TY - JOUR
T1 - Functional Assessment of Ventricular Tachycardia Circuits and Their Underlying Substrate Using Automated Conduction Velocity Mapping
AU - Hawson, Joshua
AU - Anderson, Robert D.
AU - Al-kaisey, Ahmed
AU - Chieng, David
AU - Segan, Louise
AU - Watts, Troy
AU - Campbell, Timothy
AU - Morton, Joseph
AU - McLellan, Alexander
AU - Kistler, Peter
AU - Voskoboinik, Aleksander
AU - Pathik, Bhupesh
AU - Kumar, Saurabh
AU - Kalman, Jonathan
AU - Lee, Geoffrey
N1 - Funding Information:
Dr Kistler has received funding from Abbott Medical for consultancy and speaking engagements; and has received fellowship support from Biosense Webster. Dr Kumar has received honoraria from Biosense Webster, Abbott Medical, Biotronik, and Sanofi Aventis. Dr Kalman is supported by a National Health and Medical Research Council of Australia practitioner fellowship; and has received research and fellowship support from Biosense Webster, Abbott, and Medtronic. Dr Lee has received consulting fees and speaker honoraria from Biosense Webster. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Publisher Copyright:
© 2022 American College of Cardiology Foundation
PY - 2022/4
Y1 - 2022/4
N2 - Objectives: This study sought to describe the utility of automated conduction velocity mapping (ACVM) in ventricular tachycardia (VT) ablation. Background: Identification of areas of slowed conduction velocity (CV) is critical to our understanding of VT circuits and their underlying substrate. Recently, an ACVM called Coherent Mapping (Biosense Webster Inc) has been developed for atrial mapping. However, its utility in VT mapping has not been described. Methods: Patients with paired high-density VT activation and substrate maps were included. ACVM was applied to paired VT activation and substrate maps to assess regional CV and activation patterns. A combination of ACVM, traditional local activation time maps, electrogram analysis, and off-line calculated CV using triangulation were used to characterize zones of slowed conduction during VT and in substrate mapping. Results: Fifteen patients were included in the study. In all cases, ACVM identified slow CV within the putative VT isthmus, which colocalized to the VT isthmus identified with entrainment. The dimensions of the VT isthmus with local activation time mapping were 37.8 ± 13.7 mm long and 8.7 ± 4.2 mm wide. In comparison, ACVM produced an isthmus that was shorter (length: 25.1 ± 10.6 mm; mean difference: 12.8; 95% CI: 7.5-18.0; P < 0.01) and wider (width: 18.8 ± 8.1 mm; mean difference: 10.1; 95% CI: 6.1-14.2; P < 0.01). In VT, the CV using triangulation at the entrance (8.0 ± 3.6 cm/s) and midisthmus (8.1 ± 4.3 cm/s) was not significantly different (P = 0.92) but was significantly faster at the exit (16.2 ± 9.7 cm/s; P < 0.01). In the paired substrate analysis, traditional local activation time isochronal mapping identified 6.3 ± 2.0 deceleration zones. In contrast, ACVM identified a median of 0 deceleration zones (IQR: 0-1; P < 0.01). Conclusions: ACVM is a novel complementary tool that can be used to accurately resolve complex VT circuits and identify slow conduction zones in VT but has limited accuracy in identifying slowed conduction during substrate-based mapping.
AB - Objectives: This study sought to describe the utility of automated conduction velocity mapping (ACVM) in ventricular tachycardia (VT) ablation. Background: Identification of areas of slowed conduction velocity (CV) is critical to our understanding of VT circuits and their underlying substrate. Recently, an ACVM called Coherent Mapping (Biosense Webster Inc) has been developed for atrial mapping. However, its utility in VT mapping has not been described. Methods: Patients with paired high-density VT activation and substrate maps were included. ACVM was applied to paired VT activation and substrate maps to assess regional CV and activation patterns. A combination of ACVM, traditional local activation time maps, electrogram analysis, and off-line calculated CV using triangulation were used to characterize zones of slowed conduction during VT and in substrate mapping. Results: Fifteen patients were included in the study. In all cases, ACVM identified slow CV within the putative VT isthmus, which colocalized to the VT isthmus identified with entrainment. The dimensions of the VT isthmus with local activation time mapping were 37.8 ± 13.7 mm long and 8.7 ± 4.2 mm wide. In comparison, ACVM produced an isthmus that was shorter (length: 25.1 ± 10.6 mm; mean difference: 12.8; 95% CI: 7.5-18.0; P < 0.01) and wider (width: 18.8 ± 8.1 mm; mean difference: 10.1; 95% CI: 6.1-14.2; P < 0.01). In VT, the CV using triangulation at the entrance (8.0 ± 3.6 cm/s) and midisthmus (8.1 ± 4.3 cm/s) was not significantly different (P = 0.92) but was significantly faster at the exit (16.2 ± 9.7 cm/s; P < 0.01). In the paired substrate analysis, traditional local activation time isochronal mapping identified 6.3 ± 2.0 deceleration zones. In contrast, ACVM identified a median of 0 deceleration zones (IQR: 0-1; P < 0.01). Conclusions: ACVM is a novel complementary tool that can be used to accurately resolve complex VT circuits and identify slow conduction zones in VT but has limited accuracy in identifying slowed conduction during substrate-based mapping.
KW - coherent mapping
KW - conduction velocity
KW - ventricular arrhythmias
KW - ventricular tachycardia
UR - http://www.scopus.com/inward/record.url?scp=85127866771&partnerID=8YFLogxK
U2 - 10.1016/j.jacep.2021.12.013
DO - 10.1016/j.jacep.2021.12.013
M3 - Article
C2 - 35450603
AN - SCOPUS:85127866771
SN - 2405-500X
VL - 8
SP - 480
EP - 494
JO - JACC: Clinical Electrophysiology
JF - JACC: Clinical Electrophysiology
IS - 4
ER -