A 57-year-old man with a history of palpitations and no structural heart disease underwent an EP study to help diagnose a possible arrhythmic mechanism and assess suitability for curative ablation. Figure 1 below shows the arrhythmia which was reliably induced with atrial extra-stimulus pacing.
Figure 1: Wide complex tachycardia with right bundle branch morphology and 1:1 conduction (short VA). Top to bottom: ECG leads (I, aVF & V1); Intracardiac catheters, decapolar positioned in coronary sinus (green) & quadpolar positioned in the RV apex (red)
Let’s examine this EGM carefully to see if we can identify the correct mechanism prior to possible ablation.
Firstly, there is a broad complex tachycardia with a 1:1 AV association pattern. Based on this finding the differential diagnosis includes SVT with aberrancy or VT with 1:1 retrograde conduction. The ECG morphology shows an atypical RBBB morphology with a possible superior axis. An atypical morphology like this should lead us to think this is VT until proven otherwise.
The patient was hemodynamically stable during tachycardia, has no known structural heart disease and the arrhythmia was induced with atrial programmed extra stimulus. In contrast to the QRS morphology, these findings might lead us to think that this SVT with aberrancy. It is also worth noting however, idiopathic VT and other forms of re-entry VT such as fascicular VT are not generally associated with structural heart disease and may be well tolerated by patients, especially when laying down on a bed under light sedation.
Figure 2 below shows the full 12 leads of the ECG during tachycardia. We can now confirm that along with an atypical RBBB morphology there is also a superior axis. An idiopathic VT arising from the postero-medial papillary muscle is plausible, a reentrant VT exiting from the left postero-septal region is also possible. Given the tachycardia was induced with programmed extra stimulation a reentrant mechanism is more likely, however, due to the 1:1 relationship of this tachycardia we need to exclude an SVT with an atypical form of aberrancy first.
Figure 2: Full 12L of tachycardia. There is atypical RBBB morphology with a transition at V4. A left superior axis is present.
What should you do in this situation?
What would be the best pacing manoeuvre to perform to diagnose the mechanism accurately?
For 1:1 tachycardia with a narrow QRS complex, ventricular overdrive pacing is an invaluable diagnostic manoeuvre. Similarly, for 1:1 tachycardia with a broad QRS complex, atrial overdrive pacing can provide equally valuable diagnostic information.
If this tachycardia is an SVT such as an AT, AVNRT or AVRT then atrial overdrive pacing 20-40ms faster than the tachycardia cycle length should demonstrate several key findings:
- The resultant QRS morphology from atrial pacing should be identical to the intrinsic tachycardia QRS morphology, as the pacing wavefront should follow the same pathway through the ventricular conductive system as the tachycardia.
- The response post pacing (provided tachycardia continues) should show an AVA response with either the same VA interval that is ‘hooked’ in the case of AVNRT or AVRT or a different VA interval that is ‘unhooked’ in the case of AT.
If the tachycardia is VT, then atrial overdrive pacing should demonstrate the following:
- The resultant QRS morphology from atrial pacing should change compared to the intrinsic tachycardia QRS, as the paced QRS morphology is following the native conduction system, whereas the VT QRS will be generated from a reentrant circuit or focus within the ventricle.
- The response post pacing (provided tachycardia continues) should show an AVVA response as after the ventricle has been entrained (AV), the VT will naturally resume with its usual 1:1 VA conduction pattern (VA)
Atrial overdrive pacing was performed in this case (see figure 3). Let’s see what the response shows.
Figure 3: Onset of atrial overdrive pacing at 470ms (30ms faster than the tachycardia cycle length).
Figure 3 shows the onset of atrial pacing at a rate of 470ms. There are two key findings already worth mentioning that are critical to the diagnosis of this tachycardia mechanism:
- There is a distinct change in the QRS morphology. The first four QRS’s show the underlying tachycardia morphology. The following three QRS complexes (5-7) show fusion. The remainder (8 onwards) of the QRS complexes show a narrow QRS complex.
- The RVA catheter also shows a change in activation from distal – proximal to proximal -distal in line with the change in QRS morphology.
So, what happened post atrial overdrive pacing?
Figure 4 shows the cessation of atrial overdrive pacing and continuation of the underlying broad complex tachycardia. There is an AVVA response post pacing.
Figure 4 shows the cessation of atrial overdrive pacing. Following pacing the last conducted QRS shows a narrow QRS complex, but the first return electrogram is a ventricular signal with the original intrinsic broad complex QRS and distal – proximal RVA activation. In other words, we have an ‘AVVA’ response. This is analogous to a ‘VAAV’ response that we would observe following RV overdrive pacing in an atrial tachycardia.
The combination of an ‘AVVA’ response, changes in QRS morphology, and altered RVA activation during atrial pacing confirms that the tachycardia mechanism was ventricular tachycardia with 1:1 retrograde conduction. The region of the VT re-enrant circuit was then mapped to the septal poster-inferior LV (close to the base of the posterior-medial papillary muscle) and the patient had a successful RF ablation with no reoccurrence of VT seen during the case.
VT induction is more likely to occur with ventricular pacing and programmed extra stimulation and VA dissociation is common. However, as is the case here, atrial pacing may also induce certain VT with 1:1 retrograde conduction. It is important in these situations that you correctly diagnose the true mechanism in order to select the appropriate ablation target. In this example we used a simple atrial overdrive pacing to quickly reveal the correct mechanism of tachycardia.