Author + information
- Received December 31, 2018
- Accepted January 10, 2019
- Published online May 20, 2019.
- Taihei Itoh, MD∗ (, )
- Masaomi Kimura, MD,
- Yuji Ishida, MD and
- Hirofumi Tomita, MD
- ↵∗Address for correspondence:
Dr. Taihei Itoh, Department of Cardiology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori 036-8562, Japan.
A 73-year-old man with ischemic cardiomyopathy underwent ventricular tachycardia (VT) ablation. During right ventricular pacing, substrate mapping was performed using EnSite Precision (Abbott, St. Paul, Minnesota) with an Advisor HD Grid Mapping Catheter (Abbott). The bipolar and unipolar voltage map showed a scar in the posterolateral and posterior left ventricular base and a larger scar extending to the mid-posterolateral left ventricle, respectively (Figure 1A). During the VT, endocardial activation mapping revealed a focal pattern from the mid-posterolateral left ventricle (Figure 1B), where entrainment was demonstrated with minimal fusion and a post-pacing interval equal to the VT cycle length (Figure 1C); catheter ablation was unsuccessful. Further mapping identified a mid-diastolic potential (MDP) localized in the posterolateral left ventricular base, where overdrive pacing resulted in termination of the VT followed by the first stimulus with nonglobal ventricular capture (Figure 1D); successful ablation was achieved.
The endocardial activation map illustrated the focal pattern, but the response to overdrive pacing showed that reentry was a VT mechanism, suggesting that its isthmus was located in the intramural and/or epicardial myocardium. The nonglobal capturing stimulus terminated the VT at the MDP-recorded site, around which there was no MDP, implying that the protected isthmus involved this site. This case demonstrated that in ischemic VT, a nonendocardial isthmus could be exposed to the endocardial scar surface and also that this exposed part could be protected from endocardial impulses outside the circuit.
Dr. Kimura has received speaker honoraria from Johnson & Johnson K.K., Medtronic Japan, Bayer Yakuhin Ltd., Boehringer Ingelheim Japan, Inc.; and has an affiliation with the Endowed Department of Medtronic Japan and Fukuda Denshi Co. Dr. Tomita has received research funding from Boehringer Ingelheim, Bayer, Daiichi-Sankyo, Abbott, and Pfizer; and Speakers Bureau/honorarium from Boehringer Ingelheim, Bayer, and Daiichi-Sankyo. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All 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 31, 2018.
- Accepted January 10, 2019.
- 2019 American College of Cardiology Foundation