Gemma Cadby1, Nigel McArdle2, Tom Briffa3, David R Hillman4, Laila Simpson5, Matthew Knuiman3, Joseph Hung6. 1. Centre for Genetic Origins of Health and Disease, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley. 2. School of Anatomy, Physiology and Human Biology, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley; West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, WA, Australia. Electronic address: nigel.mcardle@uwa.edu.au. 3. School of Population Health, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley. 4. School of Anatomy, Physiology and Human Biology, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley; West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, WA, Australia. 5. Centre for Genetic Origins of Health and Disease, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley; School of Anatomy, Physiology and Human Biology, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley; West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, WA, Australia. 6. School of Medicine and Pharmacology, Sir Charles Gairdner Hospital Unit, University of Western Australia, Crawley.
Abstract
BACKGROUND: OSA is a common condition that has been associated with atrial fibrillation (AF), but there is a paucity of data from large longitudinal cohorts to establish whether OSA is a risk factor for AF independent of obesity and other established risk factors. METHODS: We studied patients attending a sleep clinic referred for in-laboratory polysomnography for possible OSA between 1989 and 2001. Whole-population hospital data in Western Australia for 1970 to 2009 were linked to sleep study cases to determine incident AF hospitalization to 2009. Cox regression analyses were used to assess the independent association of OSA with incident AF. RESULTS: Study case subjects (6,841) were predominantly middle aged (48.3 ± 12.5 years old) and men (77%), and 455 developed AF during a median 11.9 years of follow-up. Univariate predictors of AF included age, BMI, hypertension, diabetes, valvular heart disease, coronary or peripheral artery disease, heart failure, and COPD (all P < .001). After multivariable adjustment, independent predictors of incident AF were an apnea/hypopnea index (AHI) > 5/h (hazard ratio [HR], 1.55; 95% CI, 1.21-2.00), log (AHI + 1) (HR, 1.15; 95% CI, 1.06-1.26), and log (time with oxygen saturation < 90% + 1) (HR, 1.12; 95% CI, 1.06-1.19). There were no interactions between age, sex, or BMI and AHI for AF development. CONCLUSIONS: OSA diagnosis and severity are independently associated with incident AF. Clinical trials are required to determine if treatment of OSA will reduce the burden of AF.
BACKGROUND: OSA is a common condition that has been associated with atrial fibrillation (AF), but there is a paucity of data from large longitudinal cohorts to establish whether OSA is a risk factor for AF independent of obesity and other established risk factors. METHODS: We studied patients attending a sleep clinic referred for in-laboratory polysomnography for possible OSA between 1989 and 2001. Whole-population hospital data in Western Australia for 1970 to 2009 were linked to sleep study cases to determine incident AF hospitalization to 2009. Cox regression analyses were used to assess the independent association of OSA with incident AF. RESULTS: Study case subjects (6,841) were predominantly middle aged (48.3 ± 12.5 years old) and men (77%), and 455 developed AF during a median 11.9 years of follow-up. Univariate predictors of AF included age, BMI, hypertension, diabetes, valvular heart disease, coronary or peripheral artery disease, heart failure, and COPD (all P < .001). After multivariable adjustment, independent predictors of incident AF were an apnea/hypopnea index (AHI) > 5/h (hazard ratio [HR], 1.55; 95% CI, 1.21-2.00), log (AHI + 1) (HR, 1.15; 95% CI, 1.06-1.26), and log (time with oxygen saturation < 90% + 1) (HR, 1.12; 95% CI, 1.06-1.19). There were no interactions between age, sex, or BMI and AHI for AF development. CONCLUSIONS: OSA diagnosis and severity are independently associated with incident AF. Clinical trials are required to determine if treatment of OSA will reduce the burden of AF.
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