Ivan F. N. Hung, MD Kwok-Yung Yuen, MD Hong Kong, China Affiliations: From the Department of Medicine (Dr Hung) and the Department of Microbiology (Dr Yuen), University of Hong Kong. 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. Correspondence to: Kwok-Yung Yuen, MD, Department of Microbiology, University of Hong Kong, Room 423, Pathology Bldg, Queen Mary Hospital Compound, 102 Pokfulam Rd, Hong Kong, China; e-mail:
[email protected] © 2013 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.13-0571
References 1. Hung IFN, To KKW, Lee C-K, et al. Hyperimmune IV immunoglobulin treatment: a multicenter double-blind randomized controlled trial for patients with severe 2009 influenza A(H1N1) infection. Chest. 2013;144(2):464-473.
CPAP in Obstructive Sleep Apnea and Atrial Flutter-Fibrillation Is This Truly Two for the Price of One? To the Editor: There is growing research interest in the association between atrial fibrillation (AF) and obstructive sleep apnea (OSA), which are independently common diseases that have a serious impact on health, quality of life, and health-care resources.1 In many cases, both these diseases show a parallelism in that appropriate early diagnosis and treatment have demonstrated positive clinical benefits.1 However, studies are promoting positive interactions of CPAP for preventing and reducing recurrences of AF, despite the lack of clear evidence-based analysis and guidelines. We read with interest the article by Bazan et al2 in CHEST (May 2013) in this area of growing interest. We would like to comment on some aspects of their study that are relevant to clinical practice. First, there are some functional and structural cardiac changes that were not evaluated in this study and could potentially influence the results. The relationship between the duration of CPAP use and echocardiographic findings were not discussed but can provide a better understanding of whether CPAP could influence AF and recurrences. Additionally, echocardiographic factors such as left atrial diameter variations, severity of mitral valve regurgitation, and left ventricular hypertrophy were not measured,3 but these are potentially strong predictive factors for AF and recurrences. Second, the authors did not describe correlations between OSA, efficacy of antiarrhythmic drugs, and CPAP therapy and AF recurrence.4 Third, there were no data on CPAP compliance and duration of CPAP use among patients who had and did not have AF recurrences following ablation therapy for atrial flutter. Fourth, the authors presented no data on other causal factors for AF. In one study, OSA was a strong predictor of recurrent AF after an ablation procedure; BMI, ejection fraction, left atrial size, and hypertension did not affect the outcomes postablation for atrial flutter.5 Finally, other relevant measurements such as levels of N-terminal pro-B-type natriuretic peptide or B-type natriuretic peptide were not provided.
We believe that the study by Bazan et al2 provides valuable information with regard to OSA and AF recurrences, but mechanisms that influence this association remain complex. Further studies that look at cardiac structural and functional modifications to identify triggers or promoters of atrial flutter recurrences are necessary. Antonio M. Esquinas, MD, PhD, FCCP Murcia, Spain Egbert Pravinkumar, MD Houston, TX Affiliations: From the Intensive Care Unit (Dr Esquinas), Hospital General Universitario Morales Meseguer; and Department of Critical Care (Dr Pravinkumar), Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center. 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. Correspondence to: Antonio M. Esquinas, MD, PhD, FCCP, Intensive Care Unit, Hospital General Universitario Morales Meseguer, Av Marques de los Velez, s/n, Murcia 30008, Spain; e-mail:
[email protected] © 2013 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.13-0621
References 1. Digby GC, Baranchuk A. Sleep apnea and atrial fibrillation; 2012 update. Curr Cardiol Rev. 2012;8(4):265-272. 2. Bazan V, Grau N, Valles E, et al. Obstructive sleep apnea in patients with typical atrial flutter: prevalence and impact on arrhythmia control outcome. Chest. 2013;143(5):1277-1283. 3. Da Costa A, Romeyer C, Mourot S, et al. Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study. Eur Heart J. 2002; 23(6):498-506. 4. Monahan K, Brewster J, Wang L, et al. Relation of the severity of obstructive sleep apnea in response to anti-arrhythmic drugs in patients with atrial fibrillation or atrial flutter. Am J Cardiol. 2012;110(3):369-372. 5. Jongnarangsin K, Chugh A, Good E, et al. Body mass index, obstructive sleep apnea, and outcomes of catheter ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 2008;19(7): 668-672.
Response To the Editor: 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.
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