REVIEW ARTICLE
Year : 2022 | Volume
: 6 | Issue : 3 | Page : 120--126
Impact of Sleep on Cardiovascular Health: A Narrative Review
Oliver Sum-Ping1, Yong-Jian Geng2,
1 Department of Psychiatry and Behavioral Sciences, The Center for Sleep Sciences and Medicine, School of Medicine, Stanford University, Stanford, CA, USA
2 Department of Internal Medicine, Division of Cardiovascular Medicine, University of Texas McGovern School of Medicine, Houston, Texas, USA
Correspondence Address:
Dr. Oliver Sum-Ping
Department of Psychiatry and Behavioral Sciences, The Center of Sleep Sciences and Medicine, Stanford University Medical School, 450 Broadway Ave., Redwood City 94063, CA
USA
Abstract
Sleep is a universal biological function but remains poorly understood and a relatively new field of science and medicine. Over the past decade, there have been rapidly accumulating scientific and clinical data around sleep, including the effects of various sleep aspects on cardiovascular health. Much of the research in the field has focused on sleep-disordered breathing, particularly obstructive sleep apnea. However, other sleep pathologies including hypersomnolence disorders, sleep-related movement disorders, and parasomnia disorders have been linked with cardiovascular health. Other areas of sleep, such as sleep duration, timing, and circadian rhythms, also have a demonstrated association with heart health. In this review, we provide an updated summary of the literature connecting sleep and cardiovascular disease.
How to cite this article:
Sum-Ping O, Geng YJ. Impact of Sleep on Cardiovascular Health: A Narrative Review.Heart Mind 2022;6:120-126
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How to cite this URL:
Sum-Ping O, Geng YJ. Impact of Sleep on Cardiovascular Health: A Narrative Review. Heart Mind [serial online] 2022 [cited 2023 May 29 ];6:120-126
Available from: http://www.heartmindjournal.org/text.asp?2022/6/3/120/357547 |
Full Text
Introduction
Sleep is a universal and critical biological function in all human life. However, despite being an experience that is familiar to all as a scientific and medical field, it has remained dormant until recently, and there are a number of fundamental scientific and clinical questions related to sleep or sleep disorders that remain unexplored. However, over the past several decades, a dawning of interest in the field has led to a rapid expansion in the scientific and medical sleep literature, and a much greater understanding of sleep and its functions has begun to develop. While numerous mysteries continue to surround sleep, an important theme that has emerged in the literature has been the important role of sleep in healthy life.
The health implications of sleep quality and quantity are broad, including the importance of sleep in the arena of cardiovascular health. Healthy sleep consists of cycles of alternating periods of nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. During NREM sleep, parasympathetic tone dominates, which reduces heart and respiratory rates as well as blood pressure. During REM sleep, sympathetic spikes trigger a variability in heart rate and blood pressure. Many sleep disorders can disrupt these patterns, often leading to cardiovascular consequences. The third edition of the International Classification of Sleep Disorders lists over 60 distinct sleep disorders.[1] Collectively, these disorders are highly prevalent worldwide. Estimates for the prevalence of insomnia symptoms alone are up to 30% of the general adult population.[2] Sleep disorders are also often under-recognized, representing a significant opportunity for the improvement of cardiovascular health.
However, sleep is multidimensional, and its quality is not simply a reflection of the presence or absence of pathology. Factors such as timing and duration play a key role in the effects of sleep on cardiovascular health. In recognition of this, the American Heart Association (AHA) has newly recognized sleep duration as a component of cardiovascular health, termed “Life's Essential 8”[3] with 7–9 h of sleep per day being recommended for most adults.
In this review, we provide a summary of literature connecting sleep and cardiovascular health.
Sleep-Disordered Breathing and Cardiovascular Health
Sleep apnea represents one of the best-researched areas of sleep medicine, with many of the most clearly established links to cardiovascular health. Central sleep apnea (CSA) is characterized by a pause in breathing associated with an absence of respiratory effort. Obstructive sleep apnea (OSA) is a more common subtype of sleep apnea characterized by the repeated collapse of the upper airway during sleep. This repeated collapse can lead to a complex cascade of downstream phenomena. Most immediately, patients with OSA may experience consequential intermittent hypoxia, recurrent arousals, and large intrathoracic pressure swings during sleep. These can provoke secondary effects, including increased sympathetic activation,[4],[5] inflammation,[6],[7],[8] endothelial dysfunction,[9] and altered hemodynamics.[10],[11] In addition to the subjective symptom burden which can result from these effects, including increased sleepiness, poor cognitive function, and mood disorders, there are more insidious consequences, most notably increased risk of cardiovascular disease.
Hypertension is a well-established cardiovascular risk factor associated with OSA. Data from the Sleep Heart Health Study, a large, multi-center community-based population study, demonstrated an increased prevalence of hypertension in participants with OSA in a dose-dependent fashion compared with controls even after adjusting for potential confounders such as Body mass index.[12] Data from another large study, the Wisconsin Sleep Cohort Study (WSCS), demonstrated a dose-response association between OSA and presence of hypertension after 4 years, even after controlling for known confounders.[13] While these data suggest that OSA increases the risk for developing hypertension, hypertension in those with OSA may not have the same characteristics as for those without OSA. Hypertension in the setting of OSA may also have a distinct profile, being more likely to take a refractory[14],[15] form that is less responsive to anti-hypertensive medication and be nondipping[16],[17] without the typically expected drop at night.
Coronary artery disease (CAD) has also been linked with OSA. Data from the WSCS demonstrated a link between severe OSA and incident CAD even after adjusting for confounding factors.[18] Other sources have suggested that this association may be clearer with men than with women.[19],[20] OSA has also been identified as a risk factor for stroke through multiple prospective cohort studies independent of other vascular risk factors. This has been demonstrated to have a dose-response relationship in some studies.[21],[22],[23] In addition to being linked to an increased risk of stroke, OSA has also been associated with worsened poststroke outcomes, including inferior functional outcomes[24],[25] and increased mortality.[26],[27] OSA has also been associated with atrial fibrillation independent of confounding factors through multiple studies,[28],[29] and respiratory events related to sleep apnea have even been suggested as an immediate triggers of paroxysms of atrial fibrillation.[30] OSA is also frequently seen in heart failure (HF), though overlap with HF symptoms such as orthopnea, nocturnal dyspnea, and nocturia may make clinical recognition of OSA more challenging. In addition, CSA may be more commonly seen in HF patients.
While several strategies can be used to manage OSA, continuous positive airway pressure (CPAP) is the gold-standard treatment. CPAP uses the constant application of positive pressure to maintain a patent upper airway during sleep. It has been consistently shown to improve daytime sleepiness and other quality-of-life measures;[31],[32],[33] however, evidence for its effects on cardiovascular health is a more mixed picture. Counter to the expectations of many, treatment of OSA with CPAP has not been consistently demonstrated to result in weight loss and has actually been associated with weight gain in recent studies.[34] However, a number of intermediate endpoints and surrogate markers of cardiovascular health have been shown to improve when OSA is treated with CPAP. For example, the treatment of OSA with CPAP has been demonstrated to result in small, but statistically significant improvements in blood pressure,[35],[36] decreases in markers of sympathetic activity,[5],[37] improve insulin resistance in patients with impaired glucose tolerance and prediabetes,[38],[39],[40] endothelial function,[41],[42] and arterial stiffness.[32]
Despite the above benefits of CPAP, its ability to reduce the risk of cardiovascular mortality or major adverse cardiovascular events in patients with OSA has not been supported by high-quality evidence thus far. While some observational evidence suggests that CPAP decreases risk of major cardiovascular events,[43] no large-scale randomized control trial has demonstrated any kind of similar benefit for either primary[44] or secondary prevention.[45],[46],[47] The most prominent of these trials to date has been the Sleep Apnea Cardiovascular Endpoints (SAVE)[47] which was a multicenter trial where 2717 patients with a history of CAD or cerebrovascular isease with untreated OSA were randomized to receive CPAP plus usual care or usual care alone. After a mean follow-up period of 3.7 years, no difference was reported between the groups in the primary endpoint of death resulting from cardiovascular causes, myocardial infarction, stroke, or hospitalization for unstable angina, HF, or transient ischemic attack. SAVE and other trials have had shared limitations including generally low CPAP adherence (mean duration of adherence of 3.3 h in the SAVE trial)[47] and the necessary exclusion of the most sleepy and hypoxemic patients who may stand to benefit most from treatment.
CSA often occurs in the setting of other medical conditions, and CSA with Cheyne–Stokes respiration (CSR) is a CSA subtype particularly closely entwined with cardiovascular health. CSA-CSR is defined by periodic breathing with a crescendo-decrescendo pattern of tidal volume alternating with a central apnea or hypopnea. The presence CSR has been identified as a predictor of mortality in patients with HF.[48] Efforts to target CSR with PAP, however, have failed to demonstrate a mortality benefit. The Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and HF study investigated the effect of CPAP on mortality for patients with chronic HF.[49] While the CPAP group demonstrated improvement in markers such as CSA events and oxygenation, no mortality benefit was seen compared to the control group. Adaptive servo-ventilation (ASV) is a form of noninvasive ventilation utilizing a dynamic inspiratory pressure support, responding to breath-by-breath changes in ventilation in a manner to create a cyclical pattern that is counter to the patient's periodic breathing. The treatment of sleep-disordered breathing with predominant CSA by Adaptive Servo-Ventilation in Patients with HF (SERVE-HF) trial tested the hypothesis that ASV may provide mortality benefit to patients with CSR in the context of chronic HF. However, there was an unexpected increase in all-cause and cardiovascular mortality in participants treated with ASV leading to the early termination of the study.
Other Sleep Disorders and Cardiovascular Health
While sleep-disordered breathing is the branch of sleep pathology most commonly considered in the context of cardiovascular health, there is evidence that links other sleep disorders to cardiovascular pathology.
Narcolepsy, a disorder of hypersomnolence, has been connected with a variety of other medical comorbidities. A retrospective medical claims analysis comparing patients with narcolepsy and healthy controls revealed a broad range of pathology with higher rates among patients with narcolepsy, including several cardiovascular diseases such as stroke, myocardial infarction, and cardiac arrest.[50] Similar findings were reported in a questionnaire-based epidemiological study where statistically significant findings included a higher prevalence of heart disease, hypertension, and hypercholesterolemia among those with narcolepsy.[51] However, there has not been complete agreement in the literature on these conclusions. The analysis of the Danish National Patient Registry revealed that patients with narcolepsy experienced higher rates of morbidity in several disease categories, including endocrine, neurologic, and musculoskeletal disorders, but there was no significant difference in the rates of cardiovascular disease between cases and controls observed.[52] One of the more consistent findings in the literature has been increased rates of obesity among patients with narcolepsy, possibly as a consequence of hypocretin deficiency, with many children, in particular, experiencing rapid weight gain at disease onset[53],[54],[55] and it has been speculated that this could be a contributing link between narcolepsy and potential cardiovascular morbidity. Even in Kleine–Levin syndrome, a rare disorder of hypersomnolence characterized by recurrent episodes of extreme sleepiness associated with cognitive and behavioral changes which can include megaphagia alternating with periods of normalcy, there is a reported case of cardiopulmonary arrest occurring during a period of autonomic instability in the setting excessive eating.[56],[57]
Restless legs syndrome (RLS) is a sleep-related movement disorder characterized by an uncomfortable urge to move the legs, typically during the evening and sometimes interfering with attempts to sleep. Periodic limb movements of sleep (PLMS) describe the leg movements commonly seen during sleep in most patients with RLS. Analyses of RLS and PLMS in relation to cardiovascular disease and risk factors have produced mixed findings. Some data suggest that RLS is associated with a higher prevalence of CAD and cardiovascular disease.[58] A proposed mechanism for this association has been that frequent periodic limb movements (PLMs) associated with more frequent sympathetic activation during sleep could result in a higher risk for cardiovascular pathology. However, some data suggest a degree of risk with RLS independent of PLMS.[59] Little consensus exists on the matter, however, as some studies have not shown any association between primary RLS and cardiovascular disease after controlling for confounding factors.[60],[61],[62]
There are fewer established connections between parasomnias and cardiovascular risk. REM sleep behavior disorder, a REM-related parasomnia marked by dream enactment behavior and frequently associated with synucleinopathies, has been linked to greater stroke risk,[63] perhaps mediated by autonomic dysfunction.
Sleep Duration, Circadian Rhythms, and Cardiovascular Health
An early observation regarding sleep duration and mortality was Hammond's 1964 finding that subjects from the American Cancer Society I study who self-reported 7 h of sleep had lower mortality than those reporting either more or <7 h of sleep.[64] Over the ensuing decades, additional studies and meta-analyses[65],[66] have reached similar conclusions, describing a U-shaped relationship between sleep duration and mortality where too short or too long of sleep duration is associated with increased all-cause mortality. Professional health organizations such as the American Academy of Sleep Medicine, Sleep Research Society, and the National Sleep Foundation have recommended a sleep duration of 7–9 h for most adults as well as the aforementioned AHA more recently.[3],[67],[68] While our understanding of the exact mechanisms for this link between sleep mortality is not complete, it is likely multifactorial with cardiovascular health serving as an important mediator. Multiple analyses have demonstrated an increase in mortality and cardiovascular events with either short or long sleep.[69] More recent work has been able to more clearly establish short sleep as a causal risk factor for CAD and HF.[70] However, in the same analysis, no causal association between long sleep time and CAD or stroke was not clearly established. In addition to data connecting sleep duration and risk of cardiovascular events[65] and CAD[71] directly, sleep duration has been linked to a number of other risk factors for cardiovascular disease, including obesity,[72] diabetes,[73] and hypertension.[74],[75]
Short sleep duration and insomnia are two distinct but overlapping conditions. Chronic insomnia is often associated with a state of constant hypervigilance, which may lead to changes in sympathetic activity[76] and alterations of endocrine function such as cortisol suggesting important connections with the hypothalamic–pituitary–adrenal axis.[77],[78],[79],[80] Elevated inflammatory markers have also been reported in patients with insomnia and short sleep duration[81],[82] as have changes in endothelial function.[83] These factors may contribute to the high rates of comorbidity of insomnia with hypertension,[84],[85],[86],[87] other cardiovascular diseases,[88],[89] and mortality.[89],[90],[91] Long sleep times have also been associated with increased risk for cardiovascular events such as stroke.[92],[93] While the mechanism of this connection is incompletely understood, it has been hypothesized that metabolic dysregulation and inflammation may play a role.[93]
While it is clear that sleep duration plays an important role in cardiovascular health, timing of sleep and other circadian factors are also valuable in the assessment of cardiovascular risk. Circadian clocks are ubiquitous within the human body and play a role in regulating a diverse array of biological processes, including many aspects of cardiovascular function. The importance of circadian rhythms in cardiovascular health is reflected in the fact that all cell types of major blood vessel layers, cardiomyocytes, myocardial stromal fibroblasts, and cardiac progenitor-like cells all have functional circadian clocks.[94] In addition, certain cardiovascular functions such as blood pressure and heart rate[95] have unique circadian patterns. Similarly, the timing of acute cardiovascular events such as stroke[96],[97] and myocardial infarction[97],[98] and sudden cardiac death[97] has a circadian pattern as they all occur more frequently in the morning. Chronic disruptions to circadian rhythms can lead to increased risk of hypertension and atherosclerosis.[99] This type of chronic circadian disruption is exemplified by shift workers who often experience repeated circadian disruptions which have been linked to cardiovascular disease.[100],[101]
Conclusion
Sleep and cardiovascular health are closely intertwined, and data continue to emerge demonstrating the many facets of this relationship, ranging from sleep-disordered breathing to parasomnias to sleep-related movement disorders and beyond. As a result, sleep has become increasingly recognized as a potential therapeutic target for reducing cardiovascular risk. One potential treatment that has captured significant attention has been CPAP for sleep-disordered breathing. However, while the literature demonstrates the existence of many benefits with CPAP use, the role of CPAP in reducing cardiovascular mortality has not been supported by results from randomized-controlled trials. Continued research in this area, including projects such as the ongoing Sleep Stroke Management and Recovery Trial[102] investigating the use of CPAP in preventing vascular events after a stroke and the ADVENT-HF trial[103] to evaluate the use of ASV in patients with HF, is of critical importance. However, efforts to improve sleep and heart health do not have to be limited to large, high-profile projects such as these. Greater recognition of the importance of sleep and simple clinical interventions such as counseling patients to get sufficient sleep and implementing good sleep hygiene could carry great benefits toward improved cardiovascular health.
The dawning of sleep as a scientific and medical field has been relatively recent. There remains fertile grounds for additional discovery in the realm of sleep. This represents a significant opportunity not just for sleep itself but also for the dream of improving cardiovascular health.
Ethical statement
Ethical statement is not applicable for this article.
Acknowledgments
The authors thank Drs. Michael Smolensky, Ramon Herminda, and Richard Castriotta for discussion and suggestions.
Financial support and sponsorship
The work of Dr. Yong-Jian Geng is supported in part by the Memorial-Hermann Foundation.
Conflicts of interest
There are no conflicts of interest.
References
| 1 | American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed.: Diagnostic and Coding Manual. Westchester, IL: American Academy of Sleep Medicine, 2014. |
| 2 | Roth T. Insomnia: Definition, prevalence, etiology, and consequences. J Clin Sleep Med 2007;3:S7-10. |
| 3 | Lloyd-Jones DM, Allen NB, Anderson CA, Black T, Brewer LC, Foraker RE, et al. Life's essential 8: Updating and enhancing the American Heart Association's construct of cardiovascular health: A presidential advisory from the American Heart Association. Circulation 2022;146:e18-43. |
| 4 | Carlson JT, Hedner J, Elam M, Ejnell H, Sellgren J, Wallin BG. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea. Chest 1993;103:1763-8. |
| 5 | Fletcher EC, Miller J, Schaaf JW, Fletcher JG. Urinary catecholamines before and after tracheostomy in patients with obstructive sleep apnea and hypertension. Sleep 1987;10:35-44. |
| 6 | Ryan S, Taylor CT, McNicholas WT. Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome. Circulation 2005;112:2660-7. |
| 7 | Ryan S, Taylor CT, McNicholas WT. Predictors of elevated nuclear factor-kappaB-dependent genes in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2006;174:824-30. |
| 8 | Yokoe T, Minoguchi K, Matsuo H, Oda N, Minoguchi H, Yoshino G, et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation 2003;107:1129-34. |
| 9 | Seif F, Patel SR, Walia H, Rueschman M, Bhatt DL, Gottlieb DJ, et al. Association between obstructive sleep apnea severity and endothelial dysfunction in an increased background of cardiovascular burden. J Sleep Res 2013;22:443-51. |
| 10 | Bradley TD, Hall MJ, Ando S, Floras JS. Hemodynamic effects of simulated obstructive apneas in humans with and without heart failure. Chest 2001;119:1827-35. |
| 11 | Parker JD, Brooks D, Kozar LF, Render-Teixeira CL, Horner RL, Douglas Bradley T, et al. Acute and chronic effects of airway obstruction on canine left ventricular performance. Am J Respir Crit Care Med 1999;160:1888-96. |
| 12 | Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000;283:1829-36. |
| 13 | Aul P, Eppard EP, Erry T, Oung Y, Alta AP, Ames J, et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-84. |
| 14 | Logan AG, Perlikowski SM, Mente A, Tisler A, Tkacova R, Niroumand M, et al. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens 2001;19:2271-7. |
| 15 | Gonçalves SC, Martinez D, Gus M, de Abreu-Silva EO, Bertoluci C, Dutra I, et al. Obstructive sleep apnea and resistant hypertension: A case-control study. Chest 2007;132:1858-62. |
| 16 | Ancoli-Israel S, Stepnowsky C, Dimsdale J, Marler M, Cohen-Zion M, Johnson S. The effect of race and sleep-disordered breathing on nocturnal BP “dipping”: Analysis in an older population. Chest 2002;122:1148-55. |
| 17 | Loredo JS, Ancoli-Israel S, Dimsdale JE. Sleep quality and blood pressure dipping in obstructive sleep apnea. Am J Hypertens 2001;14:887-92. |
| 18 | Hla KM, Young T, Hagen EW, Stein JH, Finn LA, Nieto FJ, et al. Coronary heart disease incidence in sleep disordered breathing: The Wisconsin Sleep Cohort Study. Sleep 2015;38:677-84. |
| 19 | Gottlieb DJ, Yenokyan G, Newman AB, O'Connor GT, Punjabi NM, Quan SF, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: The sleep heart health study. Circulation 2010;122:352-60. |
| 20 | Dong JY, Zhang YH, Qin LQ. Obstructive sleep apnea and cardiovascular risk: Meta-analysis of prospective cohort studies. Atherosclerosis 2013;229:489-95. |
| 21 | Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005;353:2034-41. |
| 22 | Valham F, Mooe T, Rabben T, Stenlund H, Wiklund U, Franklin KA. Increased risk of stroke in patients with coronary artery disease and sleep apnea: A 10-year follow-up. Circulation 2008;118:955-60. |
| 23 | Redline S, Yenokyan G, Gottlieb DJ, Shahar E, O'Connor GT, Resnick HE, et al. Obstructive sleep apnea-hypopnea and incident stroke: The sleep heart health study. Am J Respir Crit Care Med 2010;182:269-77. |
| 24 | Kaneko Y, Hajek VE, Zivanovic V, Raboud J, Bradley TD. Relationship of sleep apnea to functional capacity and length of hospitalization following stroke. Sleep 2003;26:293-7. |
| 25 | Aaronson JA, van Bennekom CA, Hofman WF, van Bezeij T, van den Aardweg JG, Groet E, et al. Obstructive sleep apnea is related to impaired cognitive and functional status after stroke. Sleep 2015;38:1431-7. |
| 26 | Martínez-García MA, Soler-Cataluña JJ, Ejarque-Martínez L, Soriano Y, Román-Sánchez P, Illa FB, et al. Continuous positive airway pressure treatment reduces mortality in patients with ischemic stroke and obstructive sleep apnea: A 5-year follow-up study. Am J Respir Crit Care Med 2009;180:36-41. |
| 27 | Sahlin C, Sandberg O, Gustafson Y, Bucht G, Carlberg B, Stenlund H, et al. Obstructive sleep apnea is a risk factor for death in patients with stroke: A 10-year follow-up. Arch Intern Med 2008;168:297-301. |
| 28 | Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, Kirchner HL, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J Respir Crit Care Med 2006;173:910-6. |
| 29 | Mehra R, Stone KL, Varosy PD, Hoffman AR, Marcus GM, Blackwell T, et al. Nocturnal Arrhythmias across a spectrum of obstructive and central sleep-disordered breathing in older men: Outcomes of sleep disorders in older men (MrOS sleep) study. Arch Intern Med 2009;169:1147-55. |
| 30 | Monahan K, Storfer-Isser A, Mehra R, Shahar E, Mittleman M, Rottman J, et al. Triggering of nocturnal arrhythmias by sleep-disordered breathing events. J Am Coll Cardiol 2009;54:1797-804. |
| 31 | Kawahara S, Akashiba T, Akahoshi T, Horie T. Nasal CPAP improves the quality of life and lessens the depressive symptoms in patients with obstructive sleep apnea syndrome. Intern Med 2005;44:422-7. |
| 32 | Chalegre ST, Lins-Filho OL, Lustosa TC, França MV, Couto TL, Drager LF, et al. Impact of CPAP on arterial stiffness in patients with obstructive sleep apnea: A meta-analysis of randomized trials. Sleep Breath 2021;25:1195-202. |
| 33 | Sánchez AI, Martínez P, Miró E, Bardwell WA, Buela-Casal G. CPAP and behavioral therapies in patients with obstructive sleep apnea: Effects on daytime sleepiness, mood, and cognitive function. Sleep Med Rev 2009;13:223-33. |
| 34 | Drager LF, Brunoni AR, Jenner R, Lorenzi-Filho G, Benseñor IM, Lotufo PA. Effects of CPAP on body weight in patients with obstructive sleep apnoea: A meta-analysis of randomised trials. Thorax2015;70:258-64. |
| 35 | Gottlieb DJ, Punjabi NM, Mehra R, Patel SR, Quan SF, Babineau DC, et al. CPAP versus oxygen in obstructive sleep apnea. N Engl J Med 2014;370:2276-85. |
| 36 | Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: A randomised parallel trial. Lancet 2002;359:204-10. |
| 37 | Ziegler MG, Mills PJ, Loredo JS, Ancoli-Israel S, Dimsdale JE. Effect of continuous positive airway pressure and placebo treatment on sympathetic nervous activity in patients with obstructive sleep apnea. Chest 2001;120:887-93. |
| 38 | Pamidi S, Wroblewski K, Stepien M, Sharif-Sidi K, Kilkus J, Whitmore H, et al. Eight hours of nightly continuous positive airway pressure treatment of obstructive sleep apnea improves glucose metabolism in patients with prediabetes. A randomized controlled trial. Am J Respir Crit Care Med 2015;192:96-105. |
| 39 | Weinstock TG, Wang X, Rueschman M, Ismail-Beigi F, Aylor J, Babineau DC, et al. A controlled trial of CPAP therapy on metabolic control in individuals with impaired glucose tolerance and sleep apnea. Sleep 2012;35:617-25B. |
| 40 | Lam JC, Lam B, Yao TJ, Lai AY, Ooi CG, Tam S, et al. A randomised controlled trial of nasal continuous positive airway pressure on insulin sensitivity in obstructive sleep apnoea. Eur Respir J 2010;35:138-45. |
| 41 | Schwarz EI, Puhan MA, Schlatzer C, Stradling JR, Kohler M. Effect of CPAP therapy on endothelial function in obstructive sleep apnoea: A systematic review and meta-analysis. Respirology 2015;20:889-95. |
| 42 | Xu H, Wang Y, Guan J, Yi H, Yin S. Effect of CPAP on endothelial function in subjects with obstructive sleep apnea: A meta-analysis. Respir Care 2015;60:749-55. |
| 43 | Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: An observational study. Lancet 2005;365:1046-53. |
| 44 | Barbé F, Durán-Cantolla J, Sánchez-de-la-Torre M, Martínez-Alonso M, Carmona C, Barceló A, et al. Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: A randomized controlled trial. JAMA 2012;307:2161-8. |
| 45 | Sánchez-de-la-Torre M, Sánchez-de-la-Torre A, Bertran S, Abad J, Duran-Cantolla J, Cabriada V, et al. Effect of obstructive sleep apnoea and its treatment with continuous positive airway pressure on the prevalence of cardiovascular events in patients with acute coronary syndrome (ISAACC study): A randomised controlled trial. Lancet Respir Med 2020;8:359-67. |
| 46 | Peker Y, Glantz H, Eulenburg C, Wegscheider K, Herlitz J, Thunström E. Effect of positive airway pressure on cardiovascular outcomes in coronary artery disease patients with nonsleepy obstructive sleep apnea. The RICCADSA Randomized Controlled Trial. Am J Respir Crit Care Med 2016;194:613-20. |
| 47 | McEvoy RD, Antic NA, Heeley E, Luo Y, Ou Q, Zhang X, et al. CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 2016;375:919-31. |
| 48 | Lanfranchi PA, Braghiroli A, Bosimini E, Mazzuero G, Colombo R, Donner CF, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation 1999;99:1435-40. |
| 49 | Bradley TD, Logan AG, Kimoff RJ, Sériès F, Morrison D, Ferguson K, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 2005;353:2025-33. |
| 50 | Black J, Reaven NL, Funk SE, McGaughey K, Ohayon MM, Guilleminault C, et al. Medical comorbidity in narcolepsy: Findings from the Burden of Narcolepsy Disease (BOND) study. Sleep Med 2017;33:13-8. |
| 51 | Ohayon MM. Narcolepsy is complicated by high medical and psychiatric comorbidities: A comparison with the general population. Sleep Med 2013;14:488-92. |
| 52 | Jennum P, Ibsen R, Knudsen S, Kjellberg J. Comorbidity and mortality of narcolepsy: A controlled retro- and prospective national study. Sleep 2013;36:835-40. |
| 53 | Poli F, Pizza F, Mignot E, Ferri R, Pagotto U, Taheri S, et al. High prevalence of precocious puberty and obesity in childhood narcolepsy with cataplexy. Sleep 2013;36:175-81. |
| 54 | Aran A, Einen M, Lin L, Plazzi G, Nishino S, Mignot E. Clinical and therapeutic aspects of childhood narcolepsy-cataplexy: A retrospective study of 51 children. Sleep 2010;33:1457-64. |
| 55 | Schuld A, Hebebrand J, Geller F, Pollmächer T. Increased body-mass index in patients with narcolepsy. Lancet 2000;355:1274-5. |
| 56 | Sum-Ping O, Guilleminault C. Kleine-Levin syndrome. Curr Treat Options Neurol 2016;18:24. |
| 57 | Koerber RK, Torkelson R, Haven G, Donaldson J, Cohen SM, Case M. Increased cerebrospinal fluid 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in Kleine-Levin syndrome. Neurology 1984;34:1597-600. |
| 58 | Winkelman JW, Shahar E, Sharief I, Gottlieb DJ. Association of restless legs syndrome and cardiovascular disease in the Sleep Heart Health Study. Neurology 2008;70:35-42. |
| 59 | Winkelman JW, Blackwell T, Stone K, Ancoli-Israel S, Redline S. Associations of incident cardiovascular events with restless legs syndrome and periodic leg movements of sleep in older men, for the outcomes of sleep disorders in older men study (MrOS Sleep Study). Sleep 2017;40:zsx023. |
| 60 | Winter AC, Schürks M, Glynn RJ, Buring JE, Gaziano JM, Berger K, et al. Vascular risk factors, cardiovascular disease, and restless legs syndrome in women. J Med 2013;126:220-7. |
| 61 | Szentkirályi A, Völzke H, Hoffmann W, Happe S, Berger K. A time sequence analysis of the relationship between cardiovascular risk factors, vascular diseases and restless legs syndrome in the general population. J Sleep Res 2013;22:434-42. |
| 62 | Cholley-Roulleau M, Chenini S, Béziat S, Guiraud L, Jaussent I, Dauvilliers Y. Restless legs syndrome and cardiovascular diseases: A case-control study. PLoS One 2017;12:e0176552. |
| 63 | Ma C, Pavlova M, Liu Y, Liu Y, Huangfu C, Wu S, et al. Probable REM sleep behavior disorder and risk of stroke: A prospective study. Neurology 2017;88:1849-55. |
| 64 | Cuyler Hammond E. Some preliminary findings on physical complaints from a prospective study of 1,064,004 men and women. Am J Public Health Nations Health 1964;54:11-23. |
| 65 | Yin J, Jin X, Shan Z, Li S, Huang H, Li P, et al. Relationship of sleep duration with all-cause mortality and cardiovascular events: A systematic review and dose-response meta-analysis of prospective cohort studies. J Am Heart Assoc 2017;6:e005947. |
| 66 | Cappuccio FP, D'Elia L, Strazzullo P, Miller MA. Sleep duration and all-cause mortality: A systematic review and meta-analysis of prospective studies. Sleep 2010;33:585-92. |
| 67 | Hirshkowitz M, Whiton K, Albert SM, Alessi C, Bruni O, DonCarlos L, et al. National Sleep Foundation's updated sleep duration recommendations: Final report. Sleep Health 2015;1:233-43. |
| 68 | Consensus Conference Panel, Watson NF, Badr MS, Belenky G, Bliwise DL, Buxton OM, et al. Recommended amount of sleep for a healthy adult: A joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society. J Clin Sleep Med 2015;11:591-2. |
| 69 | Kwok CS, Kontopantelis E, Kuligowski G, Gray M, Muhyaldeen A, Gale CP, et al. Self-reported sleep duration and quality and cardiovascular disease and mortality: A dose-response meta-analysis. J Am Heart Assoc 2018;7:e008552. |
| 70 | Wang S, Li Z, Wang X, Guo S, Sun Y, Li G, et al. Associations between sleep duration and cardiovascular diseases: A meta-review and meta-analysis of observational and Mendelian randomization studies. Front Cardiovasc Med 2022;9:930000. |
| 71 | Yang X, Chen H, Li S, Pan L, Jia C. Association of sleep duration with the morbidity and mortality of coronary artery disease: A meta-analysis of prospective studies. Heart Lung Circ 2015;24:1180-90. |
| 72 | Wu Y, Zhai L, Zhang D. Sleep duration and obesity among adults: A meta-analysis of prospective studies. Sleep Med 2014;15:1456-62. |
| 73 | Lu H, Yang Q, Tian F, Lyu Y, He H, Xin X, et al. A meta-analysis of a cohort study on the association between sleep duration and type 2 diabetes mellitus. J Diabetes Res 2021;2021:8861038. |
| 74 | Lusardi P, Mugellini A, Preti P, Zoppi A, Derosa G, Fogari R. Effects of a restricted sleep regimen on ambulatory blood pressure monitoring in normotensive subjects. Am J Hypertens 1996;9:503-5. |
| 75 | Lusardi P, Zoppi A, Preti P, Pesce RM, Piazza E, Fogari R. Effects of insufficient sleep on blood pressure in hypertensive patients: A 24-h study. American Journal of Hypertension 1999;12(1 Pt 1):63–8. https://doi.org/10.1016/s0895-7061(98)00200-3. |
| 76 | Carter JR, Grimaldi D, Fonkoue IT, Medalie L, Mokhlesi B, Van Cauter E. Assessment of sympathetic neural activity in chronic insomnia: Evidence for elevated cardiovascular risk. Sleep 2018;41:zsy126. |
| 77 | Vgontzas AN, Bixler EO, Lin HM, Prolo P, Mastorakos G, Vela-Bueno A, et al. Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis: Clinical implications. J Clin Endocrinol Metab 2001;86:3787-94. |
| 78 | Castro-Diehl C, Diez Roux AV, Redline S, Seeman T, Shrager SE, Shea S. Association of sleep duration and quality with alterations in the hypothalamic-pituitary adrenocortical axis: The Multi-Ethnic Study of Atherosclerosis (MESA). J Clin Endocrinol Metab 2015;100:3149-58. |
| 79 | Rodenbeck A, Huether G, Rüther E, Hajak G. Interactions between evening and nocturnal cortisol secretion and sleep parameters in patients with severe chronic primary insomnia. Neurosci Lett 2002;324:159-63. |
| 80 | Vgontzas AN, Tsigos C, Bixler EO, Stratakis CA, Zachman K, Kales A, et al. Chronic insomnia and activity of the stress system: A preliminary study. J Psychosom Res 1998;45:21-31. |
| 81 | Khan MS, Aouad R. The effects of insomnia and sleep loss on cardiovascular disease. Sleep Med Clin 2022;17:193-203. |
| 82 | Irwin MR. Why sleep is important for health: A psychoneuroimmunology perspective. Annu Rev Psychol 2015;66:143-72. |
| 83 | King CR, Knutson KL, Rathouz PJ, Sidney S, Liu K, Lauderdale DS. Short sleep duration and incident coronary artery calcification. JAMA 2008;300:2859-66. |
| 84 | Li X, Sotres-Alvarez D, Gallo LC, Ramos AR, Aviles-Santa L, Perreira KM, et al. Associations of sleep-disordered breathing and insomnia with incident hypertension and diabetes. The Hispanic community health study/study of Latinos. Am J Respir Crit Care Med 2021;203:356-65. |
| 85 | Fernandez-Mendoza J, Vgontzas AN, Liao D, Shaffer ML, Vela-Bueno A, Basta M, et al. Insomnia with objective short sleep duration and incident hypertension: The Penn State Cohort. Hypertension 2012;60:929-35. |
| 86 | Vgontzas AN, Liao D, Bixler EO, Chrousos GP, Vela-Bueno A. Insomnia with objective short sleep duration is associated with a high risk for hypertension. Sleep 2009;32:491-7. |
| 87 | Suka M, Yoshida K, Sugimori H. Persistent insomnia is a predictor of hypertension in Japanese male workers. J Occup Health 2003;45:344-50. |
| 88 | Zheng B, Yu C, Lv J, Guo Y, Bian Z, Zhou M, et al. Insomnia symptoms and risk of cardiovascular diseases among 0.5 million adults: A 10-year cohort. Neurology 2019;93:e2110-20. |
| 89 | Bertisch SM, Pollock BD, Mittleman MA, Buysse DJ, Bazzano LA, Gottlieb DJ, et al. Insomnia with objective short sleep duration and risk of incident cardiovascular disease and all-cause mortality: Sleep Heart Health Study. Sleep 2018;41:zsy047. |
| 90 | Li Y, Zhang X, Winkelman JW, Redline S, Hu FB, Stampfer M, et al. Association between insomnia symptoms and mortality: A prospective study of U.S. men. Circulation 2014;129:737-46. |
| 91 | Parthasarathy S, Vasquez MM, Halonen M, Bootzin R, Quan SF, Martinez FD, et al. Persistent insomnia is associated with mortality risk. Am J Med 2015;128:268-75.e2. |
| 92 | He Q, Sun H, Wu X, Zhang P, Dai H, Ai C, et al. Sleep duration and risk of stroke: A dose-response meta-analysis of prospective cohort studies. Sleep Med 2017;32:66-74. |
| 93 | Beaman A, Bhide MC, McHill AW, Thosar SS. Biological pathways underlying the association between habitual long-sleep and elevated cardiovascular risk in adults. Sleep Med 2021;78:135-40. |
| 94 | Crnko S, Du Pré BC, Sluijter JP, Van Laake LW. Circadian rhythms and the molecular clock in cardiovascular biology and disease. Nat Rev Cardiol 2019;16:437-47. |
| 95 | Degaute JP, van de Borne P, Linkowski P, Van Cauter E. Quantitative analysis of the 24-hour blood pressure and heart rate patterns in young men. Hypertension 1991;18:199-210. |
| 96 | Manfredini R, Boari B, Smolensky MH, Salmi R, la Cecilia O, Maria Malagoni A, et al. Circadian variation in stroke onset: Identical temporal pattern in ischemic and hemorrhagic events. Chronobiol Int 2005;22:417-53. |
| 97 | Willich SN, Goldberg RJ, Maclure M, Perriello L, Muller JE. Increased onset of sudden cardiac death in the first three hours after awakening. Am J Cardiol 1992;70:65-8. |
| 98 | Muller JE, Tofler GH, Willich SN, Stone PH. Circadian variation of cardiovascular disease and sympathetic activity. J Cardiovasc Pharmacol 1987;10 Suppl 2:S104-9. |
| 99 | Geng YJ, Smolensky MH, Sum-Ping O, Hermida R, Castriotta RJ. Circadian rhythms of risk factors and management in atherosclerotic and hypertensive vascular disease: Modern chronobiological perspectives of an ancient disease. Chronobiol Int 2022;39:1-30. |
| 100 | Knutsson A, Akerstedt T, Jonsson BG, Orth-Gomer K. Increased risk of ischaemic heart disease in shift workers. Lancet (London, England). 1986;2(8498):89–92. https://doi.org/10.1016/s0140-6736(86)91619-3. |
| 101 | Torquati L, Mielke GI, Brown WJ, Kolbe-Alexander T. Shift work and the risk of cardiovascular disease. A systematic review and meta-analysis including dose-response relationship. Scand J Work Environ Health 2018;44:229-38. |
| 102 | Brown DL, Durkalski V, Durmer JS, Broderick JP, Zahuranec DB, Levine DA, et al. Sleep for Stroke Management and Recovery Trial (Sleep SMART): Rationale and methods. Int J Stroke 2020;15:923-9. |
| 103 | Lyons OD, Floras JS, Logan AG, Beanlands R, Cantolla JD, Fitzpatrick M, et al. Design of the effect of adaptive servo-ventilation on survival and cardiovascular hospital admissions in patients with heart failure and sleep apnoea: The ADVENT-HF trial. Eur J Heart Fail 2017;19:579-87. |
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