence of Physiologic Burdens Related to Obstructive Sleep Apnea on Cardiovascular Outcomes

Sleep disorders and cardiovascular risk: Focusing on sleep fragmentation

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