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