Resetting of a Supraventricular Tachycardia by a Ventricular Premature Beat. What is the Mechanism?

A 16-year-old male patient was subjected to an electrophysiology (EP) study for evaluation of documented supraventricular tachycardia (SVT) which was refractory to medical therapy. There was no preexcitation on the baseline electrocardiogram (ECG). The EP study demonstrated normal conduction intervals. There was no evidence of dual AV nodal physiology. On incremental ventricular pacing, there was a shift in the ventriculo-atrial (VA) conduction from the septal to the left lateral location, indicating a concentric to eccentric shift in the VA conduction. A regular narrow complex tachycardia was induced by ventricular programmed stimulation and incremental ventricular pacing. A premature ventricular complex (PVC) was introduced at the right ventricular (RV) apical septal region late in the diastole when the His bundle was refractory. The response is shown in Figure 2. What is the mechanism of the tachycardia? What is the mechanism of resetting of this tachycardia by the PVC? Figure 1 shows incremental ventricular pacing. With a change in the pacing cycle length (CL) from 280 ms to 260 ms, there is a clear shift in the pattern of the VA activation from a more septal to a lateral location, distal coronary sinus (CS) bipole showing the earliest atrial activation. This is indicative of a left lateral accessory pathway conduction. Initial central conduction is either through AV node or through a septal accessory pathway. Earlier posteroseptal activation compared to anteroseptal (His-bundle region) suggests either slow AV nodal pathway conduction or a posteroseptal accessory pathway conduction. Figure 2 shows the tachycardia and response to the PVC introduced late in diastole during the tachycardia. Surface ECG shows a regular narrow complex tachycardia with partial right bundle branch block. It is an intermediate RP tachycardia with inverted P waves in inferior leads indicating a caudo-cranial atrial activation. Intracardiac recordings demonstrate earliest atrial activation at proximal CS bipole located at posteroseptal region (CS ostium). Interestingly distal CS bipole shows a near simultaneous atrial signal, which is ahead of the other CS atrial electrograms. This pattern of near simultaneous atrial activation in all available left atrial electrodes indicates that there is atrial fusion related to left lateral and a septal accessory pathways, and that a double loop tachycardia is the mechanism of this SVT. The morphology of the PVC is suggestive of fusion indicating the late diastolic timing and confirms it coincides with the refractory period of the His bundle. This PVC results in a sudden change in atrial activation shifting it from concentric to an eccentric pattern and an increase in CL of the tachycardia from 280 ms to 300 ms. One can also say that, the PVC is dissociating septal portion of the ventricle and terminating the conduction through the septal accessory pathway by concealment in to the ventricular insertion of the AP and thus making it refractory. At the same time, free wall region of the left ventricle is activated by the depolarization wavefront of the native QRS travelling through the His Purkinje system and reentering the left atrium through the left lateral accessory pathway which is maintaining the second orthodromic tachycardia. It is therefore reasonable to conclude that the original SVT was a double loop tachycardia with participation of a septal as well as left lateral accessory pathways. Near simultaneous activation of all the CS electrodes indicated atrial fusion related to conduction through septal and lateral accessory pathways. PVC is changing atrial activation by switching the retrograde limb of the AVRT lateral pathway alone from a dual loop activation. This is by terminating the shorter loop of the SVT mediated through the septal pathway by blocking it, allowing the outer loop to continue. It is evident from the ventricular pacing that the refractory period of the septal pathway is longer than that of the lateral pathway which explains preferential block of the septal pathway by the PVC apart from the fact that the location of the free wall pathway also has a role to contribute in this re setting maneuver. Thus, the effect of the PVC is not a reset in the true sense but an alteration of the atrial activation by blocking the septal pathway. Left lateral pathway is not a total bystander in the tachycardia mechanism, but in reality the bigger loop tachycardia mediated through the lateral accessory pathway was continuously entrained by the shorter loop, faster tachycardia through the septal pathway. After the termination of the shorter loop of the tachycardia, continuous concealed penetration into the atrial insertion of the septal accessory pathway prevented resumption of retrograde conduction through this accessory pathway thus preventing recurrence of the first tachycardia. Termination by a PVC which is His bundle refractory excludes the possibility of AVNRT in this case.1 Given the fact that there was no dual AV nodal physiology at baseline, AVNRT would be an unlikely mechanism for the primary tachycardia. This single electrophysiologic maneuver confirmed the diagnosis and presence of multiple accessory pathways in this tachycardia. Both pathways were successfully ablated by a trans-septal route. Left lateral accessory pathway was ablated at 3 o' clock position and septal pathway was ablated at 7 o' clock position of mitral annulus in 30 degree LAO fluoroscopic view. Postablation electrophysiological study did not reveal any evidences for accessory pathway conduction or dual AV nodal physiology. No tachycardia was inducible after ablation.

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