Association of atrial fibrillation and obstructive sleep apnea

Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St SW, Rochester, Minn 55905, USA.
Circulation (Impact Factor: 14.95). 08/2004; 110(4):364-7. DOI: 10.1161/01.CIR.0000136587.68725.8E
Source: PubMed

ABSTRACT Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion. OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown.
We prospectively studied consecutive patients undergoing electrocardioversion for AF (n=151) and consecutive patients without past or current AF referred to a general cardiology practice (n=312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and chi2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, P=0.0006).
The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) and obstructive sleep apnea (OSA) are very prevalent diseases in modern society. Recent years have seen the emergence of a wide body of literature suggesting an important association between these two diseases. This review will provide a summary of this evidence as it currently exists. First, it will review the literature suggesting an association between AF and OSA by highlighting the prevalence of AF in OSA, the correlation of AF prevalence with OSA severity and the trend towards increased AF recurrence in patients with OSA after treatment for AF. Second, it will identify the possible pathophysiologic mechanisms for this association. In doing so, it will discuss the investigated effects of intrathoracic pressure changes, autonomic instability and atrial remodeling. Finally, it will review the evidence of the effect of treatment of OSA on AF, highlighting the role of continuous positive airway pressure (CPAP) in the treatment of OSA and its impact on AF prevalence and recurrence.
    Current Cardiology Reviews 10/2012; 8(4):265-272. DOI:10.2174/157340312803760811
  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is highly associated with obstructive sleep apnea (OSA) in which AF is triggered by hyperactivity of the cardiac autonomic nervous system (CANS). Prior studies showed that low-level vago-sympathetic trunk stimulation (LLVS), at voltages not slowing sinus rate or AV conduction, inhibits AF by suppressing the CANS. We investigated whether LLVS delivered at the right vago-sympathetic trunk suppresses AF in a rabbit model of OSA. All 11 rabbits received a tracheostomy under general anesthesia. The endotracheal tube was clamped at end expiration for 1 minute to simulate OSA. Over a period of 4 hours, OSA was delivered every 6 minutes. Effective refractory period (ERP), blood pressure, intra-esophageal pressure and blood gases (O2, CO2, pH) were measured before and after each episode of OSA. AF duration and ERP were measured by programmed stimulation. Group-1 rabbits (n=6) received LLVS (50% below that which slowed the sinus rate) in the first 3 hours. Group-2 rabbits (n=5) only received OSA. Group-1 ERP began to lengthen progressively from the 2(nd) hour, compared to Group-2. AF duration increased in the 1(st) hour for both groups but it began to shorten progressively after the 1(st) hour in Group-1 rabbits. The blood pH, O2 or CO2 level, the intra-esophageal pressure and the hypertensive response during OSA were not different between the two groups. LLVS is capable of suppressing ERP shortening and AF induced by OSA. LLVS may serve as new therapeutic approach to treat OSA-induced AF. Copyright © 2014. Published by Elsevier Inc.
    Heart rhythm: the official journal of the Heart Rhythm Society 12/2014; DOI:10.1016/j.hrthm.2014.12.024 · 4.92 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Sleep deprivation contributes to the development and recurrence of ventricular arrhythmias. However, the electrophysiological changes in ventricular myocytes in sleep deprivation are still unknown. Material/Methods Sleep deprivation was induced by modified multiple platform technique. Fifty rats were assigned to control and sleep deprivation 1, 3, 5, and 7 days groups, and single ventricular myocytes were enzymatically dissociated from rat hearts. Action potential duration (APD) and transient outward current (Ito) were recorded using whole-cell patch clamp technique. Results Compared with the control group, the phases of APD of ventricular myocytes in 3, 5, and 7 days groups were prolonged and APD at 20% and 50% level of repolarization (APD20 and APD50) was significantly elongated (The APD20 values of control, 1, 3, 5, and 7 days groups: 5.66±0.16 ms, 5.77±0.20 ms, 8.28±0.30 ms, 11.56±0.32 ms, 13.24±0.56 ms. The APD50 values: 50.66±2.16 ms, 52.77±3.20 ms, 65.28±5.30 ms, 83.56±7.32 ms, 89.24±5.56 ms. P<0.01, n=18). The current densities of Ito significantly decreased. The current density-voltage (I–V) curve of Ito was vitally suppressed downward. The steady-state inactivation curve and steady-state activation curve of Ito were shifted to left and right, respectively, in sleep deprivation rats. The inactivation recovery time of Ito was markedly retarded and the time of closed-state inactivation was markedly accelerated in 3, 5, and 7 days groups. Conclusions APD of ventricular myocytes in sleep deprivation rats was significantly prolonged, which could be attributed to decreased activation and accelerated inactivation of Ito.
    Medical science monitor: international medical journal of experimental and clinical research 02/2015; 21:542-9. DOI:10.12659/MSM.893414 · 1.22 Impact Factor


Available from
May 26, 2014