Does it take two to tango?

The intracardiac tracing presented in Fig. 1 shows that one atrial beat (A¹) is followed by two QRS complexes (V¹ and V²) and that the second atrial beat (A²) produces only one QRS complex (V³). This pattern is repetitive along the tracing. We were able to reproduce this rhythm by atrial pacing (AP) (Fig. 2a) and observed that each V was preceded by a His bundle potential (H), suggesting that the rhythm is supraventricular. Ventricular pacing (VP) at a cycle length of 500 ms repeatedly resulted in a VA Wenckebach: the atrial activation sequence changes (A⁴ and A⁵), the A–A interval decreases (A³–A⁴ and A⁴–A⁵), and the VA interval lengthens (VP⁴–A⁴, VP⁵–A⁵) (Fig. 2b). Notably, a narrow QRS complex [V(P)⁶] followed after A⁵. As the activation wavefront was conducted retrogradely from VP⁵ through the fast pathway to the atrium (A⁵), the fast pathway must be refractory. Therefore, the narrow QRS complex has to result from a second AV pathway, which is, in this case, a slow pathway (Fig. 2b; [1]). Thus, Fig. 1 shows a non-reentrant AV-nodal tachycardia (dual AV-nodal response) resulting from anterograde fast and slow pathway conduction [2]. The extremely prolonged slow pathway conduction (A¹–V²) enables the His bundle to conduct the activation wavefront into a second QRS complex. Then, after A², the slow pathway is refractory, and only the fast pathway conducts the activation wavefront (V³). In Fig. 2a, the same phenomenon occurred: AP¹ initiates H¹ and H². We cannot conclude if H⁴ is a result of slow pathway conduction after AP² or fast pathway conduction after AP³. The AP³–H⁴ time is shorter than the AP²–H³ time. Therefore, we assume that this beat also conducts through the slow pathway. However, the AP²–H³ time might be prolonged because of conduction in the relative refractory period. We successfully eliminated the non-reentrant AV-nodal tachycardia via slow pathway modification.