Obstructive sleep apnoea and atrial fibrillation (AF) have presented many challenges, including identifying which patients need to be assessed for obstructive sleep apnoea and the current management options. Caroline Broughton, Shahbaz Piracha and Martin Allen write in Cardiac Rhythm News about their findings.
Sleep apnoea is a common condition affecting an unknown number of the UK population, with studies in North America suggesting the prevalence may be in double figures.1 Broadly speaking there are two types of sleep apnoea. One is the less common central apnoea that occurs when there is a lack of effort to breath, often seen in heart failure while the much more common type seen in over 90% of case is obstructive sleep apnoea associated with AF.
The mechanism of the association remains uncertain. This may be related to the recurrent hypoxaemia that occurs when the airway is obstructed by the collapse of the upper airway. An alternative explanation may be the large intrathoracic pressure swings that occur during the cessation of breathing and the large negative pressures generated. Likewise, the sympathetic activation that is associated with obstructive apnoea is also likely to be a contributory factor.2
Identifying the association is important as treatment of the obstructive sleep apnoea is often associated with an improved control of the atrial fibrillation and maintenance of rhythm control post cardioversion.3 Moreover, atrial structural remodelling and conduction changes can occur with prolonged exposure to obstructive sleep apnoea over time, which consequently impairs treatment by all modalities if left untreated.4
However, this is not always easy as the excessive daytime sleepiness that is such a feature of obstructive sleep apnoea is often absent or limited in patients with atrial fibrillation.5
The clinical syndrome of sleep apnoea where there are recurrent episodes of airway collapse, associated with arterial oxygen desaturation and sleep fragmentation as a consequence of arousal from sleep is often suggested from the clinical history of loud snoring, witnessed apnoea and daytime sleepiness. Clinical examination should take note of the commonly coexisting hypertension that is evidenced in obstructive sleep apnoea and the size of the upper airway. While obesity is associated in obstructive sleep apnoea, up to one third of patients have a normal body mass index.
This fact that you do not have to be obese to have obstructive sleep apnoea is often poorly recognised. Thus, to identify obstructive sleep apnoea in the AF population, a high index of suspicion is needed with onward referral for sleep studies to confirm the diagnosis and the severity of the sleep apnoea so patients can be triaged for the most appropriate treatment. While this may be lifestyle changes, for many patients the continuous positive airways pressure is the treatment of choice, as recommended by the National Institute for Health and Care Excellence (NICE).6 This involves the individual sleeping with a snugly fitted mask, held in place by a strap, that is connected to a flow generator that applies a pressure to the airway to prevent the collapse. Such treatment is well tolerated and highly effective in controlling symptoms, reducing hypertension and aiding control of associated medical problems, including AF.
Linz has suggested that all patients with AF who are diagnosed with obstructive sleep apnoea should be managed by multidisciplinary teams.7 This is the process we have followed at our institution for many years, with patients who are seen by the specialist AF nurse being referred for sleep studies. Additionally, all patients are referred to a cardiac rehabilitation team for exercise assessment, smoking cessation, dietary advice and hypertension management in collaboration with local GPs.
The difficulty lies in identifying which patients with AF are most likely to have obstructive sleep apnoea that is contributing to their on-going AF symptoms. The traditional association of sleepiness that exists in the general obstructive sleep apnoea population is not found in patients who have AF. Hence looking for sleepiness using the Epworth sleepiness score, as an aid to who should be referred for sleep studies appears of little use, something we found in our study.8
More work is clearly needed to identify specific risk factors for both AF and obstructive sleep apnoea in order to streamline services and optimise treatment outcomes.
Caroline Broughton is a specialty registrar in cardiology at Royal Stoke University Hospital, Stoke-on-Trent, UK.
Shahbaz Piracha is a specialty registrar in respiratory medicine at Sandwell and West Birmingham Hospitals, UK.
Martin Allen is a consultant physician in respiratory medicine at Sandwell and West Birmingham Hospitals, UK.
1. Garvey et al. J Thorac Dis. 2015;7(5):920-9.
2. Kwon et al. Sleep Med Rev 2018;39:134-42.
3. Kanagala et al. Circulation 2003;107(20):2589-94.
4. Neilan et al. J Am Heart Assoc 2013;2(6):e000421.
5. Broughton et al. EP Europace, Volume 20, Issue suppl_4,1 October 2018, Pages iv7-iv8, https://doi.org/10.1093/europace/euy198.008.
6. National Institute for Health and Care Excellence (2008). Available at: https://www.nice.org.uk/guidance/ta139 [Accessed 17/12/2018]
7. Linz et al. JAMA Cardiol 2018;3(6):532-40.
8. Albuquerque et al. Chest 2012;141(4):967-73.