Author + information
- Stavros E. Mountantonakis, MD and
- Edward P. Gerstenfeld, MD∗ ()
- ↵∗Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, MU-East 4th Floor, 500 Parnassus Avenue, San Francisco, California 94143
We would like to thank Drs. Ávila and Arenal for their comments and interest in our work (1). The demonstration of voltage “channels” during ablation of ventricular tachycardia (VT) was originally proposed in the seminal studies by Arenal et al. (2) and Hsia et al. (3); we do believe this finding continues to be of importance in the field of VT ablation. However, some have adopted these findings to the degree that “empiric” ablation of voltage channels is performed as part of a VT ablation procedure, and we have noted several limitations to the technique. First, the presence of channels is highly dependent on the density and quality of points taken on the electroanatomic map. Even on Arenal's original publication (2), the density of points in Figures 3 and 5 is high in the region of the identified channel, but sparse in other areas of the left ventricle. It is possible that if a more uniform density of points was obtained, other channels may have been identified that were not related to the clinical or induced VTs. Dr. Arenal and colleagues were also careful to perform pacing in these channels and document a prolonged stimulus to QRS duration suggestive of slow conduction. We believe this finding heightens the significance of an anatomic channel, similar to the identification of late potentials within channels in our paper. We sought to obtain the true sensitivity and specificity of such identified channels in a population of patients with tolerated VT and detailed voltage maps. Although we found that the association of such channels with the clinical VT was much lower than those identified in Arenal et al.'s paper, we did find that channels associated with late potentials were specific (81%) for identification of the VT isthmus, similar to Arenal et al. (2) findings of 75%. The difference between the upper and lower voltage cutoff in the Arenal et al. (2) paper was quite small (0.01 mV)—in our experience, this may accentuate the identification of channels that are not clinically relevant when applied uniformly.
To specifically address the 4 points raised by Drs. Ávila and Arenal:
1. It is true that complete activation maps during VT were not obtained in our study (nor Arenal et al. ) as this can be quite time consuming and technically challenging during clinical VT ablation. The voltage maps we obtained were extremely detailed, and we chose only patients with tolerated VT so we could be sure to identify the true VT isthmus using entrainment criteria, which is the gold standard target for ablation. Therefore, we feel that channels remote from any identified VT isthmus could not represent a channel for the clinically relevant VT.
2. The observation that channels typically appeared at lower cutoffs <0.5mV in the Arenal et al. (2) study is interesting. After lowering the upper cutoff, we progressively lowered the lower cutoff down to 0.01 mV and still did not find any channels corresponding to the VT isthmus in the patient depicted in Figure 5 in our paper.
3. The criticism that the spatial location of a point on an electroanatomic map during VT may be different than the same point obtained during sinus rhythm is valid. However, as stated in the Methods section of our paper, “Once the critical isthmus was identified, radiofrequency ablation was performed at the isthmus site, and upon termination of the tachycardia, a new point was tagged in sinus rhythm.” Therefore, all the isthmus points noted on the electroanatomic maps in our study were obtained during sinus rhythm after VT termination, and any change in left ventricular volume or catheter location during VT would not affect the relationship between the VT isthmus and the identified voltage map channels.
4. The authors note that in our study, VTs associated with channels were typically faster than those not associated with channels. The authors hypothesize that slower VTs may have a more complex substrate that makes identification of channels on an electroanatomic voltage map more difficult. Although it is certainly possible that slower VTs have a different mechanism and/or substrate than faster VTs, the literature on VT mechanism is based in large part on slow, tolerated VTs; there are no data we know of to suggest that slower VTs would have a different mechanism or substrate.
In summary, we find that our data provide strong evidence that the mere presence of a voltage channel demonstrated during electroanatomic mapping is not specific for a clinical VT isthmus. Additional electrophysiological surrogates such as late potentials, as described in our paper, or a long stimulus to QRS duration, as described by Dr. Arenal and colleagues, should be obtained before such channels are considered important for maintaining VT.
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