Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Sleep apnoea and atrial fibrillation: The Australian clinical picture

  Sleep apnoea and atrial fibrillation frequently share a patient. In obstructive sleep apnoea (OSA), recurrent airway obstruction causes intermittent hypoxia, chest pressure changes and repeated arousals. These stresses can favour abnormal atrial electrical activity, while AF can complicate sleep and breathing. Both influence cardiovascular risk.

  The relationship runs in both directions. Untreated OSA is associated with a greater likelihood of AF and of recurrence after cardioversion. Around respiratory programmes such as APSR 2022, the practical question is which people need combined sleep and cardiac assessment rather than treatment of an irregular rhythm in isolation.

  Australian practice gives this issue a distinctive context. A GP often first notes snoring, witnessed pauses or palpitations, and terms including OSA, AF and CPAP (continuous positive airway pressure) are familiar in local consultations. Melbourne and Sydney have dense specialist networks, while patients in regional Queensland, Western Australia or the Northern Territory may face long travel distances.

  Telehealth can bridge some distance, and Aboriginal community-controlled health services are important in remote and regional care. Access, language, housing and device affordability still shape outcomes. The aim is to recognise sleep-related breathing problems, assess their cardiovascular relevance and coordinate treatment with each person’s health needs.

  A shared clinical problem

  OSA is more common among people with AF than among comparable people without it, and more severe sleep-disordered breathing often accompanies recurrent or persistent AF. It is not the only cause: obesity, hypertension, heart failure, ageing and medication effects can all contribute, so sleep history and cardiovascular assessment belong together.

  Night-time breathlessness may be attributed to AF, while palpitations and fragmented sleep may be blamed on stress. Recording night-time events, medication use and daytime symptoms helps separate these possibilities before treatment.

  How airway obstruction can affect the heart

  Recurrent apnoeas produce intermittent hypoxaemia, negative intrathoracic pressure and arousals. The autonomic and haemodynamic changes can stretch atrial tissue and trigger abnormal electrical activity, helping explain why OSA and AF so often coexist.

  AF can worsen OSA through reduced left ventricular function, pulmonary congestion and changes in upper-airway tone. This feedback supports shared care, with sleep physicians frequently encountering AF and cardiologists regularly seeing OSA.

  Observational links do not prove causation, and some people with severe OSA never develop AF. Looking for OSA still matters because it is treatable and may complicate cardioversion, stroke prevention and maintenance of sinus rhythm.

  Recognising the combination in Australian clinics

  Useful clues include loud snoring, witnessed apnoeas, choking at night, unrefreshing sleep and morning headaches. Daytime sleepiness, resistant hypertension, obesity and a neck circumference above 40 cm increase suspicion, but no symptom confirms OSA. AF may be found on an ECG or reported as palpitations, dizziness or breathlessness.

  Australian primary care commonly uses STOP-Bang and the Epworth Sleepiness Scale. They help estimate risk and structure referral; they do not replace testing. A GP should also review alcohol, sedatives, mood, thyroid function and blood pressure rather than labelling every fatigue problem as sleep apnoea.

  Telephone and video consultations support triage in regional areas, although a remote consultation cannot observe airway obstruction during sleep. Culturally safe assessment and collaboration with local services are especially important for Aboriginal and Torres Strait Islander patients.

  Choosing an appropriate diagnostic pathway

  A sleep physician combines history, examination and testing. Full polysomnography measures airflow, oxygen saturation, arousals and sleep stages. Home sleep apnoea testing uses a smaller device and suits selected people likely to have moderate-to-severe OSA; it performs less well when other sleep disorders are present.

  For AF, an ECG, echocardiogram and blood tests help establish rhythm, ventricular function and relevant contributors. Stress testing or coronary imaging depends on symptoms and risk. Rapid heart rate, recent symptomatic AF or suspected heart failure warrants prompt review, regardless of OSA testing.

  Medicare can subsidise eligible sleep studies and CPAP treatment, but rebates and equipment pathways have eligibility rules. Private insurance, public waiting lists and out-of-pocket costs affect choices, so explaining likely costs early can prevent delays after referral.

  Treatment effects on rhythm and vascular health

  Positive airway pressure therapy keeps the airway open during sleep and is the standard first-line treatment for moderate-to-severe OSA. Good adherence can reduce sleepiness and blood pressure and may lower AF recurrence or help maintain sinus rhythm in selected patients. CPAP is not a cure for AF, and its cardiovascular effects are not uniform.

  For mild OSA, weight management, sleep position, avoiding alcohol and sedatives and treating nasal obstruction may be sufficient. A custom-fitted mandibular advancement device can suit some patients, particularly when CPAP is poorly tolerated. Upper-airway surgery may help selected anatomy.

  AF management remains essential: rate or rhythm control, anticoagulation and blood-pressure treatment depend on stroke and bleeding risk. OSA may influence AF burden, but anticoagulation decisions should not be delayed solely while awaiting sleep testing; they require the usual clinical risk assessment.

  COPD, hypoxaemia and the wider respiratory picture

  Chronic obstructive pulmonary disease (COPD) can coexist with OSA, sometimes called overlap syndrome. COPD may cause daytime sleepiness through sleep fragmentation, while OSA adds intermittent hypoxaemia and inflammatory stress. Together they can affect pulmonary pressure, right-heart function and arrhythmia risk.

  APSR 2022 coverage of lung volume reduction research in advanced COPD shows the breadth of respiratory care relevant here. Severe lung disease can increase breathlessness, hypoxaemia and right-heart strain, complicating assessment of palpitations, exercise tolerance and fluid status. Lung-function and imaging findings should be read alongside cardiac findings.

  Respiratory specialists and cardiologists often share these patients. A combined plan should identify the main cause of breathlessness, avoid duplicated tests and review inhalers, prescribed oxygen therapy, sleep treatment and cardiac medicines together.

  Practical priorities for patients and clinicians

  A useful checklist separates tasks that can occur in parallel. Patients can prepare for appointments, while clinicians ensure that sleep and cardiac care meet.

  • Mention snoring, witnessed pauses or unrefreshing sleep when AF is diagnosed, and note whether alcohol or sedatives worsen symptoms.
  • Bring a medication list, blood-pressure readings, sleep diary and any ECG or echocardiogram results to appointments.
  • Review sleep position, alcohol, nicotine and sedative use, including medicines that may affect breathing during sleep.

  The cardiovascular review should remain equally focused:

  • Assess AF symptoms, stroke and bleeding risks, blood pressure and relevant blood tests.
  • Consider sleep testing when suspicion is moderate or high, then use results to guide treatment.
  • Reassess rhythm, daytime sleepiness and treatment adherence after sleep therapy begins.

  The practical takeaway is that OSA is a treatable contributor to AF care rather than a separate footnote. Confirming sleep-disordered breathing, supporting consistent treatment and coordinating respiratory and cardiac review can improve symptoms and treatment planning. Decisions about anticoagulation and rhythm control still require individual assessment by the treating team.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)