Author + information
- Dominik Linz, MD, PhDa,
- Anthony G. Brooks, PhDb,
- Adrian D. Elliott, PhDa,
- Chrishan J. Nalliah, MBBSc,
- Jeroen M.L. Hendriks, PhDa,
- Melissa E. Middeldorpa,
- Celine Gallagher, RNa,
- Rajiv Mahajan, MD, PhDa,
- Jonathan M. Kalman, MBBS, PhDc,
- R. Doug McEvoy, MDd,
- Dennis H. Lau, MBBS, PhDa and
- Prashanthan Sanders, MBBS, PhDa,∗ ()
- aCentre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, South Australia, Australia
- bCardiac Rhythm Management, MicroPort, Scoresby, Victoria, Australia
- cDepartment of Cardiology, Royal Melbourne Hospital and Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
- dAdelaide Institute for Sleep Health, College of Medicine and Public Health, Flinders University, and Sleep Health Service, Respiratory and Sleep Services, Southern Adelaide Local Health Network, Adelaide, South Australia, Australia
- ↵∗Address for correspondence:
Dr. Prashanthan Sanders, Centre for Heart Rhythm Disorders, Department of Cardiology, Royal Adelaide Hospital, Port Road, Adelaide, 5000, Australia.
Objectives This study sought to determine night-to-night variability in the severity of sleep-disordered breathing (SDB) and the dynamic intraindividual relationship to daily risk of incident atrial fibrillation (AF) by using simultaneous long-term day-by-day SDB and AF monitoring.
Background Night-to-night variability in SDB severity may result in a dynamic exposure to SDB related conditions impacting the timing and extent of cardiovascular responses.
Methods This study was an observational cohort study. Daily data for AF burden and average respiratory disturbance index (RDI) were extracted from pacemakers capable of monitoring nightly SDB and daily AF burden in 72 patients. Nightly RDI values were grouped into quartiles of severity within each patient. AF burdens of >5 min, >1 h, and >12 h were the outcome variables.
Results A total of 32% of patients had a mean RDI of ≥20/h, indicative of overall severe SDB. There was significant night-to-night variation in RDI reflected by an absolute SD of ±6.3 events/h (range 2 to 14 events/h) within any given patient. Within each patient, the nights with the highest RDI (in their highest quartile) conferred a 1.7-fold (1.2 to 2.2; p < 0.001), 2.3-fold (1.6 to 3.5; p < 0.001), and 10.2-fold (3.5 to 29.9; p < 0.001) increase risk of having at least 5 min, 1 h, and 12 h, respectively, of AF during the same day compared with the best sleep nights (in their lowest quartiles).
Conclusions There is considerable night-to-night variability in SDB severity which cannot be detected by 1 single overnight sleep study. SDB burden may be a better metric with which to assess the extent of dynamic SDB related cardiovascular responses such as daily AF risk than the categorical diagnosis of SDB. (Night-to-Night Variability in Severity of Sleep Apnea and Daily Dynamic Atrial Fibrillation Risk [VARIOSA-AF]; ACTRN 12618000757213)
- atrial fibrillation
- dynamic substrate
- night-to-night variability
- sleep-disordered breathing
Dr. Linz is supported by a Beacon research fellowship, University of Adelaide; and is an advisory board member for LivaNova/MicroPort and Medtronic; and receives lecture and consulting fees from LivaNova/MicroPort, Medtronic, and ResMed; and has received funding from Sanofi, ResMed, and Medtronic. Drs Elliott and Hendriks are supported by Early Career Fellowships from the National Heart Foundation of Australia. Dr. Hendriks holds a Derek Frewin Lectureship, University of Adelaide, and is a consultant for Medtronic and Pfizer/BMS. Ms. Middeldorp is supported by a postgraduate scholarship from the National Health and Medical Research Council (NHMRC) of Australia. Ms. Gallagher is supported by a Leo J. Mahar scholarship, University of Adelaide. Dr. Mahajan is supported by an Early Career Fellowship, NHMRC, and a Leo J. Mahar lectureship, University of Adelaide; and receives lecture and consulting fees from Medtronic, Abbott, Bayer, and Pfizer; and has received funding through his institution from Abbott, Medtronic, and Bayer. Drs. McEvoy, Kalman, and Sanders are supported by Practitioner Fellowships, NHMRC of Australia. Dr. McEvoy has received funding from Philips Respironics, ResMed, and Fisher and Paykel. Dr. Sanders is an advisory board member of Biosense-Webster, Medtronic, St. Jude Medical, Boston Scientific, CathRx; and has received funding through his institution from Biosense-Webster, Medtronic, St. Jude Medical, Boston Scientific and LivaNova/MicroPort. Dr. Lau is supported by a Robert J. Craig Lectureship, University of Adelaide; and has received lecture and consulting fees from Abbott, Biotronik, Boehringer Ingelheim, Bayer, and Pfizer. Dr. Brooks is an employee of LivaNova/MicroPort. Dr. Lim is supported by a Neil Hamilton Fairley Early Career Fellowship, NHMRC of Australia. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. William Stevenson, MD, served as Guest Editor for this paper.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received December 17, 2018.
- Revision received February 25, 2019.
- Accepted March 13, 2019.
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.