Response to ECG Challenge
Figures 2A and 2B both demonstrate alternating nodal conduction and
pre-excitation over a left lateral (LL) AP during the drive train.
Remarkably, the subsequent introduction of AES at 240ms causes either
purely nodal (figure 2A, red arrow) or maximally pre-excited (figure 2B,
blue arrow) beats, which was reproducibly dependent on the final beat of
the drive train being conducted in the same way. Several observations
need to be made about the extrastimulus.
Firstly, when the final beat of the drive train blocks in the AP and is
conducted nodally, it is expected that, given the intermittent
pre-excitation at 400ms, the extra stimulus would meet a refractory AP
and also conduct nodally. This is consistent with the behaviour seen in
figure 2A. However, when the final beat of the drive train conducts with
pre-excitation, it is counter-intuitive that the 240ms extra-stimulus
conducts with pre-excitation as seen in figure 2B.
Secondly, during the drive train, there is evidence of nodal and AP
fusion during the pre-excited beats. Therefore, the refractory period
(RP) of the AP, which only conducts every second beat in a 400ms drive
train, can be estimated to lie somewhere between 400 and 800ms (2 x
drive cycle length). This observation makes it curious that a 240ms
extrastimulus could recruit AP conduction. The AV nodal RP in a similar
fashion, can be estimated at less than 400ms in these drive trains.
Thirdly, the His-ventricular interval (HVI) lengthens from 55ms during
the drive train to 75ms during AES when the last beat extrastimulus is
conducted via the AVN (figure 2A, black arrow). This is unusual,
particularly in a young patient and following isoproterenol, and as the
QRS remains narrow, the delay cannot occur in either of the bundle
branches unless both bundle branches delay equally.
Given the fact that both the AP and AVN display somewhat atypical
behaviour during 240ms single AES coupling intervals, it is likely that
both tissues are intermittently similarly affected by electrotonic
coupling influences directly resulting from the critically timed
impulses during the extrastimulus pacing and it is this that needs
explaining. The most likely cause is so-called ‘supernormal conduction’
(1). This is where extra-stimuli occurring during phase 3 (the relative
refractory period) of the cardiac action potential can cause
repolarizing tissue in the AP or AVN to rapidly depolarize again
allowing brisk conduction across the tissue. Input resistance, a measure
of a cell’s excitability by Ohm’s Law (V=IR), is high in the late part
of phase 3 due to ion channel closure, thus contributing to supernormal
excitability (1). It is thought that the supernormal period is dependent
upon the total refractory period and ultimately the action potential
duration. This means that the supernormal excitability will occur
earlier within the cardiac cycle at faster rates and later, at slower
rates (1,2).
In our case, the fact that AES at 240ms have the same effect on both the
AVN and the AP when the prior beat has been conducted antegradely
through the same tissue, suggests that in both instances it lands in the
supernormal phase of excitability (Figure 3A, 3B). Supernormal
conduction requires a long RP to exist in any conduction tissue,
reflected in this case by AP conduction only every second beat at a
400ms drive train. Additionally, the presence of a long HVI at faster
rates across the AVN suggests lower common pathway delay which could
cause dispersion of the RP in this area allowing for a similar effect.
Supernormal potentiation of AP conduction is a rarely described
phenomenon (2), and to our knowledge, it has never been described with a
reciprocating alternans pattern of this kind before, nor does it
typically iterate with a block-conduct-conduct (3) pattern as in this
case.
As AP conduction was unpredictable but could conduct at rates faster
than 250ms (4), radiofrequency ablation was carried out successfully.
The patient unfortunately was not put into atrial fibrillation to assess
the shortest pre-excited RR intervals in AF before ablation.
Operators should be cognizant of the potential for supernormal
conduction to unmask clinically relevant accessory pathway conduction
during extra-stimulus testing, even when it appears the refractory
period has already been reached. Amazingly, it was successive identical
extrastimulus manoeuvers which uncloaked the AP’s supernormal
conduction. As our case proves, sometimes repeating identical pacing
manoeuvres can provide additional valuable information.
Figure 1; 12 lead ECG with evidence of manifest pre-excitation