A 42-Year-Old Female with Well-Controlled Atrial Fibrillation and Mild Obstructive Sleep Apnea

A 42-year-old female with a history of atrial fibrillation (AF) controlled with medications, was referred to the a sleep disorders center for the evaluation of suspected sleep disordered breathing. Suspicion was raised because of her history of snoring and the recent diagnosis of AF. She had never been noticed to stop breathing during sleep. Review of systems was negative for nocturnal gasping, sleep walking, dream enactment, sleep related hallucinations, and sleep paralysis. There was no history of cataplexy, excessive daytime sleepiness, napping, involuntary dozing, or sleepiness while driving. There was no history of restless leg syndrome symptoms, diabetes mellitus, hypertension, or upper airway surgery. Her primary medical issue was AF, which was well controlled with flecainide 100 mg twice daily and diltiazem 180 mg daily. The only other medication that she was taking was aspirin 325 mg daily. Several of her family members snored. One brother had died of a myocardial infarction. One sister had a history of palpitations. On examination, our patient weighed 160 lb and had a BMI of 26 kg/m². She had a Mallampati III oropharynx, a mildly elongated soft palate, and a neck circumference of 13.5 inches. Because of suspected obstructive sleep apnea (OSA), we advised her to undergo an overnight polysomnogram (PSG). Hypopneas were noted during the study, and her total apneahypopnea index (AHI) was 9 events per hour, consistent with mild OSA. Her EKG showed normal sinus rhythm for the majority of the night, except for brief consecutive time intervals during which an abnormality was noted on it (Figures 1–3).

Figure 1. One-minute window from polysomnogram.

E1-M2, E2-M2: ocular channels. EMG3-EMG2: chin electromyogram. F4-M1, C3-M2, C4-M1, O2-M1: electroencephalographic channels. EKG2-EKG1: electrocardiogram. Leg/L-Leg/R: leg electromyogram. IC1-IC2: intercostal leads. Thor: respiratory effort measured by thoracic belt. Abdo: respiratory effort measured by abdominal belt.

Figure 2. Thirty-second window from polysomnogram.

E1-M2, E2-M2: ocular channels. EMG3-EMG2: chin electromyogram. F4-M1, C3-M2, C4-M1, O2-M1: electroencephalographic channels. EKG2-EKG1: electrocardiogram. Leg/L-Leg/R: leg electromyogram. IC1-IC2: intercostal leads. Thor: respiratory effort measured by thoracic belt. Abdo: respiratory effort measured by abdominal belt.

Figure 3. Thirty-second window from polysomnogram.

E1-M2, E2-M2: ocular channels. EMG3-EMG2: chin electromyogram. F4-M1, C3-M2, C4-M1, O2-M1: electroencephalographic channels. EKG2-EKG1: electrocardiogram. Leg/L-Leg/R: leg electromyogram. IC1-IC2: intercostal leads. Thor: respiratory effort measured by thoracic belt. Abdo: respiratory effort measured by abdominal belt.

QUESTION: What abnormality was noted on this patient's EKG, and what factors possibly led to this abnormality?

ANSWER: This patient can be seen going from normal sinus rhythm in to AF, the onset of which was preceded by a hypopnea associated with both EEG arousal and desaturation (Figure 1; one-minute window). These events could possibly have led to the triggering of her AF. Note that the above described EEG arousal, desaturation, and onset of AF are better seen in a 30-sec window (Figure 2), and the AF can be seen persisting in the next 30-sec window (Figure 3).

DISCUSSION

This patient had what was thought to be well controlled AF and was on flecainide and diltiazem. Her overnight in-laboratory PSG showed that she had mild OSA. Her EKG showed normal sinus rhythm for the majority of the night. During stage II sleep, immediately following one of the hypopneas, however, she was noticed to have a desaturation and an EEG arousal followed by the onset of AF.

Studies have shown that between 4.3% and 4.8% of patients with OSA have AF, compared to between 0.9% and 2.1% of those who do not have OSA.^1,2 The severity of OSA and the degree of nocturnal oxygen desaturation have been shown to be predictors for AF.² It has been shown that the initiation of CPAP therapy in patients with OSA significantly decreases their risk of developing paroxysmal atrial fibrillation.³ The intermittent hypoxia, recurrent arousals, sympathetic activation, and intrathoracic pressure swings in patients with OSA are felt to increase their risk of AF.⁴ It has been reported that between 21% and 49% of patients with AF have underlying OSA.^5,6 Another study found that patients with AF and severe OSA (AHI > 30 events/h) have a significantly higher chance of not responding to anti-arrhythmic drug therapy as compared to patients with AF and non-severe OSA (AHI ≥ 5 and ≤ 30).⁷ Note that the authors of this study defined a hypopnea as ≥ 50% reduction in airflow from baseline for ≥ 10 seconds and accompanied by a decrease in oxygen saturation ≥ 4%.

Patients with AF and OSA undergoing catheter ablation are at a significantly higher risk for recurrent AF than similar patients without OSA.^6,8,9 Patients with AF and OSA who are treated adequately with CPAP and undergo cardioversion or catheter ablation have significantly decreased risk for recurrent AF compared to similar patients not on CPAP.^6,9–11

This case highlights the clinical association between AF and OSA and strikingly shows a respiratory event apparently triggering an episode of AF. The odds of an arrhythmia after such respiratory disturbances in patients with sleep disordered breathing is estimated to be nearly 18 times the odds of an arrhythmia occurring after normal breathing.¹² Sleep physicians and other health care providers taking care of such patients need to be aware of the above associations to ensure their appropriate evaluation and management.

SLEEP MEDICINE PEARLS

1. Patients with obstructive sleep apnea are at a higher risk for developing atrial fibrillation than those patients who do not have obstructive sleep apnea.

2. A significant proportion of patients with atrial fibrillation have underlying obstructive sleep apnea.

3. The odds of an arrhythmia after a respiratory disturbance in a patient with obstructive sleep apnea is estimated to be nearly 18 times the odds of an arrhythmia occurring after normal breathing.

4. Severity of obstructive sleep apnea and degree of nocturnal oxygen desaturation have been shown to be predictors for developing atrial fibrillation.

DISCLOSURE STATEMENT

This was not an industry supported study. The authors have indicated no financial conflicts of interest.

CITATION

Kapoor M, Greenough G. A 42-year-old female with well-controlled atrial fibrillation and mild obstructive sleep apnea. J Clin Sleep Med 2015;11(3):274–276.