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Volume 14 No. 11
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Accepted Papers

Case Reports

Improvement in Sleep-Disordered Breathing Indices Downloaded From a Positive Airway Pressure Machine Following Conversion of Atrial Fibrillation to Sinus Rhythm

Ken Monahan, MD1; Raghu Upender, MD2; Kristen Sherman, PA3; James Sheller, MD3; Jay Montgomery, MD1; Robert L. Abraham, MD1
1Division of Cardiovascular Medicine, Vanderbilt Medical Center, Nashville, Tennessee; 2Department of Neurology, Division of Sleep Medicine, Vanderbilt Medical Center, Nashville, Tennessee; 3Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt Medical Center, Nashville, Tennessee


Sleep-disordered breathing (SDB) is a contributor to atrial fibrillation (AF) and treatment of obstructive sleep apnea can reduce the recurrence of AF following catheter ablation. However, the effect of AF therapies on measures of SDB severity is less robustly described. We present the case of a middle-aged man with SDB and persistent AF who exhibited improvement in SDB metrics, as characterized by data downloaded from his auto-titrating continuous positive airway pressure (AutoCPAP) machine, very shortly following procedures that restored sinus rhythm. Between procedures, when his rhythm reverted to AF, the downloaded parameters suggested more SDB events. After catheter ablation, the patient maintained sinus rhythm and the improvement in SDB metrics was sustained as well. This case provides support in favor of a bidirectional relationship between SDB and AF and suggests that data available from PAP machines may be useful in serial assessment of SDB status relative to heart rhythm.


Monahan K, Upender R, Sherman K, Sheller J, Montgomery J, Abraham RL. Improvement in sleep-disordered breathing indices downloaded from a positive airway pressure machine following conversion of atrial fibrillation to sinus rhythm. J Clin Sleep Med. 2018;14(11):1953–1957.


Over the past two decades, knowledge of the relationship between sleep-disordered breathing (SDB), including obstructive sleep apnea (OSA) and central sleep apnea (CSA), and atrial fibrillation (AF) has expanded considerably. OSA is more severe in nonresponders to antiarrhythmic drug therapy for AF than in responders1 and recurrence of AF following electrical cardioversion is more common in those with OSA relative to those without OSA.2 OSA also increases the risk of AF recurrence following catheter ablation of AF3 and treatment of OSA with continuous positive airway pressure (CPAP) reduces the risk of AF recurrence following ablation to that of individuals without OSA.4 AF is also associated with CSA in those with5 and without6 heart failure and CSA is a risk factor for incident AF regardless of baseline cardiac status.7

Although the role of SDB on the prevalence and risk of recurrence of AF continues to be elucidated, the effects of AF treatment on SDB are less well described. In a small study of Japanese patients, restoration of sinus rhythm by catheter ablation of AF was reported to decrease the apnea-hypopnea index (AHI) as assessed by formal polysomnography (PSG) 1 week after ablation.8

As a complement to these findings, we report a case of a patient with persistent AF and SDB whose SDB severity, as assessed by data downloaded from his autotitrating CPAP (AutoCPAP) machine, fluctuated with changes in heart rhythm.


The patient is a 68-year-old man in whom OSA was diagnosed 15 years prior; the initial polysomnography (PSG) showed an AHI of 25 events/h and did not separately report obstructive apnea index (OAI) or central apnea index (CAI). Subsequent diagnostic PSG performed in 2016 showed an AHI of 45 events/h and a CAI of 2.5 events/h. For the past 18 months, he has been treated with AutoCPAP at 10 to 18 cmH2O using a nasal mask with humidified air (DreamStation AutoPAP). He has been highly adherent with the AutoCPAP regimen; serial machine downloads reveal use > 4 hours on 100% of nights and an average use per night of nearly 8 hours. His wife reports cessation of snoring and the patient notes significant reduction in daytime somnolence as well as improvement in cognition.

Other cardiac risk factors include hyperlipidemia and obesity (body mass index 34 kg/m2). Several exercise-imaging evaluations over the past decade showed no inducible ischemia and standard transthoracic echocardiography showed low-normal left ventricular systolic function (left ventricular ejection fraction of 45% to 55%). Left atrial size was normal (< 4 cm) prior to arrhythmia onset and was mildly enlarged (4.7 cm) approximately 1 year prior. The patient consumes caffeine and alcohol in moderation without recent changes to these habits.

Several years prior to the implementation of his current AutoCPAP regimen, he underwent radiofrequency ablation (RFA) of typical atrial flutter. Approximately 5 years after RFA, he presented to a routine clinic visit after several months of exertional dyspnea and exercise intolerance and was found to be in AF with borderline rate control (average ventricular rate 100 bpm). He began a regimen of twice-daily flecainide (100 mg bid) and underwent successful transesophageal echocardiogram-guided direct-current cardioversion (TEE-guided DCCV) 2 weeks after initiation of antiarrhythmic drug therapy. Symptomatically and by palpation of his radial pulse, the patient felt as though he reverted to AF within 24 to 48 hours of this procedure. Return of AF was confirmed electrocardiographically at a subsequent office visit. He underwent successful AF ablation 2 months later. On the day of the ablation, the patient exhibited no signs of volume overload; specifically, the neck veins were not elevated, the lungs were clear to auscultation, and he had no lower extremity edema. The immediate preprocedure rhythm was AF and, following TEE-guided DCCV just before the ablation, the patient underwent standard pulmonary vein isolation (PVI). He was observed overnight in the hospital per our usual post-AF ablation protocol and, fortuitously, used his own AutoCPAP machine that night. No changes to his cardiac medication regimen were made following the AF ablation. Since the PVI procedure, the patient has had no AF-related symptoms and serial follow-up electrocardiograms have shown sinus rhythm.

AutoCPAP Data Review

Direct Current Cardioversion

Data before and after the patient's initial DCCV are shown in Table 1 and Figure 1. The OAI and CAI are lower the night of the procedure relative to the 5 nights prior. The percentage of recorded time spent in periodic breathing is similar on the night of the procedure compared to the 5 nights preceding the procedure, but this parameter decreases sharply on the night after the DCCV. Periodic breathing increases abruptly and returns to pre-DCCV levels on the sixth post-procedure night, several days after the patient experienced symptoms of AF. AutoCPAP usage, average pressure levels, and 90th percentile pressure levels are similar throughout the time course depicted in Figure 1.

Parameters downloaded from AutoCPAP unit before and after direct-current cardioversion and catheter ablation.


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Table 1

Parameters downloaded from AutoCPAP unit before and after direct-current cardioversion and catheter ablation.

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Temporal trend of sleep-disordered breathing parameters surrounding direct-current cardioversion.

Daily trends are shown for (A) percentage of periodic breathing and (B) CAI (lighter purple line) and OAI (darker purple line) in events/h for the 5 days prior and 6 days following direct-current cardioversion. Arrows represent the day of the procedure. There is a decrease in these metrics starting the night following the procedure (A) and the night of the procedure (B). There is an abrupt increase in all parameters on the sixth night following the procedure. CAI = central apnea index, OAI = obstructive apnea index.


Figure 1

Temporal trend of sleep-disordered breathing parameters surrounding direct-current cardioversion.

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Atrial Fibrillation Ablation

Data before and after the patient's AF ablation are shown in Table 1 and Figure 2. Similar to the DCCV, the OAI and CAI are lower the night of the procedure compared to the 5 nights prior. The percentage of periodic breathing also decreases the night of the procedure. In contrast to the DCCV, all parameters remain lower than the pre-procedure baseline nearly 1 week after the ablation was performed; the patient maintained sinus rhythm during the entire timeframe shown in Figure 2.

Temporal trend of sleep-disordered breathing parameters surrounding catheter ablation of atrial fibrillation.

Within-night trends are shown for percentage of periodic breathing (PB), central apnea index (CA), obstructive apnea index (OA), and hypopnea index (H) for (A) the night prior to catheter ablation, (B) the night of catheter ablation, (C) the night after catheter ablation, and (D) 6 nights following catheter ablation. A reduction in these indices is observed beginning the night of the ablation procedure is sustained nearly 1 week post-procedure. The horizontal axis represents recorded time in hours.


Figure 2

Temporal trend of sleep-disordered breathing parameters surrounding catheter ablation of atrial fibrillation.

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The key observation illustrated in this report is that SDB metrics, obtained from data downloaded from a patient's AutoCPAP machine, show a reduction in SDB breakthrough events (ie, events that occur on treatment) at the earliest evaluable time point following procedure-mediated conversion of AF to sinus rhythm. There are improvements in both OSA and CSA metrics suggesting that both underlying processes are affected by the change in rhythm. This case also provides circumstantial evidence that the same parameters can report on worsening of SDB in concert with reversion to AF from sinus rhythm, as occurred following the patient's initial DCCV. This experience builds on prior work that focused on changes in formal PSG parameters measured 1 week after catheter ablation of AF.8 If found to be reproducible in a larger cohort, this finding could affect the use of positive airway pressure (PAP) downloads in the evaluation and management of those with, or at risk for, atrial arrhythmias.

Downloaded data from PAP machines may serve as a readily available, albeit indirect, method of assessment for reversion to AF or AFL following DCCV or catheter ablation (or, although not presented here, pharmacologic conversion), particularly for asymptomatic AF, which can occur relatively frequently.9 If SDB indices improve following conversion to sinus rhythm, downloaded data may indicate that PAP settings should be adjusted as a result. The potential utility of this information may result in more frequent downloads surrounding an AF-related procedure. Likewise, worsening of SDB on routine download without a clear precipitant may be an indicator that an atrial arrhythmia is present and could warrant further evaluation (ie, ambulatory monitoring).

When a patient is recumbent, interstitial fluid that has accumulated in the extremities over the course of a day due to the effects of gravity can be displaced rostrally, leading to accumulation in the lungs and around the soft tissue of the airway with attendant worsening of CSA and OSA.10 In those undergoing successful DCCV or catheter ablation of AF, the restoration of sinus rhythm and subsequent return of the atrial contribution to left ventricular filling (atrial kick) could augment cardiac output and result in less interstitial fluid accumulation, and thus fewer on-treatment breakthrough events, as reflected by incremental improvements in CSA and OSA indices. The return of atrial mechanical function following conversion from AF to sinus rhythm is variable, but can occur in as little as 30 minutes to 24 hours,11,12 but may take longer following catheter ablation.13 It is therefore plausible to invoke this mechanism as playing a role in the short-term improvement of our patient's SDB indices.

Additional observations from the downloaded data merit discussion. The change in periodic breathing after conversion from AF to sinus rhythm is the most dramatic of the metrics presented. As in heart failure, AF may represent an additional destabilizing element that adversely affects ventilatory control loop gain, defined as the ventilatory response to a given ventilatory disturbance.14 Even if the cardiac output does not change in absolute magnitude, the irregular blood flow may lead to inefficient circulation and a delay in the time required for changes in peripheral CO2 levels to reach central chemoreceptors (ie, circulatory delay), thus inducing oscillation in ventilation. Plant gain (changes in pulmonary capillary blood gas tensions in response to change in ventilation) may also be affected by AF. Left atrial and pulmonary pressures are increased in AF.15 The resulting pulmonary congestion activates mechanoreceptors in the lungs and can cause relative hyperventilation.6 The reemergence of periodic breathing during the latter half of the sixth night post-ablation (Figure 2D), may reflect some degree of rostral fluid accumulation as the night progresses, though perhaps less than was present during AF. It may also be indicative of a subclinical recurrence of AF, although we do not have data to support (or refute) this hypothesis. Last, there may be a component of day-to-day biologic variation because on the seventh night post-ablation (not shown), there was minimal periodic breathing.

This report has several limitations. Although PAP machine algorithms have been validated against PSG with regard to residual AHI, they are not always able to discriminate accurately between obstructive and central apnea,16,17 especially if the airway is closed during a true central apnea. Therefore, central events may have been falsely recorded as obstructive. In addition, the information downloaded from the patient's AutoCPAP machine was not confirmed with contemporaneous PSG data. As post-conversion echocardiography is not standard of care, confirmation of return of atrial mechanical function was not obtained by echocardiography following DCCV or catheter ablation. We also do not know objectively exactly when AF recurred following the initial DCCV, although the patient previously exhibited symptoms identical to those following DCCV when he was documented to be in AF by standard 12-lead electrocardiography. An effect of anesthetics on sleep during the night of the procedure cannot be excluded completely, which may confound inferences of the effect of the change in heart rhythm. However, sleep onset was 12 hours post-procedure on the night of cardioversion and was 10 hours post-procedure on the night of AF ablation. Additionally, the primary agent used for both procedures (propofol) is very short-acting. Sedative-hypnotics are not among our patient's home medications and he did not receive any in the hospital the night of his AF ablation.

In summary, this case offers evidence of improvement in SDB following conversion of AF to sinus rhythm via electrical cardioversion and catheter ablation. These changes were detectable by AutoCPAP machine diagnostics very shortly after the change in rhythm, which may have implications regarding the use of downloadable PAP data in the peri-procedural timeframe.


All authors have seen and approved the manuscript. The authors report no conflicts of interest.



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