Commentary
Creating a complete linear block is essential for preventing recurrent
PMAT. Therefore, evaluating conduction across the MI linear lesion is
important, and entrainment pacing and post-pacing interval (PPI) mapping
during tachycardia are effective tools for identifying tachycardia
circuits.1 However, this is sometimes challenging
because of the small or invisible potential after extensive ablation of
the MI and inside the CS. Epicardial CS electrograms can be used as a
surrogate for LA signals. However, CS activation can differ from
contiguous LA activation. Careful signal analysis and discrimination of
the local CS from the far-field LA electrograms are necessary.
In this case, the first ablation was performed at the 3’o clock line of
the MI and inside the CS, but the second ablation was performed because
the PMAT recurred. Figures 1A and 2A show intracardiac
electrocardiograms taken during the low-output entrainment pacing at a
pacing CL of 240ms from CS 3,4 corresponding to the 4’o clock position
of the MA. The PPI was 291ms, longer than the tachycardia CL. Therefore,
CS 3,4 are outside of the tachycardia circuit.
This case highlights the importance of the location of a multielectrode
catheter (2 mm interspacing) in the LA close to the CS 3,4 to interpret
the activation sequence during entrainment pacing. As shown in Figure
2A, the intervals between the CS 7,8 potentials during the first and
second pacing were the same as the tachycardia CL (250 ms), while those
after the third pacing coincided with the pacing CL (240 ms).
Immediately after capturing the CS 7,8 potentials, the intervals between
the LA potentials on LA 1,2 and 3,4 close to CS 3,4 coincided with the
pacing CL. These findings indicate that low-output pacing from CS 3,4
captured only the CS musculature.
Figures 1B, 2B, and 2C show the intracardiac electrocardiograms taken
during the high-output entrainment pacing at a pacing CL of 240ms from
CS 3,4. In Figure 2B, only the terminal component of the CS 7,8
potential overlapped with the first pacing stimulus artifact at the same
interval as the tachycardia CL. The CS 3,4 potential was observed
immediately before the second pacing stimulus artifact, and the
intervals between CS 3,4 potential after the second pacing were
consistent with the pacing CL. In contrast, the LA potentials on LA 1,2
and 3,4 were captured by the first pacing stimulation. In Figure 2C, the
PPI to LA 1,2 potential was 252ms, which was almost consistent with the
tachycardia CL. Paradoxically, concealed fusion was demonstrated by
selective LA capture only, although no clear far-field LA potential was
observed at the site of pacing from CS 3,4 despite amplification. What
mechanism underlies the unexpected inability to capture near-field CS
potentials during high-output entrainment pacing from CS 3,4?
Entrainment pacing can be influenced by current strength. Different
current strengths are helpful for distinguishing near-field form
far-field component.2 Theoretically, a relatively
lower current strength probably results in selective capture of the CS
musculature, while a relatively higher current strength results in
nonselective capture of the LA and the CS owing to the capture of
adjacent myocardium beyond the intracardiac electrocardiogram interest.
In this case, the antidromic wavefront from the first pacing stimulation
from CS 3,4 collided inside the CS with the orthodromic wavefront of the
tachycardia. The orthodromic wavefront of the first pacing stimulation
turns the MA counterclockwise and conducts into the CS, making the local
CS musculature refractory to the second pacing stimulation. Therefore,
subsequent entrainment pacing with concealed fusion was performed by
direct LA capture; thus, only an orthodromic wavefront was observed and
the CS potentials preceded the pacing stimulus artifacts. This mechanism
is pseudo-selective LA capture by concealed remote capture from the CS
3,4.
Focal LA endocardial radiofrequency ablation at the gap site terminated
the PMAT and caused a bidirectional complete block of the MI.