Tachycardia with VA Dissociation: An Unusual Tachycardia Mechanism

A 56-year-old man with a history of congestive heart failure and a biventricular ICD was referred for assessment of frequent episodes of antitachycardia pacing and occasional shocks for tachycardia. An EP study was performed for further assessment. During catheter manipulation in the right ventricle, tachycardia was observed (Fig. 1). At baseline, the AH interval was 100 msec and the HV interval was 50 msec at 58 bpm. Preexcitation was not demonstrated with atrial pacing, and VA conduction was absent at all cycle lengths tested. Tachycardia was easily reproduced by ventricular and atrial pacing (Fig. 2). What is the differential diagnosis of the tachycardia? ECG during tachycardia. Three beats paced from the atrium followed by tachycardia (and a 4th atrial paced beat which does not conduct to the ventricle). Note very similar QRS morphology. Intracardiac tracings are shown in Figure 3. Administration of 6 mg of intravenous adenosine consistently resulted in termination of the tachycardia. Attempts to entrain the tachycardia by right atrial pacing were unsuccessful. Catheter manipulation in the right ventricle during tachycardia resulted in transient right bundle branch block (RBBB) with delayed activation recorded at the RV apex. A premature ventricular beat was introduced at a time when the His bundle was refractory, demonstrated in Figure 4. What is the mechanism of the tachycardia determined at EP study? Intracardiac recordings during tachycardia. PVC introduced while His is refractory advances and resets tachycardia. Figure 1 demonstrates tachycardia with left bundle branch block. Dissociation of the atrium from the ventricle is evident, as P waves are visible intermittently. The differential diagnosis of a tachycardia with VA dissociation and QRS identical or at least similar to sinus rhythm includes: bundle branch reentry, interfascicular reentry, orthodromic reentrant tachycardia using a nodoventricular or nodofascicular pathway as the retrograde limb, reentry using a fasciculoventricular AP as the retrograde limb, junctional ectopic tachycardia (JET), and AV nodal reentrant tachycardia (AVNRT). The mechanism could not be discerned without intracardiac assessment. Figure 2 illustrates the onset of tachycardia after three atrial-paced beats. The morphology of the tachycardia is identical to that of the intrinsic QRS complexes produced by atrial pacing. The onset of the tachycardia, after a paced atrial beat which does not conduct to the ventricles, may be compatible with a “two-for-one” phenomenon. The second-last atrial-paced beat may have conducted to the ventricles via a fast and also a slow anterograde pathway, resulting in two conducted beats and the onset of AVNRT. No VA conduction was present, and intracardiac recordings during tachycardia confirm dissociation of the atrium from the ventricle (Fig. 3). His bundle activation precedes ventricular activation during tachycardia, with an HV interval of 50 msec. The normal HV interval at baseline and during tachycardia makes the diagnosis of bundle branch reentry unlikely.1 Continuation of tachycardia with RBBB, as seen in Figure 3, effectively rules out this diagnosis. The observation that the right-ventricular apex was activated later during tachycardia with RBBB, suggests that the tachycardia circuit uses the normal conduction pathway as the anterograde limb of the circuit. This, along with the observation that the QRS morphology during tachycardia was identical to sinus rhythm, effectively excludes interfascicular reentry as the tachycardia mechanism. Reproducible termination of the tachycardia with adenosine generally supports participation of the AV node in the tachycardia circuit. This suggests that the mechanism is not fasciculoventricular reentry, an already unlikely diagnosis which has not been previously described.2 AVNRT can persist with exit block to the atrium.3–5 In this case, entrance block to the AV node was also demonstrated by the inability to affect the tachycardia circuit with atrial pacing. The diagnosis is now established by introduction of PVCs into the tachycardia when the His is refractory (Fig. 4). The diagnoses of AVNRT and JET are excluded by the ability to advance and reset the tachycardia with a ventricular-paced beat while the His bundle is refractory. By exclusion, the diagnosis of orthodromic reentrant tachycardia using a nodoventricular pathway as the retrograde limb was reached. As the patient had a biventricular device, the decision was made to ablate the AV junction. After ablation, no further tachycardia was inducible, and the tachycardia has subsequently not recurred. Nodoventricular connections were first postulated by Wellens6 to account for accessory atrioventricular pathways that demonstrated decremental conduction. However, many of the accessory pathways which were initially believed to be nodoventricular were in fact decremental atrioventricular or atriofascicular connections.7 This case illustrates what we believe to be a rare entity, a true nodoventricular pathway with unidirectional retrograde conduction. Participation of such a pathway as the retrograde limb of orthodromic reentrant tachycardia has been previously described.8,9 In complex cases, it is important to formulate a differential diagnosis based on observations from the 12-lead ECG and results of EP testing, and methodically test the possibility of each using appropriate maneuvers. In this case, the diagnosis was clarified by programmed electrical stimulation, the use of adenosine, and a systematic exclusion of the other possibilities in the differential diagnosis. Had administration of adenosine been inconclusive, participation of the AV node in the tachycardia could have been proven by temporary cooling of the node using a cryocatheter during tachycardia.10 Finally, ablation of the AV node with elimination of tachycardia supported the essential role of the AV node in the tachycardia mechanism. Hypothesis testing based on the differential diagnosis remains a classical method for arriving at a definitive diagnosis, with ablation providing a verification of the postulated mechanism.

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