2 │ DISCUSSION
The broad differential diagnoses of this narrow complex supraventricular
tachycardia (SVT) with VA interval >70 ms and earliest
atrial activation recorded at the His bundle region includes
atrioventricular nodal reentrant tachycardia (AVNRT), orthodromic AV
re-entrant tachycardia (ORT) utilizing a paraseptal accessory pathway as
the retrograde limb, paraseptal atrial tachycardia (AT), and junctional
tachycardia with retrograde conduction to the atrium.
Reproducible initiations of SVT with AH decrement following a single
AEST (Figure 2a) favor an AV node dependent mechanism (AVNRT/ORT). This
is further attested by the fact that the slight wobble in the SVT CL is
driven predominantly by changes in the AH interval. Furthermore, VOP
during SVT (Figure 2b) results in a 1:1 retrograde conduction to atrium
without a change in atrial activation sequence followed by a VAHV
response upon cessation of pacing. This also argues against an atrial
tachycardia.
The first SVT beat following AEST (Figure 2a) demonstrates a slight
longer VA interval than subsequent beats. In addition, the VA interval
during VOP from the RV is longer than that during SVT. The corrected
post-pacing interval minus tachycardia CL (cPPI – TCL) is also 180 ms
(> 115 ms) (Figure 2b).1 In the context
of a presumed AV node dependent mechanism, these findings presumptively
favor a diagnosis AVNRT over a non-decremental right paraseptal
accessory pathway. However, a decremental right paraseptal accessory
pathway is not theoretically excluded.
A relatively late coupled HRVES delivered from the RV apex does not
reset the tachycardia (Figure 2c). Note that this HRVES ‘pulled in’ the
local V at the anteroseptal (His bundle) region. However, it failed to
‘pull’ in or perturb the local VEGM in the postero-septal or adjacent
mitral annular region along any of the CS electrodes. This particular
response evoked by the fusion beat (HRVES) excludes an ORT due to a
retrograde conducting right anteroseptal accessory pathway.
Thus far, all findings seem to be consistent with a diagnosis of AVNRT.
Interestingly, another HRVES delivered from the LV apex (RF catheter via
retrograde aortic approach) did indeed reset the tachycardia (Figure 2d
and Figure 3). This LV HRVES (fusion beat) pulled in the local VEGM in
the distal CS electrodes (CS 1-2 and 3-4), but not in the other CS
electrodes (CS 5-6, 7-8, and 9-10) or His bundle region. This suggests
an ORT due to a retrograde conducting accessory pathway with its
ventricular insertion near the vicinity of the distal CS electrodes
despite their paradoxical later local atrial activation.
Subsequent efforts should be directed towards localizing the atrial
insertion of accessory pathway (earliest atrial activation during SVT)
and clarifying if it connects to left atrium or CS musculature. During
VOP, HRVES, as well as intermittently during SVT (Figure 2 and 3) there
are two distinct atrial electrogram signals visible on the proximal CS
electrode 9-10. The first likely represents a far-field left atrial (LA)
signal. The second (or latest) appears to be a sharper near field
electrogram likely originating from the local CS musculature itself. At
other times during SVT, those two signals are fused (far field followed
by near field) with minimal decrement. In addition, the atrial
electrogram signals on CS electrodes 3-4 and 5-6 are fused. The far
field LA component still precedes the near field CS component. Hence, we
can infer that the atrial insertion is unlikely to be to the proximal or
mid CS musculature. The CS muscular coat usually extends only upto the
level of Vieussens valve and not distally into the great cardiac
vein.3 The distal CS electrode 1-2 shows only a far
field LA electrogram. In case of slanted/oblique accessory pathway along
the posterior/lateral mitral annulus the atrial insertion is expected to
be more lateral/superior to its ventricular
insertion.4 When there is minimal/no slant the atrial
and ventricular insertions should be adjacent.
Pursuant to the above stipulations, a possible inference here is that
the accessory pathway has a LA insertion lateral to the mitral annulus
corresponding to the distal CS electrodes with mitral annular block
between the former and later. This is speculated to be the result of the
unsuccessful first ablation causing a line of block in the lateral
mitral isthmus between the mitral valve and the left inferior pulmonary
vein. The preserved atrial insertion of the accessory pathway further
lateral to the line of block is then expected to result in a peculiar
counterclockwise activation of the mitral annulus during SVT.
To demonstrate mitral annular block, the RF/mapping catheter was placed
in the LA just lateral to the distal CS electrodes via retrograde aortic
approach (Figure 4a; LAO view). The earliest retrograde atrial
activation was also recorded here during SVT (Figure 4b). After
termination of SVT, overdrive pacing from the RF catheter during sinus
rhythm (Figure 4c) reproduced the characteristic mitral annular block
atrial activation pattern (lateral mitral annulus > His
> proximal > mid > distal CS
activation medial to RF catheter). This was validated during SVT using 3
D Electro anatomic activation mapping. A counterclockwise mitral annular
activation was demonstated proceeding from the earliest site of
activation at the lateral mitral annulus (Figure 4d and 4e). Successful
RF ablation was performed at the site of earliest LA activation during
SVT with an 8F TactiCathTM SE catheter (Abbott). There
was abrupt termination of tachycardia followed by no residual VA
conduction or any inducible SVT.
As explicated here, attempted RF ablation of a left-sided AP can result
in intra-atrial conduction block along the mitral
annulus.4 An anatomical predisposition with a narrow
lateral mitral isthmus (morphological or functional) may render some
individuals more vulnerable to this sequelae.5 A
strong index of suspicion is pre requisite to accurately elucidate this
mechanism in the setting of recurrent SVT following prior ablation. In
our case a HRVES delivered from the LV apex clarified the diagnosis.
Alternative maneuvers during SVT are also suggested. The simplest
maneuver is always to advance the CS catheter further distally beyond
the line of block to document the earliest atrial activation. Secondly,
delivering a double extra stimulus from the RV apex could potentially
‘pull in’/advance the local V along the mitral annulus thus resetting
the tachycardia. If the second extra stimulus also shows a fused
morphology then ORT is diagnosed. A single HRVES delivered from the RV
outflow tract septum usually results in counterclockwise ventricular
activation pattern along the mitral annulus. This is more likely to
‘pull in’ the local V along the lateral mitral annulus and reset the
tachycardia thus confirming ORT.