Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventricular premature stimulation in the Wolff-Parkinson-White syndrome.

Abstract

The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V(2) method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V(1)V(1)) ranging from 550 to 900 ms (mean, 657.1+/-139.5), closely coupled V(2) (mean V(1)V(2), 357.3+/-59.2 ms, range 320-500) produced retrograde His bundle (H(2)) activation via the bundle branches and retrograde atrial (A(2)) activation via the AP. As the V(1)V(2) were further shortened, the V(2) showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A(2) impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V(2) when the latter produced retrograde H(2) activation via the bundle branches. In 10 of 14 cases, however, the retrograde H(2) was followed by a V(3), due to macroreentry in the HPS. The V(3) in turn blocked retrogradely in the HPS while producing A(3) via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V(2) and/or V(3) in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none of the patients in this series was the PSVT initiated with a retrograde block of V(2) in the atrioventricular node with or without concomitant retrograde A(2) activation via the AP. We conclude that within the ranges of cycle lengths tested, a retrograde block of V(2) and/or V(3) in the HPS is the most common mechanism for initiation of PSVT during ventricular premature stimulation in patients with the Wolff-Parkinson-White Syndrome.