Author + information
- Received February 20, 2018
- Revision received March 19, 2018
- Accepted March 21, 2018
- Published online July 16, 2018.
- Vidal Essebag, MD, PhDa,b,∗ (, )
- Jacqueline Joza, MDa,
- Pablo B. Nery, MDc,
- Steve Doucette, MScd,
- Isabelle Nault, MDe,
- Lena Rivard, MDf,
- Lorne Gula, MDg,
- Marc Deyell, MDh,
- Jean-Marc Raymond, MDi,
- Chris Lane, MDj and
- John L. Sapp, MDk
- aMcGill University Health Centre Research Institute, Montreal, Canada
- bHôpital Sacré-Coeur de Montréal, Montreal, Canada
- cResearch Methods Unit, University of Ottawa Heart Institute, Ottawa, Canada
- dDepartment of Community Health and Epidemiology, Dalhousie University, Halifax, Canada
- eInstitute Universitaire de Cardiologie et de Pneumologie de Quebec, Quebec, Canada
- fMontreal Heart Institute, Montreal, Canada
- gWestern University, London, Canada
- hSt. Paul’s Hospital, Vancouver, Canada
- iCentre Hospitalier de L’Universite de Montreal, Montreal, Canada
- jRoyal Jubilee Hospital, Victoria, Canada
- kDepartment of Medicine, QEII Health Sciences Centre and Dalhousie University, Halifax, Canada
- ↵∗Address for correspondence:
Dr. Vidal Essebag, Cardiac Electrophysiology, McGill University Health Centre, 1650 Cedar Avenue, Room E5-200, Montreal QC H3G 1A4, Canada.
Objectives This study sought to evaluate the predictive value of noninducibility on long-term outcomes.
Background The traditional endpoint for catheter ablation of ventricular tachycardia (VT) is noninducibility of VT by programmed stimulation; however, the definition of inducibility remains variable and its prognostic value limited by nonstandardized periprocedural antiarrhythmic drug therapy and implantable cardioverter-defibrillator programming in prior observational studies. The VANISH trial randomized patients with prior myocardial infarction and VT to ablation (with an endpoint of noninducibility of VT ≥300 ms after ablation) versus antiarrhythmic drug escalation.
Methods Patients enrolled in the VANISH study randomized to catheter ablation were included. The relationship between post-ablation inducibility and the primary composite endpoint (death, VT storm >30 days, or appropriate implantable cardioverter-defibrillator shock >30 days) was assessed using a time-to-event analysis, adjusting for other clinical and procedural characteristics.
Results A total of 129 patients from the ablation arm were included in the primary analysis, of which 51 were noninducible post-ablation compared with 78 who had inducible VT or in whom inducibility testing was not performed. There were no significant baseline characteristic or procedural differences except for increased implantable cardioverter-defibrillator shocks before randomization in the noninducible group. In multivariate analysis, inducibility significantly increased the risk of death, appropriate shock, or VT storm after 30 days (HR: 1.87; p = 0.017).
Conclusions Inducibility of any VT post-ablation was associated with an increased risk of the composite endpoint in the VANISH trial. A randomized trial is required to confirm whether more aggressive ablation targeting faster induced VTs (<300 ms) can improve outcomes.
This study was supported by an operating grant from the Canadian Institutes of Health Research, with additional funding from St. Jude Medical and Biosense Webster, and a Clinical Research Scholar Award to Dr. Essebag from Fonds de recherché du Quebec-Santé. Canadian Arrhythmic Network (CANet) Investigators (to Drs. Essebag, Joza, Nery, Nault, Rivard, Gula, Deyell, Lane, Sapp). Dr. Essebag has received honoraria from Biosense Webster Inc., Boston Scientific, St. Jude Medical, Abbott, and Medtronic Inc. Dr. Rivard has received consulting fees from Biosense Webster. Dr. Deyell has received research funding from Biosense Webster; and honoraria from Biosense Webster and Abbott. Dr. Raymond has received lecture fees from Biosense Webster. Dr. Lane has received honoraria from Medtronic, Biosense Webster, Forest Laboratories Canada, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb/Pfizer, and Servier. Dr. Sapp has received research funding from Biosense Webster, Abbott, St. Jude Medical, and Philips; is a consultant for Biosense Webster; and received speaker honoraria from Abbott and Medtronic Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology. author instructions page.
- Received February 20, 2018.
- Revision received March 19, 2018.
- Accepted March 21, 2018.
- 2018 American College of Cardiology Foundation
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.