Sleep apnea may induce distinct form of atrial fibrillation

Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice and is associated with increased morbidity and mortality due to thromboembolism, stroke, and worsening of pre-existing heart failure. Both its incidence and prevalence are increasing as AF risk increases with advancing age.1 While the strategies of heart rate control and anticoagulation to lower stroke risk and rhythm control have been found comparable with regard to survival, many patients remain highly symptomatic because of palpitations and reduced cardiac output.1

Structural abnormalities of the atria, including fibrosis and dilation, accompanied by conduction abnormalities, provide the underlying substrate for AF. It is well established that AF episodes perpetuate atrial remodeling leading to more frequent and prolonged AF episodes. Hence, there is the long-standing notion that “AF begets AF.” While a variety of antiarrhythmic drugs have been employed over the years to prevent AF recurrences and to maintain sinus rhythm, their use has decreased over the past 2 decades due to their major side effects and their potential of proarrhythmia.

Catheter-based ablation techniques have gained widespread acceptance for the prevention of AF recurrences and the maintenance of sinus rhythm. Since the junction between the pulmonary veins and the left atrium has long been appreciated as a contributer to AF initiation and/or perpetuation, catheter-based radiofrequency ablation directed at the junction of the pulmonary veins and left atrium has become the mainstay of nonpharmacologic treatment of AF.2 The efficacy of this technique has been found comparable if not superior to anti­arrhythmic drug therapy.2 Recently, the use of a cryoablation technique, which produces a large and more homogeneous lesion, has been tested and found comparable to radiofrequency ablation in terms of safety and efficacy.3 Despite considerable improvement in the understanding and application of catheter-based ablation, published technical success rates have ranged from 51%-77% and are likely considerably lower in “real world” practice.4 Therefore there is strong need and opportunity for technical refinement.

Since AF patients represent a heterogeneous group of patients with CV diseases of varying type and severity as well as comorbidities, it stands to reason that the pulmonary venous–left atrial junction may not be the sole culprit region of all cases of AF and that other anatomical locations might serve as triggers for AF.

In support of this notion are the results of the prospective multicenter study presented by Dr. Elad Anter at the annual International AF Symposium. This important study is consistent with and expands upon prior studies that have suggested that sites within the atria remote from the pulmonary veins may serve as triggers for AF, rather than lower technical success of pulmonary vein ablation.5 It further highlights the importance of fibrosis and associated electrical dispersion to the pathogenesis of AF.6 However, the recommendation that patients with AF be screened for OSA is not new, as nearly half of patients with AF also have OSA.7 While AF and OSA share common risk factors/comorbidities such as male gender, obesity, hypertension, coronary artery disease, and congestive heart failure, OSA has been found to be an independent risk factor for AF development.

It is important to know whether OSA was treated, as the presence of OSA raises the risk of AF recurrence and OSA treatment decreases AF recurrence after ablation.8,9 Conversely, in the setting of OSA, AF is more resistive to rhythm control. Enhanced vagal activation, elevated sympathetic tone, and oxidative stresses due to oxygen desaturation and left atrial distension have all been implicated in the pathogenesis linking OSA to the development of AF. Repeated increases in upper airway resistance during airway obstruction have been shown to lead to atrial stretch, dilation, and fibrosis.10 Since patients with heart failure, coronary artery disease, and other underlying causes for AF were excluded from the onset, the results may not be applicable to a large segment of AF patients. Exclusion of underlying cardiac conditions potentially raised the yield of patients found to have OSA and the potential value of OSA screening. Of note: Less than half of patients that were enrolled had complete data for analysis, which may further limit applicability of the study findings. All patients had paroxysmal AF and were in sinus rhythm while the mapping procedure was performed, leaving questions as to how to approach patients presenting acutely with persistent or long standing AF, or those recently treated with antiarrhythmic therapy. Also, since arrhythmia-free survival decreases from 1 to 5 years after AF ablation, and short-time success rates do not predict longer success rates, the present study results should be interpreted with cautious optimism.11

However, these limitations should not detract from the major implications of the study. In the setting of AF, OSA should be clinically suspected not only because of the frequent coexistence of the two disorders but because the presence of OSA should prompt electrophysiologists to consider non–pulmonary vein triggers of AF prior to ablation attempts. The consideration of alternative ablation sites might help to explain the lack of ablation procedure endpoints to predict long-term success of ablation and holds promise for increasing technical success rates. Given that airway obstruction may occur in other clinical settings such as seizure-induced laryngospasm and that seizures may induce arrhythmias and sudden death, there is potential for non–pulmonary vein sites to trigger AF and other arrhythmias in settings other than OSA as well.12 Whether other disease states are associated with a higher likelihood of non-pulmonary veins trigger sites also merits further study. Moreover, this study underscores the notion that with regard to AF ablation, “no one site fits all” and “clinical mapping” may serve as a valuable adjunct to anatomical mapping. It also serves as a reminder of the multidisciplinary nature of Chest Medicine and the need of a team oriented approach..

References
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