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.