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Mechanism of wide QRS tachycardia: Guest interpretation

What is the mechanism of Wide QRS Tachycardia: Another Point of ViewGuest Tracing Interpretation by Dr. George J Klein. This is a very interesting and challenging case1 and the authors have laid out a logical argument to support their case. The reader might get the most of this and other electrophysiology rounds by initially just looking at the figures and drawing their own conclusions before reading those of the authors. It is, after all, an exercise in tracing interpretation. To this end, I usually scan the figure or place the digital version if available into a PowerPoint presentation. This allows me to use my own calipers formeasurements,makes it easy to enlarge areas of interest whenmore precision is required, and, finally, cut and paste sections for side-by-side analysis. The following are my observations prepared from looking at the figures alone, “without” reading the text on the first go-round. Figure1 shows theonset of awide complex tachycardia (WCT) after cessation of atrial pacing. The QRS during pacing is normal and the AH interval appears to be normal. TheWCT tachycardia begins with a ventricular event after a pause. The QRSmorphology is of right bundle branch block (RBBB) type with left axis deviation. Although only three surface leads are available, the electrocardiogram is not easily compatible with usual ventricular pre-excitation over an atrioventricular (AV) pathway, which has a basal ventricular insertion. I would also note that a bifascicular block pattern is a very unusual aberrancy pattern without either RBBB or left anterior fascicular block being present at baseline. It is, however, compatible with idiopathic left ventricular tachycardia (LVVT). The His bundle electrogram, well seen in sinus rhythm, is absent during WCT and reasonably assumed to be buried in theQRS. This, of course, leaves only ventricular tachycardia (VT) or preexcited tachycardia in the differential diagnosis of theWCT. The atrial activation sequence is central based on the atrial electrograms available to us, a fact not helpful as being compatible with either of our contenders for the diagnosis. The onset of tachycardia is unusual, theWCT starting after a pause following cession of atrial pacing. It is certainly compatible with VT. If one tries to link the onset directly to pacing, it is plausibly atrioventricular nodal reentry tachycardia (AVNRT) with a “2 for 1” phenomenon over a fast and slow atrioventricular node (AVN) pathway with bystander participation of an accessory pathway, or alternatively nodoventricular tachycardia with anterograde nodoventricular conductionand retrograde conductionover thenormalAVconduction system or a septal AP. After interpreting Figure 1, it is reasonable to conclude that one is dealing with ventricular tachycardia (idiopathic LVVT specifically, known to be inducible with atrial pacing) or alternatively preexcited tachycardia utilizing an atypical accessory pathway. Of course, the former would be statistically considerably more probable. I am not surewhat Figure 2 tells us. The CL of pacing is within 10ms of the tachycardia CL, making reliance on slight measurement differences a little risky especially when the length of transition is relatively brief. An entrainment allowing the measurements after cessation of pacing might of course be helpful in distinguishing AVNRT from AVRT, although the onset of tachycardia in Figure 1made AVRT unlikely. I will accept a 10-ms shortening of the atrial cycle length after a transition of several fusedQRSuntil theQRSbecomes fully paced. This would seemcompatiblewithVT froma left ventricular (LV) sourcewith several cycles required before total capture from the right ventricular (RV) apical source and passive retrograde conduction over the AV node. Figure 3 shows us termination of theWCTwith a short run of atrial pacing. The third cycle shows slight ventricular fusion and also shows the H advanced. The timing of S3 to V onset is unchanged from S2 to V onset, showing that the fusion is caused by His advancement, i.e., conduction over the normal AV conduction system. Consider that one postulated a nodoventricular pathway as the anterograde limb of a circuit, bystander, or other. In this instance, atrial activation would have to retain conduction time over the part of the AVN that leads to the AP but advance only the part that leads to the H for that one beat. The following cycle is completely normal with a normal HV interval and this likely signals the end of the tachycardia. The AH remains the same until pacing is stopped and no tachycardia is observed. This would be an unusual termination with AVNRT with little change in anterograde fast pathway conduction and termination after only a couple of cycles. On the other hand, termination of idiopathic LVVT by atrial pacing is well known and anterograde His capture typically precedes this method of termination. The reentrant mechanism has a close relationship to the His Purkinje system in the former, allowing both induction and termination of VT with atrial stimuli. Mypreferreddiagnosis looking initially only at the tracingswas idiopathic LVVT. I am not, however, convinced that the diagnosis can be unconditionally made from the three tracings shown alone. What would support AVNRT with bystander nodoventricular (NV) fiber?