Commentary:
In our case, His plus myocardium (HMc) vs. only myocardial capture (Mc)
was differentiated on the basis of QRS morphology and width, although it
is not the ideal way. The best way of concluding it is by analyzing
whether H-signal is obscured inside or released from ventricular signal
on the His catheter [1,2]. However, this was not well appreciated in
our index case, hence, QRS width was used as a surrogate.
In fig 1A, the first beat represented a Mc only capture (QRS width
138ms) and second beat was a HMc (i.e. Para-His capture, QRS width
-114ms) capture. In both cases, the atrial activation sequence remained
identical suggesting only one route for VAC . The Stimulus-A
electrogram (SA) measurements were also identical. This would be called
an extra-nodal response (i.e. in both the beats the VAC took place over
an AP). This proves the presence of an AP, although participation of the
AP in supraventricular tachycardia cannot be ascertained from PHP
maneuver.
Fig 1B shows (at a different time during the same pacing protocol as Fig
1A): a very short SA (40 ms CS-12, 50 ms in HRA) was recorded in the
first beat. The differentials of such a short SA are – (i) simultaneous
atrial capture (SAC), (ii) Capture of ventricular end of AP. One of the
ways to differentiate them is looking for ‘Schmutz’ after the pacing
spike at the catheter near the pacing pole, MAPp and His here. But
sometimes it is difficult to discriminate ‘Schmutz’ from myocardial
V-EGM recorded at nearly the same time. However, if anytime pure his
capture (PHc) without any local myocardial capture can be achieved with
and without SAC (also encountered in this case, described below), the
difference of EGM attached to pacing spike could be compared to
delineate presence or absence of ‘Schmutz’, respectively. Second and
easier way to validate SAC, is to look for SA prolongation when the QRS
morphology remains unchanged, as happened in the second beat (Fig 1B).
Among the common responses during PHP, nodal response can also have
prolongation of VA, but only during concomitant QRS widening and His-EGM
release (if visible). In our case, nodal response was ruled out as the
SA interval widened in spite of identical QRS width in the second beat.
Hence, everything was suggestive of SAC in the first beat. Moreover, a
short SA of <60 or 70 ms on the proximal CS or high right
atrial electrodes respectively, is highly suggestive of SAC by itself as
shown in an earlier study [3]. An ‘intermittent’ direct AP capture,
although very rare, cannot be ruled out from above observations.
Subsequently, Fig 2A shows there is SAC in both the beats. It also
reveals a pure his capture (PHc) with loss of myocardial capture in the
narrower second beat, as compared to HMc in the previous wider beat. The
way to recognize PHc is the 12-lead ECG morphology having isoelectric
segment after pacing spike. In addition, the convincing proof of PHc
came from intracardiacs having late V-EGM recorded separately from the
pacing artifact in the second beat (best appreciated in MAPd). Unless
this is promptly recognized there could be a mistaken consideration of
the wider beat as Mc and narrower beat as HMc, hence the interpretation
for the VAC might completely change[2]. Moreover, as the ventricular
EGM of the second beat is delayed and recorded separately from the
pacing spike, it rendered an opportunity to analyze the ‘Schmutz/SAC’(*)
properly (MAPp). The absence of Schmutz was distinctly noted when the
SAC disappeared during PHc (Fig 2B, next discussion) and genuine VA
conduction finally took place.
The next intriguing observation noted in Fig 2B during the PHP was
prolongation of SA during PHc (second beat) as compared to HMc (first
beat). This resulted in 48-50 ms increment in SA. In contrast theVA interval was fixed (78 ms) during both the beats with
similar activation pattern. From this it can be inferred that the VAC
was dependent on V capture and not His capture (as here the SA i.e. the
HA in these two beats were not the same). Therefore, the route of VAC
could be concluded to be an extra-nodal route even from these 2 beats.
An additional interesting observation was the underlying RBBB getting
unmasked during PHP, when antegrade AP conduction disappeared. We
believe, the prolongation of SA by 48-50 ms in second beat was
exaggerated due to the existing/underlying RBBB as during PHc the
impulse has to travel down via left bundle (LB) and exit into myocardium
followed by trans-septal conduction and then VAC via right sided AP. We
did not get an opportunity to demonstrate the SA prolongation in absence
of RBBB as it was a fixed RBBB. We speculate, even in absence of RBBB,
the SA still would have prolonged, but by a lesser magnitude, when
myocardial capture is lost (Appendix 2). Hence, the PHc although
infrequently encountered, can indeed help to delineate the route of VAC,
irrespective of distal antegrade RBBB.
To summarize, this single case illustrates several pitfalls and
challenges encountered during PHP maneuver. We speculate, many of these
happened because the pacing bipole (His-D) was more proximate to the
atrial side of proximal His region (Fig 3A). To complete the case, the
VAC after ablation (in Fig 3B) revealed nodal response (although the PCL
was 500 ms, as sinus rate interval was approx. 600-650 ms). We believe,
unwarranted findings like SAC might be avoided by placing the pacing
catheter at more preferable distal His region [1,2]. PHc, a rare
finding, can confound the interpretations if not recognized by subtle
differences from HMc. However, when identified correctly, PHc can offer
important electrophysiological inputs and supporting evidence regarding
the route of VAC.