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Research Article Free access | 10.1172/JCI113307

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

R Mahmud, S T Denker, P J Tchou, M Jazayeri, and M Akhtar

Natalie and Norman Soref & Family Electrophysiology Laboratory, University of Wisconsin, Milwaukee 53233.

Find articles by Mahmud, R. in: PubMed | Google Scholar

Natalie and Norman Soref & Family Electrophysiology Laboratory, University of Wisconsin, Milwaukee 53233.

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Natalie and Norman Soref & Family Electrophysiology Laboratory, University of Wisconsin, Milwaukee 53233.

Find articles by Tchou, P. in: PubMed | Google Scholar

Natalie and Norman Soref & Family Electrophysiology Laboratory, University of Wisconsin, Milwaukee 53233.

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Natalie and Norman Soref & Family Electrophysiology Laboratory, University of Wisconsin, Milwaukee 53233.

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Published January 1, 1988 - More info

Published in Volume 81, Issue 1 on January 1, 1988
J Clin Invest. 1988;81(1):39–46. https://doi.org/10.1172/JCI113307.
© 1988 The American Society for Clinical Investigation
Published January 1, 1988 - Version history
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Abstract

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

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