Sleep-Disordered Breathing and Excessive Daytime Sleepiness in Patients With Atrial Fibrillation

Albuquerque, Felipe N.; Calvin, Andrew D.; Kuniyoshi, Fatima H. Sert; Konečný, Tomáš; López-Jiménez, Francisco; Pressman, Gregg S.; Kara, Thomas; Friedman, Paul A.; Ammash, Naser M.; Somers, Virend K.; Caples, Sean M.

doi:10.1378/chest.11-0975

Cited by 89 publications

(52 citation statements)

References 30 publications

(22 reference statements)

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“…The relationship between SDB and EDS is also inconsistent in patients with atrial fibrillation31 and with heart failure 32. The reason for the absence of EDS in some post‐MI patients with SDB is not completely understood.…”

Section: Discussionmentioning

confidence: 99%

Excessive Daytime Sleepiness Independently Predicts Increased Cardiovascular Risk After Myocardial Infarction

Xie

Kuniyoshi

Covassin

et al. 2018

JAHA

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BackgroundExcessive daytime sleepiness (EDS), a common symptom among patients with sleep‐disordered breathing, is closely associated with the development of cardiovascular diseases, but its long‐term prognostic value is not completely understood. The aim of this study was to investigate whether EDS would be an independent prognostic factor after myocardial infarction.Methods and ResultsWe prospectively recruited 112 post–myocardial infarction patients. The Epworth Sleepiness Scale was completed before polysomnography, and EDS was defined as a score ≥11. After exclusion of 8 patients who accepted treatment with continuous positive airway pressure, 104 patients were followed up for 48 months. The primary composite end point was major adverse cardiac events. Patients with EDS had higher rates of major adverse cardiac events (48.4% versus 27.4%, χ2=5.27, P=0.022) and reinfarction (29.0% versus 5.5%, χ2=13.51, P=0.0002) compared with those without EDS. In the Cox proportional hazards model, patients with EDS had 2.15 times (95% confidence interval, 1.08–4.18; P=0.030) higher crude risk of major adverse cardiac events, with prognostic significance persisting after adjusting for age, diabetes mellitus, depression, left ventricular ejection fraction, apnea–hypopnea index, and nocturnal nadir oxygen saturation (hazard ratio: 2.13, 95% confidence interval, 1.04–4.26, P=0.039). Furthermore, among participants with moderate to severe sleep‐disordered breathing, the presence of EDS was associated with higher risk of major adverse cardiac events than those without EDS, after adjusting for age and nadir oxygen saturation (hazard ratio: 3.17, 95% confidence interval, 1.22–7.76, P=0.019).Conclusions EDS may be an independent prognostic factor of adverse outcome in post–myocardial infarction patients with moderate to severe sleep‐disordered breathing. Evaluation of EDS may shed new light on risk stratification and identify treatment responders for this patient population.

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Section: Discussionmentioning

confidence: 99%

Excessive Daytime Sleepiness Independently Predicts Increased Cardiovascular Risk After Myocardial Infarction

Xie

Kuniyoshi

Covassin

et al. 2018

JAHA

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“…[2][3][4]10 Although obesity is associated with OSA in patients with coronary artery disease and hypertension 2,3 among patients with HF and stroke, in comparison with the general population, a larger proportion with OSA patients are nonobese, and there is little or no relationship between body mass index and severity of OSA. 8,11 OSA arises when sleep-related withdrawal of respiratory drive to the upper airway (UA) dilator muscles is superimposed on an UA predisposed to collapse because it is narrow and highly compliant.…”

Section: Obstructive Sleep Apneamentioning

confidence: 99%

“…However, most patients with OSA and CVD do not report excessive daytime sleepiness and report lower Epworth Sleepiness Scale scores for any given AHI in comparison with the general population. 8,10,11 Thus, the majority of CVD patients lack this usual indication for treatment, and despite considerable observational, nonrandomized data, it remains uncertain whether OSA patients who do not report excessive daytime sleepiness require therapy at all. Similarly, most patients with CSA and CVD do not report excessive daytime sleepiness.…”

Section: Treating Sleep Apneamentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Kasai

Floras²,

Bradley³

2012

Circulation

330

207

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Sleep apnea occurs in Ϸ5% to 10% of the general population, regardless of race and ethnicity. 1 By contrast, in patients with cardiovascular diseases (CVDs), its prevalence, depending on the specific disorder surveyed, can range between 47% and 83%. [2][3][4] One form, central sleep apnea (CSA), is rare in the general population, but is detected often in conditions characterized by sodium and water retention, such as heart failure (HF). 2 Such epidemiological observations raise several important and as yet unresolved questions: What accounts for this remarkable concentration of sleep apnea among patients with CVD and its association with fluid retaining states? Does obstructive sleep apnea (OSA) predispose at-risk individuals to develop, over time, hypertension, coronary artery disease, stroke, or HF? Conversely, could mechanisms engaged by CVD, such as activation of the sympathetic nervous and renin-angiotensin-aldosterone systems, with consequences including renal sodium retention, contribute over time to the development or exacerbation of sleep apnea? From the clinical perspective, is sleep apnea, when present in patients with CVD an epiphenomenon, perhaps related to ageing, or a causal contributor to worse prognosis? And if so, are there now sufficient data to recommend randomized controlled trials to determine whether specific treatment of sleep apnea can reduce mortality or cardiovascular event rates? Our objectives, in this review, are to provide novel insight into each of these specific questions by integrating into our contemporary understanding of relationships between sleep apnea and CVD 5 newer epidemiological, observational, mechanistic, and trial data; to introduce a hypothetical model of bidirectional causality; and to consider directions for future research. Normal SleepIn healthy subjects, during non-rapid eye movement sleep (which constitutes Ϸ85% of total sleep time), efferent sympathetic nerve activity (SNA) diminishes and vagal tone increases, resulting in reductions in metabolic rate, blood pressure (BP), and heart rate (HR). 6,7 Thus, although sleep is, in general, a stable state of cardiovascular quiescence, this tableau can be interrupted both normally, by the intermittent surges in SNA, BP, and HR characteristic of rapid eye movement sleep (but comprising only 15% of total sleep time), 6 and pathologically, whether because of fitful sleep or shorter overall sleep time, as evident in patients with HF or drug-resistant hypertension, 8,9 or by coexisting sleep apnea, whether obstructive (OSA) or central (CSA).

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“…However, the prevalence of daytime symptoms like excessive daytime sleepiness in OSA patients with cardiac disease like AF or congestive heart failure is rare [14]. Therefore, the prevalence of OSA in AF patients may be even underestimated.…”

Section: Prevalence and Incidence Of Atrial Fibrillation In Sleep Apneamentioning

confidence: 99%

Atrial arrhythmogenesis in obstructive sleep apnea: Therapeutic implications

Linz

Hohl

et al. 2016

Sleep Medicine Reviews

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Sleep-Disordered Breathing and Excessive Daytime Sleepiness in Patients With Atrial Fibrillation

Cited by 89 publications

References 30 publications

Excessive Daytime Sleepiness Independently Predicts Increased Cardiovascular Risk After Myocardial Infarction

Excessive Daytime Sleepiness Independently Predicts Increased Cardiovascular Risk After Myocardial Infarction

Sleep Apnea and Cardiovascular Disease

Atrial arrhythmogenesis in obstructive sleep apnea: Therapeutic implications

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