Author + information
- Robert D. Anderson, MBBSa,b,c,d,
- Geoffrey Lee, MBChB, PhDa,b,
- Ivana Trivic, BScc,d,
- Timothy Campbell, BScc,d,
- Timmy Pham, BMedScic,d,
- Chrishan Nalliah, MBBS, PhDc,
- Eddy Kizana, MBBS, PhDc,d,
- Stuart P. Thomas, MBBS, PhDc,
- Siddharth J. Trivedi, BSc, BMedSci, MBBSc,d,
- Troy Watts, BSca,b,
- Jonathan Kalman, MBBS, PhDa,b and
- Saurabh Kumar, BSc(Med)/MBBS, PhDc,d,∗ ()
- aDepartment of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
- bFaculty of Medicine, Dentistry, and Health Science, University of Melbourne, Melbourne, Australia
- cDepartment of Cardiology, Westmead Hospital, Sydney, Australia
- dWestmead Applied Research Centre, University of Sydney, Sydney, Australia
- ↵∗Address for correspondence:
Associate Prof. Saurabh Kumar, Department of Cardiology, Westmead Hospital, Westmead Applied Research Centre, University of Sydney, Darcy Road, Westmead, New South Wales-2145, Australia 2145.
Objectives This study sought to summarize the procedural characteristics and outcomes of patients with structural heart disease (SHD) who have focal ventricular tachycardia (VT).
Background Scar-mediated re-entry is the predominant mechanism of VT in SHD. Some SHD patients may have a focal VT mechanism that remains poorly described.
Methods An extended induction protocol incorporating programmed electrical stimulation, right ventricular burst pacing and isoprenaline was used to elucidate both re-entrant and focal VT mechanisms.
Results Eighteen of 112 patients (16%) with SHD undergoing VT ablation over 2 years had a focal VT mechanism elucidated (mean age 66±13 years; ejection fraction 46±14%; nonischemic cardiomyopathy 10). Repetitive failure of termination with antitachycardia pacing (ATP) (69% of patients) or defibrillator shocks (56%) was a common feature of focal VTs. A median of 3 VTs per patient were inducible (28 focal VTs, 34 re-entrant VTs; 53% of patients had both focal and re-entrant VT mechanism). Focal VTs more commonly originated from the right ventricle (RV) than the left ventricle (LV) (67% vs. 33%, respectively). In the RV, the RV outflow tract was the most common site (33% of all focal VTs), followed by the RV moderator band (22%), apical septal RV (6%), and lateral tricuspid annulus (6%). The lateral LV (non-Purkinje) was the most common LV focal VT site (16%), followed by the papillary muscles (17%). After median follow-up of 289 days, 78% of patients remained arrhythmia-free; no patients had recurrence of focal VT at repeat procedure. In patients with recurrence, defibrillator therapies were significantly reduced from a median of 53 ATP episodes pre-ablation to 10 ATP episodes post-ablation. During follow-up, 2 patients (11%) underwent repeat VT ablation; none had recurrence of focal VT.
Conclusions Focal VTs are common in patients with SHD and often coexist with re-entrant forms of VT. High failure rate of defibrillator therapies was a common feature of focal VT mechanisms. Uncovering and abolishing focal VT may further improve outcomes of catheter ablation in SHD.
Dr. Anderson has been supported by postgraduate scholarships co-funded by the National Health and Medical Research Council (NHMRC), National Heart Foundation (NHF), and Royal Australasian College of Physicians NHMRC Woodcock Scholarships. Dr. Campbell was a former employee of Johnson and Johnson Medical within the last 12 months; and was a previously salaried employee of Johnson and Johnson Medical. Dr. Kalman has received fellowship support from Biosense Webster, Medtronic, and Abbott. Dr. Kumar has received research grants from Biotronik, Abbott, Bayer-Cardiac Society of Australia and New Zealand, Perpetual Ramaciotti Foundation, Sylvia and Charles Viertel Foundation, Westmead Hospital Charitable Trust, and Westmead Hospital Research and Education Network; has received honoraria from Abbott Medical, Biosense Webster, Biotronik, and Sanofi Aventis; and has received fellowship support from NSW Early to Mid Career Fellowship. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Francis Marchlinski, MD, served as Guest Editor for this paper.
The 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 June 6, 2019.
- Revision received July 29, 2019.
- Accepted September 4, 2019.
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