From the Electrophysiology Unit (Dr Bazan), Cardiology Department; and Sleep Disorders Unit (Dr Grau), Respiratory Medicine Department, Hospital del Mar, Parc de Salut Mar, Universitat Autònoma de Barcelona.
Correspondence: Victor Bazan, PhD, Hospital del Mar, Parc de Salut Mar, Universitat Autònoma de Barcelona, 25 Passeig Marítim, 08003 Barcelona, Spain; e-mail: firstname.lastname@example.org
Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.
We sincerely appreciate the comments of Drs Esquinas and Pravinkumar regarding our article in CHEST1 on obstructive sleep apnea (OSA), atrial flutter (AF), and reduction of new-onset atrial fibrillation (AFib) by CPAP treatment. We hypothesized about a selective physiopathologic interaction between OSA and AF (as suggested by an 82% prevalence of OSA in patients with AF), in which pulmonary hypertension during apnea episodes or other mechanisms would induce right atrial overload and/or remodeling, thus favoring the occurrence of AF.2 We further theorized a beneficial impact of CPAP early in the atrial remodeling process leading to AFib (before any AFib documentation), independent or not of AF being documented.3
In our study, no serial echocardiography was performed to evaluate the structural changes induced by CPAP. Therefore, hemodynamic mechanisms through which CPAP presumably protects from AFib remain unclear.
Only six patients without previous AFib were given antiarrhythmic drugs (AADs), and interaction between AADs and CPAP did not influence the incidence of AFib during follow-up among them (P =1) (our unpublished data, 2013). CPAP did not add any clinical benefit to AADs in patients with previous AFib documentation (P = .53, unpublished data). Compliance and duration of CPAP use was not higher in patients who did not have AFib during follow-up, and lack of “antiarrhythmic” efficacy of CPAP in patients with previous AFib cannot be attributed to a lower use of this therapy in this subgroup.
A prior history of AFib is the strongest risk factor for recurrent AFib after AF ablation.4 It would appear by our results that other acknowledged variables (left atrial size, hypertension, ejection fraction, atrial stretching biomarkers, BMI, etc) are not as predictive. Again, this study was not designed to assess for risk factors of AFib, but to determine the impact of an intervention (CPAP) on a reduction of AFib after AF ablation (from 46% to 6% of cases, P = .025).
We may conclude that documentation of AF sets for the identification of a subset of patients in whom underlying OSA is highly likely. This fact has notable implications in terms of cardiovascular morbidity and mortality.5 This also appears to include a lower incidence of AFib after CPAP initiation if this arrhythmia has never been documented.1 Further investigation will be needed to assess the etiopathogenic relationship between OSA and AF and the physiologic changes induced by CPAP that prevent AFib in some patients with AF.
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