Temporal relationships between esophageal injury type and progression in patients undergoing atrial fibrillation catheter ablation.


Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
02 2019
Historique:
received: 10 08 2018
pubmed: 3 10 2018
medline: 3 10 2020
entrez: 2 10 2018
Statut: ppublish

Résumé

Currently, little is known about the onset, natural progression, and management of esophageal injuries after atrial fibrillation (AF) ablation. We sought to provide a systematic review on esophageal injury after AF ablation and identify temporal relationships between various types of esophageal lesions, their progression, and clinical outcomes. A comprehensive search of PubMed and Web of Science was conducted until September 21, 2017. All AF ablation patients who underwent upper gastrointestinal endoscopy within 1 week of the procedure were included. Patients with esophageal lesions were classified into 3 types by using our novel Kansas City classification: type 1: erythema; type 2a: superficial ulcers; type 2b: deep ulcers; type 3a: perforation without communication with the atria; and type 3b: perforation with atrioesophageal fistula. Thirty studies met our inclusion criteria. Of the 4473 patients, 3921 underwent upper gastrointestinal evaluation. The overall incidence of esophageal injuries was 15% (570). There were 206 type 1 lesions (36%), 222 type 2a lesions (39%), and 142 type 2b lesions (25%). Six of 142 type 2b lesions (4.2%) progressed further to type 3, of which, 5 were type 3a and 1 was type 3b. All type 1 and type 2a and most type 2b lesions resolved with conservative management. One type 3a and 1 type 3b lesions were fatal. Based on our classification, all type 1 and most type 2 lesions resolved with conservative management. A small percentage (4.2% [6 of 142]) of type 2b lesions progressed to perforation and/or fistula formation, and these patients need to be followed closely.

Sections du résumé

BACKGROUND
Currently, little is known about the onset, natural progression, and management of esophageal injuries after atrial fibrillation (AF) ablation.
OBJECTIVES
We sought to provide a systematic review on esophageal injury after AF ablation and identify temporal relationships between various types of esophageal lesions, their progression, and clinical outcomes.
METHODS
A comprehensive search of PubMed and Web of Science was conducted until September 21, 2017. All AF ablation patients who underwent upper gastrointestinal endoscopy within 1 week of the procedure were included. Patients with esophageal lesions were classified into 3 types by using our novel Kansas City classification: type 1: erythema; type 2a: superficial ulcers; type 2b: deep ulcers; type 3a: perforation without communication with the atria; and type 3b: perforation with atrioesophageal fistula.
RESULTS
Thirty studies met our inclusion criteria. Of the 4473 patients, 3921 underwent upper gastrointestinal evaluation. The overall incidence of esophageal injuries was 15% (570). There were 206 type 1 lesions (36%), 222 type 2a lesions (39%), and 142 type 2b lesions (25%). Six of 142 type 2b lesions (4.2%) progressed further to type 3, of which, 5 were type 3a and 1 was type 3b. All type 1 and type 2a and most type 2b lesions resolved with conservative management. One type 3a and 1 type 3b lesions were fatal.
CONCLUSION
Based on our classification, all type 1 and most type 2 lesions resolved with conservative management. A small percentage (4.2% [6 of 142]) of type 2b lesions progressed to perforation and/or fistula formation, and these patients need to be followed closely.

Identifiants

pubmed: 30273767
pii: S1547-5271(18)31010-5
doi: 10.1016/j.hrthm.2018.09.027
pii:
doi:

Types de publication

Journal Article Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

204-212

Informations de copyright

Copyright © 2018. Published by Elsevier Inc.

Auteurs

Bharath Yarlagadda (B)

Division of Electrophysiology, University of Kansas Medical Center, Kansas City, Kansas.

Thomas Deneke (T)

Department of Cardiology and Angiology, Philipps University Marburg, Marburg, Germany.

Mohit Turagam (M)

Division of Electrophysiology, Icahn School of Medicine, New York, New York.

Tawseef Dar (T)

Division of Electrophysiology, University of Kansas Medical Center, Kansas City, Kansas.

Swathi Paleti (S)

Division of Gastroenterology, University of New Mexico, Albuquerque, New Mexico.

Valay Parikh (V)

Division of Electrophysiology, University of Kansas Medical Center, Kansas City, Kansas.

Luigi DiBiase (L)

Montefiore Medical Center, Albert Einstein College of Medicine, New York, New York.

Philipp Halfbass (P)

Heart Center Bad Neustadt, Clinic for Interventional Electrophysiology, Bad Neustadt an der Saale, Germany.

Pasquale Santangeli (P)

Division of Electrophysiology, University of Pennsylvania, Philadelphia, Pennsylvania.

Srijoy Mahapatra (S)

Abbott Medical, Chicago, Illinois.

Jie Cheng (J)

Memorial Hermann Medical Center, Houston, Texas.

Andrea Russo (A)

Division of Electrophysiology, Cooper University Hospital, Cherry Hill, New Jersey.

James Edgerton (J)

Center for Advanced Cardiovascular Care, Baylor Health, Plano, Texas.

Moussa Mansour (M)

Division of Electrophysiology, Mass General Hospital, Boston, Massachusetts.

Jeremy Ruskin (J)

Division of Electrophysiology, Mass General Hospital, Boston, Massachusetts.

Srinivas Dukkipati (S)

Division of Electrophysiology, Icahn School of Medicine, New York, New York.

David Wilber (D)

Division of Electrophysiology, Loyola Medical Center, Chicago, Illinois.

Vivek Reddy (V)

Division of Electrophysiology, Icahn School of Medicine, New York, New York.

Douglas Packer (D)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.

Andrea Natale (A)

St. David's - Texas Cardiac Arrhythmia Institute, Austin, Texas.

Dhanunjaya Lakkireddy (D)

Kansas City Heart Rhythm Institute, Overland Park, Kansas. Electronic address: dhanunjaya.lakkireddy@hcahealthcare.com.

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