A 29-year-old male presented with palpitations without a documented tachycardia. ECG showed minimal preexcitation ( Figure 1A), and echo confirmed a normal heart. At electrophysiological study in the drug-free state, the HV interval was 13 ms in sinus rhythm, and ventricular (V) activation in the right paraHisian region preceded the surface delta wave (Figure 2A). Programmed stimulation from the septal right atrium (A) increased preexcitation at shorter S1-S2 intervals (below 600-360 ms), as evidenced by a subtle loss of physiological left-to-right ventricular (RV) septal activation (loss of r wave in V1 and q waves in I, aVL) and an increasingly negative HV interval. The S2-δ interval also prolonged with progressive preexcitation. Figures 1B and 2B show increased preexcitation elicited at an S1-S2 interval of 220 ms. Atrioventricular (AV) effective refractory period was shorter than 600-220 ms, and dual AV nodal physiology was absent. These features along with the existence of escape junctional preexcited beat ( Figure 1C and 2C) supported the presence of a right-sided manifest nodoventricular (NV) pathway bypassing a portion of the AV node, and ruled against typical anterograde AV bypass tracts, Mahaim fibers from AV ring, and fasciculoventricular pathways.
See Editor's Perspective by Asirvatham and StevensonRetrograde conduction was through a concealed left lateral accessory pathway (AP) that had slow decremental conduction and a long ventriculoatrial (VA) effective refractory period of 600-340 ms. Despite multiple atrial and ventricular programmed or burst stimulation attempts, no tachycardia was induced. However, coincidental with decrement in retrograde AP conduction (VA interval increasing from 112 to 136 ms), single reciprocating ventricular echo beats were easily reproducible, even during fixed RV pacing at rates moderately faster than the sinus rate (Figure 3). After intravenous adenosine 12-mg, VA block developed during RV pacing (cycle length: 550 ms) consistent with the decremental nature of VA conduction and the lack of typical retrograde bypass tracts ( Figure 1A in the Data Supplement). Soon after recovery of VA block, during ongoing RV pacing, a nonsustained 1:1 VA reciprocating tachycardia (cycle length: 310-345 ms) was induced (lasting 35 s) with an atrial activation pattern identical to that of the ventricular echo beats ( Figure 4A; Figure 1B in the Data Supplement). An His-refractory RV pacing stimulus advanced the subsequent A with resetting of the tachycardia without change in atrial activation ( Figure 4B), thereby confirming participation of the left lateral AP in the tachycardia. The QRS morphology of the ventricular echo beats, the tachycardia and the beat subsequent to the atrial advancement brought by the His-refractory extrastimulus represented variably fused anterograde NV fiber and AV nodal conduction (Figures 3 and 4).In light of these features: (1) Why was the induction and maintenance of tachycardia so difficult, despite easily provoked ventricular echo beats? (2) What was the...