- Email: [email protected]
To the Editor—Left atrium, vagal nerve, and esophagus: A neighborhood with close relations
Author's Accepted Manuscript
Left Atrium, Vagal Nerve and Esophagus: a Neighborhood with close relations Claudia Stö llberger, Josef Finsterer
www.elsevier.com/locate/buildenv
PII: DOI: Reference:
S1547-5271(14)00616-X http://dx.doi.org/10.1016/j.hrthm.2014.05.030 HRTHM5793
To appear in:
Heart Rhythm
Cite this article as: Claudia Stö llberger, Josef Finsterer, Left Atrium, Vagal Nerve and Esophagus: a Neighborhood with close relations, Heart Rhythm, http://dx.doi.org/ 10.1016/j.hrthm.2014.05.030 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Left atrium, vagal nerve and esophagus: a neighborhood with close relations Letter to the Editor
Claudia Stöllberger, Josef Finsterer Krankenanstalt Rudolfstiftung, Juchgasse 25, 1030 Wien,
Address of the corresponding author Univ. Prof. Dr. Claudia Stöllberger Steingasse 31/18 A-1030 Wien, Österreich Tel. & Fax: +43 1 945-42-91 [email protected]
No funding No conflict of interest
With interest we read the article by Knopp et al. about endoscopic findings in patients after radiofrequency ablation (RFA) of atrial fibrillation (AF).[1] Gastrointestinal abnormalities were detected by esophagogastroduodenoscopy (EGD) in 77 % of 425 patients 1-3 days after RFA. Since EGD was carried out only after RFA, it cannot be assessed, how many of these abnormalities were indeed the direct consequence of RFA and how many were present already before RFA and contributed to the pathogenesis of AF. How many of the 328 patients with lesions on EGD took proton-pump-inhibitors or H2-blockers already before RFA? An association of gastroesophageal reflux disease (GERD) with AF is suggested by clinical and epidemiological studies.[2][3] One pathomechanism of AF in GERD may be local inflammation penetrating the esophageal wall and thus affecting the adjacent vagal nerves. The innervation of the esophageal mucosa is altered in response to inflammation.[4] Inflammation of the esophageal mucosa may trigger afferent-efferent reflex mechanisms with involvement of the cerebral representation of cardiac modalities and thus lead to secondary stimulation of the vagal nerves. Additionally, GERD may lead to a release of inflammatory mediators or to an autoimmune response, which may affect the atrial myocardium or the cardiac conduction system. Thus it would be of interest if the included patients with gastroesophageal abnormalities had a higher recurrence rate of AF after RFA than patients with normal EGD-findings. How was gastroparesis defined and how was regression of gastroparesis diagnosed during follow-up? Based on which observations do the authors conclude that gastroparesis can be attributed to RFA when they do not have evidence for gastroparesis before RFA? Gastroparesis may be multicausal including vagal denervation or direct affection of smooth muscle cells. Were there any patients who developed atrioesophageal fistula during the recruitment period? Did these patients show any abnormalities at EGD?
Patients with AF receive frequently oral anticoagulant drugs, and some of them, like dabigatran, are known to have gastrointestinal side effects.[5] Was there any association between the type of anticoagulant drugs between patients with and without gastrointestinal abnormalities? Many patients with AF develop stroke/embolism. Was there a difference in the frequency of EGD abnormalities between those with and without a previous stroke/embolism? AF may be due to cardiac involvement in a neuromuscular disorder. How many of the patients undergoing RFA had a muscle disease? In conclusion, more data about the complex relation between esophagus, left atrium and its nerval connections are necessary.
References 1.
Knopp H, Halm U, Lamberts R, Knigge I, Zachäus M, Sommer P, Richter S, Bollmann A, Hindricks G, Husser D. Incidental and ablation-induced findings during upper gastrointestinal endoscopy in patients after ablation of atrial fibrillation: A retrospective study of 425 patients. Heart Rhythm 2014;11:574-578.
2.
Weigl M, Gschwantler M, Gatterer E, Finsterer J, Stöllberger C. Reflux esophagitis in the pathogenesis of paroxysmal atrial fibrillation: results of a pilot study. South Med J 2003;96:1128-1132.
3.
Huang CC, Chan WL, Luo JC, Chen YC, Chen TJ, Chung CM, Huang PH, Lin SJ, Chen JW, Leu HB. Gastroesophageal reflux disease and atrial fibrillation: a nationwide population-based study. PLoS One 2012;7:e47575.
4. Newton M, Kamm MA, Soediono PO, Milner P, Burnham WR, Burnstock G. Oesophageal epithelial innervation in health and reflux oesophagitis. Gut 1999; 44:317-322 5. Bytzer P, Connolly SJ, Yang S, Ezekowitz M, Formella S, Reilly PA, Aisenberg J. Analysis of upper gastrointestinal adverse events among patients given dabigatran in the RE-LY trial. Clin Gastroenterol Hepatol 2013;11:246-52.
Left Atrium, Vagal Nerve and Esophagus: a Neighborhood with close relations Claudia Stö llberger, Josef Finsterer
www.elsevier.com/locate/buildenv
PII: DOI: Reference:
S1547-5271(14)00616-X http://dx.doi.org/10.1016/j.hrthm.2014.05.030 HRTHM5793
To appear in:
Heart Rhythm
Cite this article as: Claudia Stö llberger, Josef Finsterer, Left Atrium, Vagal Nerve and Esophagus: a Neighborhood with close relations, Heart Rhythm, http://dx.doi.org/ 10.1016/j.hrthm.2014.05.030 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Left atrium, vagal nerve and esophagus: a neighborhood with close relations Letter to the Editor
Claudia Stöllberger, Josef Finsterer Krankenanstalt Rudolfstiftung, Juchgasse 25, 1030 Wien,
Address of the corresponding author Univ. Prof. Dr. Claudia Stöllberger Steingasse 31/18 A-1030 Wien, Österreich Tel. & Fax: +43 1 945-42-91 [email protected]
No funding No conflict of interest
With interest we read the article by Knopp et al. about endoscopic findings in patients after radiofrequency ablation (RFA) of atrial fibrillation (AF).[1] Gastrointestinal abnormalities were detected by esophagogastroduodenoscopy (EGD) in 77 % of 425 patients 1-3 days after RFA. Since EGD was carried out only after RFA, it cannot be assessed, how many of these abnormalities were indeed the direct consequence of RFA and how many were present already before RFA and contributed to the pathogenesis of AF. How many of the 328 patients with lesions on EGD took proton-pump-inhibitors or H2-blockers already before RFA? An association of gastroesophageal reflux disease (GERD) with AF is suggested by clinical and epidemiological studies.[2][3] One pathomechanism of AF in GERD may be local inflammation penetrating the esophageal wall and thus affecting the adjacent vagal nerves. The innervation of the esophageal mucosa is altered in response to inflammation.[4] Inflammation of the esophageal mucosa may trigger afferent-efferent reflex mechanisms with involvement of the cerebral representation of cardiac modalities and thus lead to secondary stimulation of the vagal nerves. Additionally, GERD may lead to a release of inflammatory mediators or to an autoimmune response, which may affect the atrial myocardium or the cardiac conduction system. Thus it would be of interest if the included patients with gastroesophageal abnormalities had a higher recurrence rate of AF after RFA than patients with normal EGD-findings. How was gastroparesis defined and how was regression of gastroparesis diagnosed during follow-up? Based on which observations do the authors conclude that gastroparesis can be attributed to RFA when they do not have evidence for gastroparesis before RFA? Gastroparesis may be multicausal including vagal denervation or direct affection of smooth muscle cells. Were there any patients who developed atrioesophageal fistula during the recruitment period? Did these patients show any abnormalities at EGD?
Patients with AF receive frequently oral anticoagulant drugs, and some of them, like dabigatran, are known to have gastrointestinal side effects.[5] Was there any association between the type of anticoagulant drugs between patients with and without gastrointestinal abnormalities? Many patients with AF develop stroke/embolism. Was there a difference in the frequency of EGD abnormalities between those with and without a previous stroke/embolism? AF may be due to cardiac involvement in a neuromuscular disorder. How many of the patients undergoing RFA had a muscle disease? In conclusion, more data about the complex relation between esophagus, left atrium and its nerval connections are necessary.
References 1.
Knopp H, Halm U, Lamberts R, Knigge I, Zachäus M, Sommer P, Richter S, Bollmann A, Hindricks G, Husser D. Incidental and ablation-induced findings during upper gastrointestinal endoscopy in patients after ablation of atrial fibrillation: A retrospective study of 425 patients. Heart Rhythm 2014;11:574-578.
2.
Weigl M, Gschwantler M, Gatterer E, Finsterer J, Stöllberger C. Reflux esophagitis in the pathogenesis of paroxysmal atrial fibrillation: results of a pilot study. South Med J 2003;96:1128-1132.
3.
Huang CC, Chan WL, Luo JC, Chen YC, Chen TJ, Chung CM, Huang PH, Lin SJ, Chen JW, Leu HB. Gastroesophageal reflux disease and atrial fibrillation: a nationwide population-based study. PLoS One 2012;7:e47575.
4. Newton M, Kamm MA, Soediono PO, Milner P, Burnham WR, Burnstock G. Oesophageal epithelial innervation in health and reflux oesophagitis. Gut 1999; 44:317-322 5. Bytzer P, Connolly SJ, Yang S, Ezekowitz M, Formella S, Reilly PA, Aisenberg J. Analysis of upper gastrointestinal adverse events among patients given dabigatran in the RE-LY trial. Clin Gastroenterol Hepatol 2013;11:246-52.