Robert D Anderson1, Geoffrey Lee2, Ivana Trivic3, Timothy Campbell3, Timmy Pham3, Chrishan Nalliah4, Eddy Kizana3, Stuart P Thomas4, Siddharth J Trivedi3, Troy Watts2, Jonathan Kalman2, Saurabh Kumar5. 1. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Faculty of Medicine, Dentistry, and Health Science, University of Melbourne, Melbourne, Australia; Department of Cardiology, Westmead Hospital, Sydney, Australia; Westmead Applied Research Centre, University of Sydney, Sydney, Australia. 2. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Faculty of Medicine, Dentistry, and Health Science, University of Melbourne, Melbourne, Australia. 3. Department of Cardiology, Westmead Hospital, Sydney, Australia; Westmead Applied Research Centre, University of Sydney, Sydney, Australia. 4. Department of Cardiology, Westmead Hospital, Sydney, Australia. 5. Department of Cardiology, Westmead Hospital, Sydney, Australia; Westmead Applied Research Centre, University of Sydney, Sydney, Australia. Electronic address: saurabh.kumar@health.nsw.gov.au.
Abstract
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. Crown
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 SHDpatients 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. Crown
Authors: Richard G Bennett; Timothy Campbell; Ashish Sood; Ashwin Bhaskaran; Kasun De Silva; Lloyd Davis; Pierre Qian; Gopal Sivagangabalan; Mark J Cooper; Clara K Chow; Aravinda Thiagalingam; A Robert Denniss; Stuart P Thomas; Eddy Kizana; Saurabh Kumar Journal: Heliyon Date: 2021-12-06