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Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome
Masood Akhtar, … , Mohammad Shenasa, Donald H. Schmidt
Masood Akhtar, … , Mohammad Shenasa, Donald H. Schmidt
Published April 1, 1981
Citation Information: J Clin Invest. 1981;67(4):1047-1055. https://doi.org/10.1172/JCI110116.
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Research Article

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

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Abstract

The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V2 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 (V1V1) ranging from 550 to 900 ms (mean, 657.1±139.5), closely coupled V2 (mean V1V2, 357.3±59.2 ms, range 320-500) produced retrograde His bundle (H2) activation via the bundle branches and retrograde atrial (A2) activation via the AP. As the V1V2 were further shortened, the V2 showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A2 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 V2 when the latter produced retrograde H2 activation via the bundle branches. In 10 of 14 cases, however, the retrograde H2 was followed by a V3, due to macroreentry in the HPS. The V3 in turn blocked retrogradely in the HPS while producing A3 via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V2 and/or V3 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 V2 in the atrioventricular node with or without concomitant retrograde A2 activation via the AP. We conclude that within the ranges of cycle lengths tested, a retrograde block of V2 and/or V3 in the HPS is the most common mechanism for initiation of PSVT during ventricular premature stimulation in patients with the Wolff-Parkinson-White Syndrome.

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Masood Akhtar, Mohammad Shenasa, Donald H. Schmidt

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