CPAP in AF Patients With OSA (CPAPAF)
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|ClinicalTrials.gov Identifier: NCT04513483|
Recruitment Status : Recruiting
First Posted : August 14, 2020
Last Update Posted : September 4, 2020
|Condition or disease||Intervention/treatment||Phase|
|Atrial Fibrillation Sleep Apnea||Device: continuous positive airway pressure Device: Placebo||Not Applicable|
Traditional risk factors for AF were established from the original Framingham Heart Study cohort which showed aging, hypertension, congestive heart failure, coronary artery disease, valvular heart disease and diabetes mellitus (DM) as independent risk factors. In the past decade, several important risk factors not encompassed in previous studies have also been found to have a link with AF. One of these newly-identified risk factors is obstructive sleep apnea (OSA), which has been listed as one of the risk factor needed to be assessed and treated in AF patients.
OSA and AF often co-exist and indeed share some risk factors, such as hypertension. AF Patients are more likely to have OSA, with reported prevalence rates of OSA (apnea-hypopnea index [AHI] ≥15) as high as 62% in AF cohorts from hospital-based studies. In community-based cohort studies, a cross-sectional analysis from sleep heart health study (SHSS) found those with sleep-disordered breathing(SDB)/sleep apnea (SA) (respiratory disturbance index [RDI] ≥ 30) had four times the odds of a polysomnography (PSG)-detected nocturnal AF as compared to those without SDB/SA after adjusting confounders. Following from this, a cross-sectional study on Outcomes of Sleep Disorders in Older Men Study (MrOS Sleep Study) showed a dose-response association between RDI and AF.
There are several pathophysiological mechanisms by which OSA could potentially increase the risk of development of new AF, or trigger a recurrence of AF in a patient with an established history of AF. OSA is characterized by repetitive collapse of the upper airway (UA) during sleep. The UA collapses when sleep-related loss in UA dilator muscle tone is superimposed upon a narrow and/or collapsible airway. These obstructive apneas or hypopneas, characterized by unsuccessful inspiratory efforts against an occluded airway, lead to 1) exaggerated negative intrathoracic pressure swings 2) hypoxia, and 3) co-activation of sympathetic and parasympathetic systems, all of which have been shown to potentiate a pro-arrhythmic state. Given that these mechanisms are pro-arrhythmic, CPAP (continuous positive airway pressure), the gold standard therapy for OSA, works by splinting the upper airway open during sleep with subsequent abolition of swings in pressure, hypoxia and arousals, can potentially modify the risk of development of AF or recurrence of AF in OSA patients.
There is a growing body of literature supporting that OSA being as a risk factor for recurrence of AF after cardioversion or ablation and treatment of OSA with CPAP decreased the risk of recurrence of AF. Nevertheless, all of the aforementioned studies are observational or retrospective in nature. Recently, Caples et al. conducted the first randomized control trial using CPAP in patients with AF and OSA but failed to find a difference of recurrence of AF between those treated with CPAP versus usual care. Notably, there are several issues in the study design and methodology that do not allow for firm conclusion from the results of this study. It was a single-center study, enrolling very small number of patients, and used a low cut-off AHI>5/h as inclusion criteria. More importantly, only patients with persistent AF scheduled for cardioversion were included. Given the natural time-course from paroxysmal AF to persistent AF, long-term remodeling or established atrial arrythmogenic substrate in persistent AF may be less or not reversible even when the initial risk factor is removed. In this regard, early intervention with CPAP in patients with paroxysmal AF and OSA, which has never been done in previous studies, should confer a better antiarrythmic effect. Therefore, the investigators aim to test the hypothesis that treatment of OSA with CPAP would reduce the burden of AF in patients with paroxysmal AF.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||100 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||None (Open Label)|
|Official Title:||The Effect of Continuous Positive Airway Pressure in Patients With Obstructive Sleep Apnea and Paroxysmal Atrial Fibrillation|
|Actual Study Start Date :||August 7, 2020|
|Estimated Primary Completion Date :||June 30, 2022|
|Estimated Study Completion Date :||June 30, 2022|
Experimental: CPAP treatment for 12 months
CPAP treatment for 12 months
Device: continuous positive airway pressure
CPAP treatment at night. Treat AF as cardiologist's discretion.
Placebo Comparator: Placebo
Observation. Treat AF as cardiologist's discretion.
- Change of AF burden [ Time Frame: 0, 6, 12 months ]The duration in AF on 14-day ECG monitor (percent)
- change of left atrium volume [ Time Frame: 0, 6, 12 months ]LA volume index measured by ultrasonocardiography
- change of Quality of Life [ Time Frame: 0, 6, 12 months ]Questionnaire (Short Form Health Survey-36); higher scores means a better quality of life; maximal score 100%
- Number of participants hospitalized for cardiovascular or all causes [ Time Frame: 12 months ]Hospitalization for cardiovascular or all causes within the follow-up period
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04513483
|Contact: Chih-Chieh C Yu, MD.PhD||886-2-23123456 ext firstname.lastname@example.org|
|National Taiwan University Hospital||Recruiting|
|Contact: Chih-Chieh Yu, MD.PhD. 886-2-23123456 ext 65257 email@example.com|
|Principal Investigator:||Chih-Chieh Yu, MD.PhD||National Taiwan University Hospital|