Journal of Sleep Disorders: Treatment and CareISSN: 2325-9639

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Research Article, J Sleep Disor Treat Care Vol: 4 Issue: 2

Obstructive Sleep Apnea is Associated with Increased Frequency of Nocturnal Cardiac Arrhythmias

Davies SE1, Turton AR2, DMonte N3, Hamilton GS2,4 and O’Driscoll DM4,5*
1Department of General Medicine, Monash Health, Victoria, Australia
2Monash Lung and Sleep, Monash Health, Victoria, Australia
3Monash Heart, Monash Health, Victoria, Australia
4Department of Medicine, School of Clinical Sciences, Monash University, Victoria, Australia
5Department of Respiratory and Sleep Medicine, Eastern Health, Victoria, Australia
Corresponding author : Dr Denise M O’Driscoll
Department of Respiratory and Sleep Medicine Eastern Health, 8 Arnold St., Box Hill 3128, Australia
Tel: +61 (0)39975 6538
E-mail: [email protected]
Received: March 02, 2015 Accepted: June 01, 2015 Published: June 03, 2015
Citation: Davies SE, Turton AR, DMonte N, Hamilton GS, O’Driscoll DM (2015) Obstructive Sleep Apnea is Associated with Increased Frequency of Nocturnal Cardiac Arrhythmias. J Sleep Disor: Treat Care 4:2. doi:10.4172/2325-9639.1000155


Obstructive Sleep Apnea is Associated with Increased Frequency of Nocturnal Cardiac Arrhythmias

Objectives: Obstructive sleep apnea (OSA) is associated with increased cardiovascular mortality secondary to ischaemic heart disease and stroke. Evidence surrounding cardiac arrhythmia is limited and conflicting. We aimed to test the hypothesis that patients with OSA have an increased frequency of nocturnal cardiac arrhythmias compared to those without OSA. Secondly, to determine if CPAP reduces the frequency of OSA associated arrhythmias.
Methods: 61 patients with an AHI <5events/hr (No OSA) and 72 patients with an AHI >20 events/hr (moderate to severe OSA) were included from consecutive referrals for suspected OSA. 28 patients with moderate-severe OSA returned for further overnight study with CPAP. The electrocardiogram from polysomnography (PSG) was reviewed for cardiac arrhythmias whilst blinded to subject group.
Results: Significantly more subjects in the OSA group had arrhythmia compared with the no-OSA group (74% vs. 56%, p<0.05). Significantly more subjects in the OSA group exhibited ventricular premature complexes (VPCs) (18% vs. 5%, p<0.05). Stepwise multiple linear regression found OSA was the only significant independent predictor for VPCs. There was no significant difference in the percentage of subjects identified with non-sustained ventricular tachycardia, atrial premature complexes, atrial fibrillation, or heart block. There was no significant difference in arrhythmia with CPAP.
Conclusion: Individuals with moderate or severe OSA are atincreased risk of VPCs, which may predispose this group to further significant cardiac arrhythmias, and subsequently be a contributory factor to the increased morbidity and mortality seen in this patient group.  

Keywords: Sleep apnea; Arrhythmia; Ventricular; Cardiac


Sleep apnea; Arrhythmia; Ventricular; Cardiac


Obstructive sleep apnea (OSA) has a prevalence of approximately 2% in Western populations [1] and is associated with an increased cardiovascular morbidity and mortality that includes both fatal and non-fatal cardiovascular events [2,3]. Studies have found that patients with untreated severe OSA are at increased risk of hypertension, stroke, ischaemic heart disease and cardiovascular mortality. Continuous Positive Airway Pressure (CPAP) is an established treatment for moderate and severe OSA. It has beneficial effects on hypertension [4] and the incidence of cardiovascular events [3,5].
The evidence surrounding OSA and cardiac arrhythmia is limited and mainly from observational and retrospective studies. Studies have shown that patients with severe OSA have up to a fourfold higher odds of arrhythmia after adjusting for confounders [3,6] and that patients without arrhythmia have less severe apnea and nocturnal hypoxaemia [7]. Whilst a randomized controlled trial of CPAP treatment for OSA showed no change in frequency of arrhythmias [8], a large Japanese study demonstrated that treatment with CPAP reduces frequency of arrhythmia in patients with OSA [9]. The exact mechanism for an increase in nocturnal arrhythmia in patients with OSA is uncertain. One suggested theory is that alterations in the autonomic nervous system occur during the hypoxia, respiratory acidosis, apneas and arousals that are associated with OSA [6,10,11].
OSA clearly has important public health implications, particularly as treatment with CPAP has been shown to reduce the incidence of hypertension and cardiovascular events in these patients. However, evidence surrounding nocturnal cardiac arrhythmia is more limited and requires further research. The main aim of this study was to determine if there is an increased frequency of nocturnal cardiac arrhythmia in patients with OSA compared to those without OSA in a clinical cohort. Secondly, we looked at patients with OSA who returned for CPAP to see if the frequency of cardiac arrhythmia was reduced with treatment


The Monash Health Human Research Ethics Committees granted ethical approval for this project.
A total of 133 adults aged >18 years took part in this study. Subjects were randomly selected from consecutive referrals to the sleep laboratory for investigation of OSA. Consecutive and unselected patients with an apnea hypopnea index (AHI) <5events/hr (No OSA) and an AHI >20 events/hr (moderate to severe OSA) were included. Exclusion criteria included a sleep efficiency <60%, history of congestive cardiac failure, and chronic obstructive pulmonary disease requiring oxygen therapy. A total of 61 subjects were categorised as No OSA and 72 categorised as moderate-severe OSA. A total of 28 patients with moderate-severe OSA also returned for further overnight polysomnography (PSG) during a CPAP implementation study.
All participants underwent routine overnight PSG using a commercially available PSG system (Grael Sleep System, Compumedics). Electroencephalograms, electrooculograms, chin electromyogram (EMG), electrocardiogram (ECG, single modified lead II), left and right leg EMG and body position were recorded. Oxygen saturation (SaO2) was measured by pulse oximetry, thoracic and abdominal breathing movements recorded via uncalibrated respiratory inductance plethysmography, and airflow was recorded via nasal pressure. Prior to PSG, height and weight were recorded, and BMI calculated. The Epworth Sleepiness Scale (ESS) [12] was recorded. Patients filled in a standardised questionnaire regarding smoking status, past medical history (including diabetes, hypercholesterolaemia and hypertension), and medications including anti-arrhythmics.
Data analysis
Sleep and arousals were scored from the EEG, EOG and chin EMG channels in 30 s epochs according to standard criteria [13]. Respiratory events ≥ 10s in duration were scored. Obstructive apneas, mixed apneas and hypopneas were defined according to 2007 American Academy of Sleep Medicine standard criteria (hypopneas scored using the alternative criteria) [13]. An AHI was calculated, defined as the total number of obstructive apneas, mixed apneas, and hypopneas per hour of total sleep time.
The ECG was reviewed by an investigator (an experienced cardiac technologist working in a large teaching and University affiliated hospital) blinded to the subject’s group (i.e. OSA or No OSA). The ECG trace was reviewed for presence of cardiac arrhythmias and average heart rate was calculated. The arrhythmias classified were: Ventricular premature complexes (VPC) and Atrial premature complexes (APC) (both separated in number count as <20 and >20), Atrial fibrillation (AF), Heart Block – all types (HB), Non-sustained ventricular tachycardia (NSVT). An original example of an identified arrhythmia (NSVT) is shown in Figure 1.
Figure 1: Original 60 second polysomnographic trace during NREM2 showing non-sustained ventricular tachycardia (see expanded box) concurrent with an obstructive apnoea (Thor, Thoracic belt; Abdo, Abdominal belt, Mic, Microphone).
Statistical analysis
Statistical analysis was performed using Sigma Plot (Version 11, Systat Software Inc) and Intercooled Stata (Version 10, Stata Corp). Patient demographics and sleep characteristics were compared between groups using unpaired t-tests or Mann-Whitney Rank Sum Test where data failed normality. Patient demographics and sleep characteristics before and after CPAP were compared between groups using paired t-tests. Proportions of subjects with each arrhythmia type were compared between groups using Z-tests. Stepwise multiple logistic regressions for predictors of arrhythmias were performed by entering the following variables: gender, BMI, diagnosis of hypertension, diabetes, hypercholesterolemia, smoking status, OSA grouping and age (40+). Data are presented as mean ± SEM or Median (interquartile range) where appropriate. Statistical significance was taken at the p<0.05 level.


Patient demographics and sleep characteristics are presented in Table 1. As expected, the OSA group had a significantly higher BMI, AHI, arousal index (AI) and 3% oxygen desaturation index (ODI) (p<0.01 for all). The OSA group were also significantly older with a higher proportion of males and subjects identified as having hypertension (p<0.05 for all).
Table 1: Patient demographics and sleep characteristics.
A significantly higher proportion of subjects in the OSA group had cardiac arrhythmias as a whole compare with the no-OSA group (74% vs. 56%, p<0.05, Figure 2). When explored further, a significantly higher proportion of subjects in the OSA group had VPC >20 in number (18% vs. 5%, p<0.05) and APC <20 in number (49% vs. 26%, p<0.05) compared with the no-OSA group. There was no significant difference in the percentage of subjects identified as VPC <20, NSVT, APC>20, AF, Heart Block.
Figure 2: Percentage of subjects with OSA and without OSA exhibiting cardiac arrhythmias (*p<0.05).
Stepwise multiple logistic regression revealed that the only significant predictor for nocturnal cardiac arrhythmias was increased age (OR 3.61, p<0.001). However the only significant independent predictor for VPC>20 was having OSA (OR 3.93, p=0.04, Table 2).
Table 2: Stepwise multiple logistic regression for predictors of nocturnal arrhythmias.
Of the 72 subjects identified as having moderate-severe OSA, 28 returned for an in-laboratory CPAP implementation study. There was a significant reduction in AHI, ODI 3% and AI in the treatment study compared with the original diagnostic study (AHI: 6.7 ± 1.9 vs. 28.8 ± 1.6 events/h, ODI 3%: 8.6 ± 2.3 vs. 25.6 ± 3.3 events/h, AI: 12.7 ± 1.4 vs. 24.9 ± 2.4 events/h, p<0.001 for all). No significant differences in the presence of arrhythmias was found between the original sleep study and the CPAP implementation study.


This study has demonstrates an increased frequency of nocturnal cardiac arrhythmias in patients with moderate severe OSA compared to patients without OSA in a clinical population. Furthermore OSA was found to be a significant independent predictor for VPBs.
These findings correlate with previous studies that have shown an increase in cardiac arrhythmia with OSA. Guilleminault et al. [14] studied 400 patients with sleep apnea and reported that 48% of patients had arrhythmia, and that VPCs were seen in 20%. Hoffstein et al. [7] found that patients with OSA had an increased prevalence of cardiac arrhythmia when compared with non-apnoeic controls. Importantly, the patients with arrhythmia had both more severe obstructive apnea and nocturnal hypoxaemia. These initial studies were confirmed by findings from the Sleep Heart Health Study demonstrating a higher prevalence of AF, NSVT and complex ventricular ectopy in subjects with OSA after adjusting for potential confounders such as age, gender and BMI [6]. VPCs were also significantly higher in the OSA group compared to the no-OSA group, supporting our findings. Conversely, a study by Felmons et al. [15] found that cardiac arrhythmia was not increased in patients with obstructive sleep apnea compared to nonapnoeic control. Of note, however the OSA patients in this study were noted to have little oxygen desaturation associated with respiratory events.
The association between AF and OSA has received particular attention in the literature given the rapidly increasing prevalence of AF over the last few decades. Gami et al. [16] observed a significantly higher proportion of patients with AF had OSA (determined by Berlin screening questionnaire) (49%) compared to a control group referred for general cardiovascular disease management (32%). However a smaller case-control study that matched patients to age, gender and cardiovascular morbidity did not demonstrate an increased frequency of OSA determined by limited channel sleep study in patients with lone AF (i.e. no known cause of AF) compared to age, gender and cardiovascular morbidity matched controls suggesting that other pathophysiologic pathways such as hypertension may be important in association between OSA and AF [17]. The present study found that 2.8% of patients with OSA had AF compared to 0% of patients in the no-OSA group. This is not dissimilar to the Sleep Heart Health Study [6] in which 4.8% of patients with OSA had AF compared to 0.9% in the no-OSA group.
The present study adds to the literature describing increased cardiac arrhythmias with OSA in an Australian clinical cohort. Our finding that OSA is independently associated with increased frequency of VPCs is of particular note as these aberrant rhythms may herald more detrimental arrhythmias if OSA was to remain untreated. We analysed the occurrence of arrhythmias over the entire sleep period, however the uniquely pro-arrhythmic state of REM sleep should be acknowledged. REM sleep is characterised by surges of sympathetic activity and decreased baroreceptor regulation and control. VPCs have been shown to be a precursor to developing potentially lifethreatening arrhythmias and cardiovascular conditions in subsequent years. There is evidence to indicate that VPCs are associated with increased risk of other arrhythmias, stroke [18-20] and death. One observational study that followed patients over a ten year period found that after adjusting for confounders patients with VPCs were twice as likely to die due to coronary heart disease [19]. Patients with a higher mean frequency of VPCs post myocardial infarction have also been shown to have a significantly higher incidence of sudden death, cardiac death and arrhythmic events compared to those with a lower frequency of VPCs [20,21]. Furthermore, increased VPCs have been reported to occur during the apnoeic phase in OSA and at the end of apnea when hypoxia is maximal, supporting the notion that acute apneas have the potential to be arrhythmia-inducing [22-24].
A number of physiological changes occurring in OSA are potential mechanisms promoting cardiac arrhythmia. Increased respiratory effort against an occluded airway and the associated changes in negative intrathoracic pressure are known to cause acute cardiac structural changes that may trigger arrhythmia. Indeed, simulated obstructive apneas have been shown to be associated with increased premature beats and prolonged cardiac repolarisation in healthy subjects [25]. Obstructive apneas are also well known to illicit a large cyclical variation in heart rate including a marked bradycardia during airway occlusion following a by a large, albeit transient, tachycardia post event coinciding with an arousal-related sympathetic surge [26]. This repetitive augmented autonomic response could serve as a stimulus for arrhythmias. Other potential arrhythmic mediators associated with OSA include increased inflammation (e.g. C Reactive Protein, which is known to be linked to AF), elevated catecholamines or simply the known arrhythmic properties of hypoxia and hypercapnia [27].
In our study we demonstrated a reduction in AHI and AI with one night of CPAP treatment in a subset of OSA patients (28 out of 61) who proceeded on to a CPAP implementation study. Despite this improvement in OSA, we found no change in the frequency of arrhythmias. Treatment with CPAP has been found to reduce the risk of cardiovascular events in relation to stroke and ischaemic heart disease, however review of the literature suggests there is only limited evidence with regard to the effect of CPAP on cardiac arrhythmia in these patients. Earlier studies focus on pre and post tracheostomy in patients with severe OSA. Gilleminault et al. [28] found that 50 patients with OSA pre-tracheostomy had cardiac arrhythmias that included ventricular tachycardia, sinus arrest, second degree atrioventricular block and VPCs. Three to six months post-tracheostomy there were no cardiac arrhythmias detected in 46 of these patients. VPCs were still present in the remaining 4 but decreased during sleep in all 4 patients. Tilikan et al. [29] looked at the effect of atropine and tracheostomy on 15 patients with obstructive sleep apnea and arrhythmia. Arrhythmias included marked sinus arrhythmia, extreme sinus bradycardia, second degree AV block, ventricular arrhythmias, ventricular tachycardias and VPCs. In this study, tracheostomy was found to be highly effective at eliminating these arrhythmias. The data on CPAP treatment are more conflicting. A randomised controlled trial of CPAP in OSA demonstrated that one month of CPAP reduced mean heart rate, but did not reduced the frequency of arrhythmias [8]. However, a much larger Japanese study demonstrated that CPAP treatment significantly reduced the frequency of paroxysmal AF, VPCs, sinus bradycardia and sinus pause [9].


This study includes over 130 patients recruited via referral to a general sleep clinic for investigation. The patients in the OSA group were older than the non OSA group, and had a higher proportion of patients with hypertension. However, when these confounders were controlled for in logistic regression, OSA remained a significant predictor for VPCs. Other limitations of this study include the fact that we used only a single-night PSG with AHI to categorize "no OSA" and "OSA", and did not compare the OSA group to an asymptomatic/ healthy group. Our comparison group was rather patients referred for investigation of OSA, but who were found not to have the condition. However it should be acknowledged that this comparison group included snorers and by definition reside on the continuum of sleep disordered breathing, and may potentially be exhibiting the associated negative cardiovascular profile. A further limitation was the reduced subset of patients with OSA returning for subsequent in-laboratory CPAP titration. Whilst the effect of treatment of OSA on the presence of cardiac arrhythmias is key to understanding the cardiovascular morbidity in this group, the reduced sample size in our data set must be acknowledged. Finally, given the uncontrolled study design and sampling approach, the possibility of a Type II error needs to be acknowledged. The study is, by design, exploratory in nature.


This study has shown that patients with moderate or severe obstructive sleep apnea have an increased frequency of nocturnal cardiac arrhythmias, including a significantly increased risk of VPCs. Further studies are needed to determine the temporal relationship between apnea and arrhythmia, and whether arrhythmia in untreated OSA is a contributory factor to the increased morbidity and mortality seen in this patient group.

Conflict of Interest

The authors declare that they have no conflict of interest.


  1. Stradling JR, Davies RJ (2004) Sleep. 1: Obstructive sleep apnoea/hypopnoea syndrome: definitions, epidemiology, and natural history. Thorax 59: 73-78.

  2. Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N, De la Cruz-Moron I, Perez-Ronchel J, et al. (2005) Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure. Chest 128:624-633.

  3. Marin JM, Carrizo SJ, Vicente E, Agusti AG (2005) Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 365: 1046-1053.

  4. Duran-Cantolla J, Aizpuru F, Montserrat JM, Ballester E, Teran-Santos J, et al. (2010) Continuous positive airway pressure as treatment for systemic hypertension in people with obstructive sleep apnoea: randomised controlled trial. BMJ 341: c5991.

  5. Martinez-Garcia MA, Soler-Cataluna JJ, Ejarque-Martinez L, Soriano Y, Roman-Sanchez P, et al. (2009) 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, 180:36-41.

  6. Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, et al. (2006) Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J Respir Crit Care Med 173: 910-916.

  7. Hoffstein V, Mateika S (1994) Cardiac arrhythmias, snoring, and sleep apnea. Chest 106: 466-471.

  8. Craig S, Pepperell JC, Kohler M, Crosthwaite N, Davies RJ, et al. (2009) Continuous positive airway pressure treatment for obstructive sleep apnoea reduces resting heart rate but does not affect dysrhythmias: a randomised controlled trial. J Sleep Res 18:329-36.

  9. Abe H, Takahashi M, Yaegashi H, Eda S, Tsunemoto H, et al. (2010) Efficacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients. Heart Vessels 25: 63-69.

  10. Narkiewicz K, van de Borne PJ, Pesek CA, Dyken ME, Montano N, et al. (1999) Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea. Circulation 99: 1183-1189.

  11. Narkiewicz K, van de Borne PJ, Cooley RL, Dyken ME, Somers VK (1998) Sympathetic activity in obese subjects with and without obstructive sleep apnea. Circulation 98: 772-776.

  12. Johns MW (1991) A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep, 14:540-545.

  13. Iber C, Ancoli-Israel S, Chesson A, Quan S (2007) The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications (1st edtn.), American Academy of Sleep Medicine, Westchester, IL.

  14. Guilleminault C, Connolly SJ, Winkle RA (1983) Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 52: 490-494.

  15. Flemons WW, Remmers JE, Gillis AM (1993) Sleep apnea and cardiac arrhythmias. Is there a relationship? Am Rev Respir Dis 148: 618-621.

  16. Gami AS, Pressman G, Caples SM, Kanagala R, Gard JJ, et al. (2004) Association of atrial fibrillation and obstructive sleep apnea. Circulation 110: 364-367.

  17. Porthan KM, Melin JH, Kupila JT, Venho KK, Partinen MM (2004) Prevalence of sleep apnea syndrome in lone atrial fibrillation: a case-control study. Chest 125: 879-885.

  18. Carrim ZI, Khan AA (2005) Mean frequency of premature ventricular complexes as predictor of malignant ventricular arrhythmias. Mt Sinai J Med 72: 374-380.

  19. Meyerfeldt U, Schirdewan A, Wiedemann M, Schütt H, Zimmerman F, et al. (1997) The mode of onset of ventricular tachycardia. A patient-specific phenomenon. Eur Heart J 18: 1956-1965.

  20. Agarwal SK, Heiss G, Rautaharju PM, Shahar E, Massing MW, et al. (2010) Premature ventricular complexes and the risk of incident stroke: the Atherosclerosis Risk In Communities (ARIC) Study. Stroke 41: 588-593.

  21. Statters DJ, Malik M, Redwood S, Hnatkova K, Staunton A, et al. (1996) Use of ventricular premature complexes for risk stratification after acute myocardial infarction in the thrombolytic era. Am J Cardiol 77: 133-138.

  22. Koshino Y, Satoh M, Katayose Y, Yasuda K, Tanigawa T, et al. (2008) Association of sleep-disordered breathing and ventricular arrhythmias in patients without heart failure. Am J Cardiol 101:882-826.

  23. Ryan CM, Juvet S, Leung R, Bradley TD (2008) Timing of nocturnal ventricular ectopy in heart failure patients with sleep apnea. Chest 133: 934-940.

  24. Monahan K, Storfer-Isser A, Mehra R, Shahar E, Mittleman M, et al. (2009) Triggering of nocturnal arrhythmias by sleep-disordered breathing events. J Am Coll Cardiol 54: 1797-1804.

  25. Camen G, Clarenbach CF, Stöwhas AC, Rossi VA, Sievi NA, et al. (2013) The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects. Eur J Appl Physiol 113: 489-496.

  26. O'Driscoll DM, Morrell MJ (2005) The interaction between respiratory and autonomic function during sleep-related changes in pharyngeal airway patency. Auton Neurosci120:18-25.

  27. Shepard JW Jr (1985) Gas exchange and hemodynamics during sleep. Med Clin North Am 69: 1243-1264.

  28. Guilleminault C, Simmons FB, Motta J, Cummiskey J, Rosekind M, et al. (1981) Obstructive sleep apnea syndrome and tracheostomy. Long-term follow-up experience. Arch Intern Med 141: 985-988.

  29. Tilkian AG, Guilleminault C, Schroeder JS, Lehrman KL, Simmons FB, et al. (1977) Sleep-induced apnea syndrome. Prevalence of cardiac arrhythmias and their reversal after tracheostomy. Am J Med 63: 348-358.

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