Obstructive sleep apnea (OSA) is caused by intermittent episodes of partial or complete closure of the upper airway, leading to apneic episodes while the patient is asleep. Atrial fibrillation (AF) leads to more than 750,000 hospitalizations per year and accounts for an estimated 130,000 deaths each year. The death rate from AF as the primary or a contributing cause of death has been rising for more than two decades. The material reviewed in this paper focuses on the association between OSA and arrhythmias. It goes into the details of the epidemiology, pathophysiology, and types of arrhythmias and the therapies seen in association with OSA.
Introduction & Background
Sleep-disordered breathing (SDB) is a cumulative term for sleep-related breathing disorders and abnormalities of respiration during sleep. SDB consists of obstructive sleep apnea (OSA), central sleep apnea syndrome, sleep-related hypoventilation disorder, sleep-related hypoxemia, primary snoring, and nocturnal groaning. OSA is caused by intermittent episodes of partial or complete closure of the upper airway, leading to apneic episodes while the patient is asleep . OSA is diagnosed by a combination of positive patient history and positive findings on polysomnography. An apnea-hypopnea index (AHI) of greater than five is diagnostic of OSA.
The incidence and prevalence of OSA vary based on age in the general population. The prevalence is higher in the middle-aged and 65-years and above populations . Based on an AHI of more than five, the prevalence ranges from 9%-38% and is higher in men than in women . At an AHI of more than 15, the prevalence in the general adult population ranged from 6%-17% and was 49% in the 65-years and above group .
Atrial fibrillation (AF) has a prevalence of 9% in the 65-year-old and above population as compared to the 2% prevalence in the younger than 65-year-old population . An estimated 2.7-6.1 million people in the United States have AF . AF leads to more than 750,000 hospitalizations per year and accounts for an estimated 130,000 deaths each year [4-5]. Medical costs for AF patients are about $8,705 higher than for people without AF [3,6]. The death rate from AF as the primary or a contributing cause of death has been rising for more than two decades [4-5].
Over the years, attempts have been made to determine how arrhythmias develop in OSA patients. In OSA, the frequent collapse of the airway causes oxyhemoglobin desaturation, which leads to persistent inspiratory efforts made against a collapsed airway, often resulting in the patient’s arousal from sleep .
One hypothesis is that OSA causes reduced blood oxygen and increased carbon dioxide levels due to problems with the baroreflex and chemoreflex activities, leading to the activation of the sympathetic nervous system, causing electrical remodeling of the heart [7-10]. This remodeling can lead to arrhythmia development [1,7-10].
Another hypothesis is that co-existing hypertension in OSA patients may be responsible for the development of AF. Past studies have shown a strong association between OSA and hypertension, as well as hypertension and AF. Hypertension has been shown to cause atrial remodeling. Similarly, in OSA patients with hypertension, it is hypothesized that persistent inspiratory efforts made against a collapsed airway cause dramatic shifts in intracardiac pressures, leading to the activation of atrial ion channels, thus creating an acute change in cardiac chamber dimensions [11-12]. This change in size can lead to AF development [11-12].
The third hypothesis is the OSA effect of applying negative intrathoracic pressure on both atrial and ventricular free walls, which will lead to cardiac stretching, thus activating cardiac ion channels, causing a change in cardiac chamber size, which can lead to arrhythmias .
The fourth hypothesis is related to OSA causing hypoxemia that stimulates the vagal nerve, leading to cardiac vagal reflex activation. In approximately 10% of OSA patients, the resulting hypoxemia activates the cardiac vagal reflex, leading to the development of bradyarrhythmias even in the absence of cardiac conduction disease .
Types of arrhythmias
Different types of arrhythmias may be found in patients of OSA. Based on past research studies (see Table 1), there are several observed associations between OSA and arrhythmias.
Atrial fibrillation is a commonly seen arrhythmia in OSA patients . AF occurs when disordered atrial electric activity causes an abnormal electrical rhythm that replaces the normal sinus mechanism . It can be caused by hypertension, myocardial infarction, hyperthyroidism, caffeine use, and abnormal heart valves and is seen in sleep apnea patients. AF often goes undiagnosed for a long time because 10%-40% of AF patients are asymptomatic . Symptomatic patients will present with palpitations, shortness of breath, exercise intolerance, chest pain, or malaise . AF is responsible for an estimated 130,000 deaths per year and for the worsening morbidity in other diseases like stroke and heart failure [4-5,30]. AF is found in 2% of the general population, with an increasing prevalence to 9% in the above 65 years population [3,30].
Sick sinus syndrome (SSS) refers to a collection of disorders marked by the heart's inability to perform its pacemaking function . SSS mostly affects older adults and consists of bradyarrhythmias with or without accompanying tachyarrhythmias . At least 50% of SSS patients develop alternating bradycardia and tachycardia, also known as Tachy-Brady syndrome . SSS results from degenerative fibrosis, ion channel dysfunction, and the remodeling of the sinoatrial node . Signs and symptoms are often subtle early on and become more obvious as the disease progresses . They are commonly related to end-organ hypoperfusion, like syncope secondary to cerebral hypoperfusion .
Atrioventricular block (AV block) is an arrhythmia that is caused by a delay or disturbance in the transmission of an electrical impulse from the atria to the ventricles . This can be due to an anatomical or functional impairment in the heart’s conduction system . In general, there are three degrees of AV nodal blocks: first-degree, second-degree (Mobitz type 1 or 2), and third-degree . The causes of AV blocks are myocardial infarction, post-cardiac surgery, electrolyte imbalances, idiopathic fibrosis, and medications that slow atrioventricular conduction . Patients may be asymptomatic or they may present with palpitations, syncope, and dizziness.
Sudden cardiac death is defined as natural death due to cardiac causes, which will present as an abrupt loss of consciousness within the first hour of symptoms . The mechanisms can be ventricular fibrillation, ventricular tachycardia, and flutter with subsequent ventricular fibrillation, torsades de pointes, and, lastly, bradyarrhythmias and asystolic arrest .
There are no conclusive epidemiologic or longitudinal intervention studies that relate specifically to the prevalence, severity, and consequences of cardiac arrhythmias and the effects of OSA treatment . Despite this, there have been many observations made from previous studies regarding the effectiveness of continuous positive airway pressure (CPAP) therapy for OSA patients and their therapeutic effect on arrhythmia incidence in the same patients. Based on the studies (see Table 2), CPAP therapy had an effect on reducing the incidence and prevalence of cardiac arrhythmias in OSA patients.
The material reviewed in this paper focuses on the association between OSA and arrhythmias. It goes into the details regarding the epidemiology, pathophysiology, and types of arrhythmias seen in association with OSA. It also addresses observations regarding CPAP therapy in reducing arrhythmias. Despite these key points being addressed, larger and more prospective studies are needed to understand the true benefits of CPAP therapy. This is a review article for busy, practicing physicians to have a cumulative view of our current situation regarding the need for CPAP therapy in patients of both OSA and arrhythmias.
- Hersi AS: Obstructive sleep apnea and cardiac arrhythmias. Ann Thorac Med. 2010, 5:10-17. 10.4103/1817-1737.58954
- Senaratna CV, Perretac JL, Lodge CJ, et al.: Prevalence of obstructive sleep apnea in the general population: a systematic review. Sleep Med Rev. 2017, 34:70-81. 10.1016/j.smrv.2016.07.002
- January CT, Wann LS, Alpert JS, et al.: AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014, 64:1-76. 10.1016/j.jacc.2014.03.022
- Agency for Healthcare Research and Quality. Weighted national estimates. HCUP National Inpatient Sample [online]. (2012). Accessed: March 19, 2019: https://www.hcup-us.ahrq.gov/db/nation/nis/NISIntroduction2010.pdf.
- Centers for Disease Control and Prevention. About multiple cause of death 1999-2011. CDC WONDER Online Database. (2014). Accessed: March 19, 2019: https://mchb.hrsa.gov/chusa14/special-features/child-mortality.html.
- Mozaffarian D, Benjamin EJ, Go AS, et al.: Heart disease and stroke statistics--2015 update: a report from the American Heart Association. Circulation. 2015, 131:e29-322. 10.1161/CIR.0000000000000152
- Parati G, Di Rienzo M, Bonsignore M, et al.: Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep. J Hypertens. 1997, 2:1621-1626.
- Narkiewicz K, Pesek CA, Kato M, Phillips BG, Davison DE, Somers VK: Baroreflex control of sympathetic nerve activity and heart rate in obstructive sleep apnea. Hypertension. 1998, 32:1039-1043. 10.1161/01.HYP.32.6.1039
- de Paula PM, Tolstykh G, Mifflin S: Chronic intermittent hypoxia alters NMDA and AMPA-evoked currents in NTS neurons receiving carotid body chemoreceptor inputs. Am J Physiol Regul Integr Comp Physiol. 2007, 292:2259-2265. 10.1152/ajpregu.00760.2006
- Narkiewicz K, van de Borne PJH, Montano N, Dyken ME, Phillips BG, Somers VK: Contribution of tonic chemoreflex activation to sympathetic activity and blood pressure in patients with obstructive sleep apnea. Circulation. 1998, 97:943-945. 10.1161/01.CIR.97.10.943
- Condos WR Jr, Latham RD, Hoadley SD, Pasipoularides A: Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography. Circulation. 1987, 76:1020-1028. 10.1161/01.CIR.76.5.1020
- Hall MJ, Ando S-I, Floras JS, Bradley TD: Magnitude and time course of hemodynamic responses to Mueller maneuvers in patients with congestive heart failure. J Appl Physiol. 1998, 85:1476-1484. 10.1152/jappl.1918.104.22.1686
- Franz MR: Mechano-electrical feedback in ventricular myocardium. Cardiovasc Res. 1996, 32:15-24. 10.1016/S0008-6363(96)00074-0
- Guilleminault C, Connolly SJ, Winkle RA: Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol. 1983, 52:490-494. 10.1016/0002-9149(83)90013-9
- Mehra R, Benjamin EJ, Shahar E, et al.: Association of nocturnal arrhythmias with sleep-disordered breathing: the sleep heart health study. Am J Respir Crit Care Med. 2006, 173:910-916. 10.1164/rccm.200509-1442OC
- Gami AS, Pressman G, Caples SM, et al.: Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004, 110:364-367. 10.1161/01.CIR.0000136587.68725.8E
- Porthan KM, Melin JH, Kupila JT, Venho KK, Partinen MM: Prevalence of sleep apnea syndrome in lone atrial fibrillation: a case-control study. Chest. 2004, 125:879-885. 10.1378/chest.125.3.879
- Javaheri S, Parker TJ, Liming JD, Corbett WS, Nishiyama H, Weller L, Rossell GA: Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation. 1998, 97:2154-2159. 10.1161/01.CIR.97.21.2154
- Flemons WW, Remmers JE, Gillis AM: Sleep apnea and cardiac arrhythmias: is there a relationship?. Am Rev Respir Dis. 1993, 148:618-621. 10.1164/ajrccm/148.3.618
- Mooe T, Gullsby S, Rabben T, Eriksson P: Sleep-disordered breathing: a novel predictor of atrial fibrillation after coronary artery bypass surgery. Coron Artery Dis. 1996, 7:475-478.
- Simantirakis EN, Schiza SI, Marketou E, et al.: Severe bradyarrhythmias in patients with sleep apnoea: the effect of continuous positive airway pressure treatment: a long-term evaluation using an insertable loop recorder. Eur Heart J. 2004, 25:1070-1076. 10.1016/j.ehj.2004.04.017
- Garrigue S, Pépin JL, Delaye P, Murgatroyd F, Poezevara Y, Clémenty J, Lévy P: High prevalence of sleep apnea syndrome in patients with long-term pacing: the European multicenter polysomnographic study. Circulation. 2007, 115:1703-1709. 10.1161/CIRCULATIONAHA.106.659706
- Grimm W, Hoffman J, Kohler U, Heitmann J, Peter J, Wichert P, Maisch B: Invasive electrophysiological evaluation of patients with sleep apnoea-associated ventricular asystole—methods and preliminary results. J Sleep Res. 1995, 4:160-165. 10.1111/j.1365-2869.1995.tb00207.x
- Steiner S, Schueller PO, Hennersdorf MG, Strauer BE: Obstructive sleep apnea in heart failure patients: evidence for persistent conduction disturbances or sinus node dysfunction. J Physiol Pharmacol. 2008, 59:669-674.
- Velasco A, Hall C, Perez-Verdia A, Nugent K: Association of high-risk scores for obstructive sleep apnea with symptomatic bradyarrhythmias. J Cardiovasc Med. 201, 15:407-410. 10.2459/JCM.0b013e3283630d07
- Becker H, Brandenburg U, Peter JH, von Wichert P: Reversal of sinus arrest and atrioventricular conduction block in patients with sleep apnea during nasal continuous positive airway pressure. Am J Respir Crit Care Med. 1995, 151:215-218. 10.1164/ajrccm.151.1.7812557
- Gami A, Olson E, Shen W, et al.: Obstructive sleep apnea and the risk of sudden cardiac death: a longitudinal study of 10,701 adults. J Am Coll Cardiol. 2013, 62:610-616. 10.1016/j.jacc.2013.04.080
- Gami AS, Howard DE, Olson EJ, Somers VK: Day-night pattern of sudden death in obstructive sleep apnea. N Engl J Med. 2005, 352:1206-1214. 10.1056/NEJMoa041832
- Zimetbaum P: Atrial fibrillation. Ann Intern Med. 2017, 166:33-48. 10.7326/AITC201703070
- Boriani G, Pettorelli D: Atrial fibrillation burden and atrial fibrillation type: clinical significance and impact on the risk of stroke and decision making for long-term anticoagulation. Vascul Pharmacol. 2016, 83:26-35. 10.1016/j.vph.2016.03.006
- Semelka M, Gera J, Usman S: Sick sinus syndrome: a review. Am Fam Physician. 2013, 87:691-696.
- Kashou AH, Kashou HE: Rhythm, atrioventricular block. StatPearls [Internet]. 2018,
- Evéquoz D, Zuber M, Erne P: Sudden cardiac death: definition, mechanisms and risk factors [Article in French]. Praxis (Bern 1994). 1994, 85:188-196.
- Kufoy E, Palma JA, Lopez J, Alegre M, Urrestarazu E, Artieda J, Iriarte J: Changes in the heart rate variability in patients with obstructive sleep apnea and its response to acute CPAP treatment. PLoS One. 2012, 7:e33769. 10.1371/journal.pone.0033769
- Ryan CM, Usui K, Floras JS, Bradley TD: Effect of continuous positive airway pressure on ventricular ectopy in heart failure patients with obstructive sleep apnoea. Thorax. 2005, 60:781-785. 10.1136/thx.2005.040972
- Kurlykina NV, Pevzner AV, Litvin A, Galitsin PV, Chazova IE, Sokolov SF, Golitsyn SP: Treatment of patients with long nocturnal asystoles and obstructive sleep apnea syndrome by creating continuous positive air pressure in the upper respiratory tract [Article in Russian]. Kardiologiia. 2009, 49:36-42.
- Kanagala R, Murali NS, Friedman PA, Ammash NM, Gersh BJ, Ballman KV: Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003, 107:2589-2594. 10.1161/01.CIR.0000068337.25994.21
- Harbison J, O'Reilly P, McNicholas WT: Cardiac rhythm disturbances in the obstructive sleep apnea syndrome: effects of nasal continuous positive airway pressure therapy. Chest. 2000, 118:591-595. 10.1378/chest.118.3.591
- 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, 19:1046-1053.
The Association Between Obstructive Sleep Apnea and Arrhythmias
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Cite this article as:
Patel A R, Patel A R, Singh S, et al. (April 10, 2019) The Association Between Obstructive Sleep Apnea and Arrhythmias. Cureus 11(4): e4429. doi:10.7759/cureus.4429
Received by Cureus: March 27, 2019
Peer review began: April 02, 2019
Peer review concluded: April 06, 2019
Published: April 10, 2019
© Copyright 2019
Patel et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 3.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.