BACKGROUND: Monomorphic ventricular premature depolarizations (VPDs) have been found to initiate ventricular fibrillation (VF) or polymorphic ventricular tachycardia (PMVT) in patients with and without structural heart disease. OBJECTIVE: The purpose of this study was to describe and characterize sites of origin of VPDs triggering VF and PMVT. METHODS: The distribution of mapping-confirmed VPDs, electrophysiology laboratory findings, and results of radiofrequency catheter ablation were analyzed. RESULTS: Among 1132 consecutive patients who underwent ablation for ventricular arrhythmias, 30 patients (2.7%) with documented VF/PMVT initiation were identified. In 21 patients, VF/PMVT occurred in the setting of cardiomyopathy; in 9 patients, VF/PMVT was idiopathic. The origin of VPD trigger was from the Purkinje network in 9, papillary muscles in 8, left ventricular outflow tract in 9, and other low-voltage areas unrelated to Purkinje activity in 4. Each distinct anatomic area of origin was associated with VF/PMVT triggers in patients with and without heart disease. Acute VPD elimination was achieved in 26 patients (87%), with a decrease in VPDs in another 3 patients (97%). During median follow-up of 418 days (interquartile range [IQR] 144-866), 5 patients developed a VF/PMVT recurrence after a median of 34 days (IQR 1-259). Rare recurrence was noted in patients with and without structural disease and from each distinct anatomic origin. The total burden of VF/PMVT episodes/shocks was reduced from a median of 9 (IQR 2.5-22.5) in the 3 months before ablation to 0 (IQR 0-0, total range 0-2) during follow-up (P <.0001). CONCLUSION: Catheter ablation of VPD-triggered VF/PMVT is highly successful. Left ventricular outflow tract and papillary muscles are common and are previously unrecognized sites of origin of these triggers in patients with and without structural heart disease.
BACKGROUND: Monomorphic ventricular premature depolarizations (VPDs) have been found to initiate ventricular fibrillation (VF) or polymorphic ventricular tachycardia (PMVT) in patients with and without structural heart disease. OBJECTIVE: The purpose of this study was to describe and characterize sites of origin of VPDs triggering VF and PMVT. METHODS: The distribution of mapping-confirmed VPDs, electrophysiology laboratory findings, and results of radiofrequency catheter ablation were analyzed. RESULTS: Among 1132 consecutive patients who underwent ablation for ventricular arrhythmias, 30 patients (2.7%) with documented VF/PMVT initiation were identified. In 21 patients, VF/PMVT occurred in the setting of cardiomyopathy; in 9 patients, VF/PMVT was idiopathic. The origin of VPD trigger was from the Purkinje network in 9, papillary muscles in 8, left ventricular outflow tract in 9, and other low-voltage areas unrelated to Purkinje activity in 4. Each distinct anatomic area of origin was associated with VF/PMVT triggers in patients with and without heart disease. Acute VPD elimination was achieved in 26 patients (87%), with a decrease in VPDs in another 3 patients (97%). During median follow-up of 418 days (interquartile range [IQR] 144-866), 5 patients developed a VF/PMVT recurrence after a median of 34 days (IQR 1-259). Rare recurrence was noted in patients with and without structural disease and from each distinct anatomic origin. The total burden of VF/PMVT episodes/shocks was reduced from a median of 9 (IQR 2.5-22.5) in the 3 months before ablation to 0 (IQR 0-0, total range 0-2) during follow-up (P <.0001). CONCLUSION: Catheter ablation of VPD-triggered VF/PMVT is highly successful. Left ventricular outflow tract and papillary muscles are common and are previously unrecognized sites of origin of these triggers in patients with and without structural heart disease.
Authors: Edmond M Cronin; Frank M Bogun; Philippe Maury; Petr Peichl; Minglong Chen; Narayanan Namboodiri; Luis Aguinaga; Luiz Roberto Leite; Sana M Al-Khatib; Elad Anter; Antonio Berruezo; David J Callans; Mina K Chung; Phillip Cuculich; Andre d'Avila; Barbara J Deal; Paolo Della Bella; Thomas Deneke; Timm-Michael Dickfeld; Claudio Hadid; Haris M Haqqani; G Neal Kay; Rakesh Latchamsetty; Francis Marchlinski; John M Miller; Akihiko Nogami; Akash R Patel; Rajeev Kumar Pathak; Luis C Saenz Morales; Pasquale Santangeli; John L Sapp; Andrea Sarkozy; Kyoko Soejima; William G Stevenson; Usha B Tedrow; Wendy S Tzou; Niraj Varma; Katja Zeppenfeld Journal: J Interv Card Electrophysiol Date: 2020-10 Impact factor: 1.900
Authors: David E Krummen; Justin Hayase; Stephen P Vampola; Gordon Ho; Amir A Schricker; Gautam G Lalani; Tina Baykaner; Taylor M Coe; Paul Clopton; Wouter-Jan Rappel; Jeffrey H Omens; Sanjiv M Narayan Journal: J Cardiovasc Electrophysiol Date: 2015-09-06
Authors: Edmond M Cronin; Frank M Bogun; Philippe Maury; Petr Peichl; Minglong Chen; Narayanan Namboodiri; Luis Aguinaga; Luiz Roberto Leite; Sana M Al-Khatib; Elad Anter; Antonio Berruezo; David J Callans; Mina K Chung; Phillip Cuculich; Andre d'Avila; Barbara J Deal; Paolo Della Bella; Thomas Deneke; Timm-Michael Dickfeld; Claudio Hadid; Haris M Haqqani; G Neal Kay; Rakesh Latchamsetty; Francis Marchlinski; John M Miller; Akihiko Nogami; Akash R Patel; Rajeev Kumar Pathak; Luis C Sáenz Morales; Pasquale Santangeli; John L Sapp; Andrea Sarkozy; Kyoko Soejima; William G Stevenson; Usha B Tedrow; Wendy S Tzou; Niraj Varma; Katja Zeppenfeld Journal: Europace Date: 2019-08-01 Impact factor: 5.214
Authors: Gordon Ho; Christopher T Villongco; Omid Yousefian; Aaron Bradshaw; Andrew Nguyen; Yonatan Faiwiszewski; Justin Hayase; Wouter-Jan Rappel; Andrew D McCulloch; David E Krummen Journal: J Cardiovasc Electrophysiol Date: 2017-08-04
Authors: David E Krummen; Gordon Ho; Kurt S Hoffmayer; Franz N Schweis; Tina Baykaner; A J Rogers; Frederick T Han; Jonathan C Hsu; Mohan N Viswanathan; Paul J Wang; Wouter-Jan Rappel; Sanjiv M Narayan Journal: Circ Arrhythm Electrophysiol Date: 2021-02-07