Author + information
- Received December 9, 2019
- Revision received March 26, 2020
- Accepted April 1, 2020
- Published online July 20, 2020.
- Antonio Frontera, MD, PhD∗ (, )
- Francesco Melillo, MD,
- Luca Baldetti, MD,
- Andrea Radinovic, MD,
- Caterina Bisceglia, MD, PhD,
- Giuseppe D’Angelo, MD,
- Luca Foppoli, ME,
- Lorenzo Gigli, MD,
- Giovanni Peretto, MD,
- Manuela Cireddu, MD,
- Simone Sala, MD,
- Patrizio Mazzone, MD and
- Paolo Della Bella, MD
- ↵∗Address for correspondence:
Dr. Antonio Frontera, Arrhythmia Unit and EP Laboratories, Via Olgettina 60, San Raffaele Hospital, Milan 20132, Italy.
Objectives The aim of this study was to characterize, during sinus rhythm, the electric activation abnormalities in post–myocardial infarction patients undergoing ablation of ventricular tachycardia (VT) in order to identify specific signatures of those abnormal electrograms (EGMs).
Background In the setting of VT ablation, substrate characterization hinges on the identification of local abnormal ventricular activity (LAVA) and late potentials (LPs) that are considered to be related to the VT circuit.
Methods Patients scheduled for VT ablation underwent high-density ventricular substrate mapping. The substrate map during sinus rhythm was then compared with the activation maps of the clinical VT. Abnormal EGMs (LAVA and LPs) during sinus rhythm were characterized according to their configuration, duration, and amplitude and distinguished as belonging to bystander region or to the re-entrant circuit. Underlying electrophysiological mechanisms (wave-front collision, slow conduction) were identified on the activation maps and assigned to corresponding EGMs.
Results Ten patients satisfied the criteria to be enrolled in the study. A mean of 5 ± 1 slow-conduction areas and 4 ± 2 wave-front collisions were identified. LAVA was due to slow conduction in 60.5%, followed by wave-front collision (17.5%). LPs were caused by slow conduction in 52% of cases and by wave-front collision in 43% of cases. During sinus rhythm, entrance and exit sites were characterized by LAVA, while at the VT isthmus, only LPs were identified. Cutoff values of duration <24.5 ms (95% sensitivity and 99% specificity) and amplitude <0.14 mV (90% sensitivity and 48.1% specificity) discriminated those LPs belonging to the circuit from those playing a bystander role.
Conclusions In the setting of post–myocardial infarction cardiomyopathy, specific EGM signatures are expressions of distinct electrophysiological phenomena. LAVA and LPs may play a bystander or an active role in the VT circuit, but only LPs with low amplitude and short duration predicted the VT isthmus.
Drs. Frontera, Bisceglia, and Della Bella have received travel and consulting fees from Boston Scientific, Biosense Webster, and Abbott Medical. Dr. Radinovic has received travel fees from Biotronik. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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 December 9, 2019.
- Revision received March 26, 2020.
- Accepted April 1, 2020.
- 2020 American College of Cardiology Foundation
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