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Research Article Free access | 10.1172/JCI110116

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, and Donald H. Schmidt

Natalie and Norman Soref and Family Electrophysiology Laboratory, University of Wisconsin Mount Sinai Medical Center, Milwaukee, Wisconsin 53201

Find articles by Akhtar, M. in: JCI | PubMed | Google Scholar

Natalie and Norman Soref and Family Electrophysiology Laboratory, University of Wisconsin Mount Sinai Medical Center, Milwaukee, Wisconsin 53201

Find articles by Shenasa, M. in: JCI | PubMed | Google Scholar

Natalie and Norman Soref and Family Electrophysiology Laboratory, University of Wisconsin Mount Sinai Medical Center, Milwaukee, Wisconsin 53201

Find articles by Schmidt, D. in: JCI | PubMed | Google Scholar

Published April 1, 1981 - More info

Published in Volume 67, Issue 4 on April 1, 1981
J Clin Invest. 1981;67(4):1047–1055. https://doi.org/10.1172/JCI110116.
© 1981 The American Society for Clinical Investigation
Published April 1, 1981 - Version history
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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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