Discussion
The tachycardia in Figure 1, left
panel, shows an eccentric atrial activation pattern with the earliest
‘A’ in channels CS34 and CS12, located in the left posterolateral
region. The ventriculoatrial (VA) time even at this site is quite long
and there is no bracketing. A His-refractory PVC delivered from the left
ventricle terminates the tachycardia without activation of the atrium,
confirming ORT as the mechanism, using a left free wall accessory
pathway. The second tachycardia (Figure 1, right panel) has a clearly
different atrial activation pattern with the earliest atrial activation
in CS78 and CS910, near the mouth of the coronary sinus, though with a
relatively long VA interval. This is also an ORT, being terminated by a
His-refractory PVC delivered from the left ventricle, without activation
of the atrium. Hence the differential diagnoses include: i) Only 1 left
free wall accessory pathway, with intermittent local periannular (mitral
isthmus) conduction block resulting in coronary sinus disconnection, due
to the previous ablation; ii) Two APs, left lateral and inferoparaseptal
(posteroseptal) and iii) Two APs, left lateral and right sided. A single
left ventricular His-refractory PVC terminating tachycardia made a right
sided AP unlikely and this was ruled out by mapping the tricuspid
annulus during the tachycardia.
Figure 2 shows tachycardia with two different atrial activation
patterns. A later His-refractory
PVC from the left ventricle results in following changes: i) Fusion QRS
complex; ii) Prolongation of tachycardia CL from 255 ms to 300 ms and
iii) Change in mitral annular atrial activation pattern from concentric
to eccentric with a longer initial local VA time. So here differential
diagnoses could be either 1) Two left sided APs, the ORT utilising the
left posterior AP being terminated by the PVC and the ORT utilising the
left lateral AP being immediately initiated or ii) ORT using the same
left lateral AP, with concentric mitral annular atrial activation in the
initial two beats due to local mitral isthmus block; the PVC ‘peels
away’ this conduction block.
The left Panel of Figure 3 explains the concentric activation pattern.
Local conduction block due to previous ablation does not allow the
coronary sinus to get activated from the atrial end of the AP during
tachycardia. The activation then could have proceeded up the left atrium
to the Bachman’s bundle and thence, to the right atrium. However, in
that case the atrium in the peri-AV nodal area would have been activated
before the coronary sinus ostium region. In our case, the coronary sinus
ostium is activated earlier, with the ‘A’ in the His bundle region
later. So the previous ablation energies had also produced a conduction
block higher up, preventing the Bachman’s bundle from getting engaged.
This is further confirmed by Figure 2, where we see that the ‘A’
maintains the same rsr’S’R” morphology in the HISD channel and the same
delay after the ‘A’ in CS910 during both types of tachycardia.
Hence it was decided to map in the lateral mitral annular region during
left ventricular pacing. At the left posterolateral region 1 cm above
the mitral annulus, the earliest fragmented atrial activation was found.
Upon starting radiofrequency energy the AP conduction was immediately
abolished and retrograde AV nodal conduction was seen. After this
successful ablation, complete VA block was seen with adenosine during
left ventricular pacing. Despite isoprenaline, no AP conduction was seen
and no tachycardia was inducible.
Left atrial- coronary sinus disconnection, also termed mitral isthmus
conduction delay or block, is a peculiar phenomenon that can occur
during ablation of a left free wall AP, when several energies are
delivered inferiorly while the actual AP inserts higher
up.1,2 This is one of the important reasons for
failure of ablation, as the operator may erroneously think that the AP
pathway conduction was abolished when retrograde conduction changes from
an eccentric to a concentric pattern.