Journal of Interventional Cardiac Electrophysiology 4, 231±239(2000) #2000 Kluwer Academic Publishers. Manufactured in The Netherlands. Conduction Time Oscillations Precede the Spontaneous Termination of Human Atrioventricular Reciprocating Tachycardia Derek V. Exner MD, MPH, L. Brent Mitchell MD, D. George Wyse MD, Ph.D., Robert S. Sheldon MD, Ph.D., Anne M. Gillis MD, Peggy Cassidy BN, and Henry J. Duff MD Department of Medicine, Division of Cardiology, University of Calgary, Canada Abstract. Prior clinical research indicates that conduc- tion slowing is the primary mechanism leading to the spontaneous termination of reentrant tachycardia in humans. Yet, some experimental models indicate that cycle length oscillations and enhanced conduction are important prerequisites. The role of oscillations in conduction times and enhanced conduction in the spontaneous termination of human reentrant tachycar- dia has not been adequately investigated. The electrophysiologic features preceding the spon- taneous termination of orthodromic atrioventricular (AV) reciprocating tachycardia (RT) were evaluated in 21 patients, each of whom had a sustained (> 60 seconds) and a spontaneously terminating ( 10 beats and  60 seconds) episode of AVRT during the same electrophysiologic study. Atrio-His, His-ventricular, interventricular, ventriculoatrial and atrial conduc- tion times were measured for each beat of sponta- neously terminating AVRT and for paired beats of sustained AVRT. Beats of spontaneously terminating and sustained tachycardia were pooled and Hadi multi- variate outlier analysis was used to identify whether signi®cant beat-to-beat alterations in conduction times preceded the spontaneous termination of reentry. Cycle lengths of sustained (348  62 msec) and spon- taneously terminating AVRT (351  70 msec) were simi- lar. Signi®cant beat-to-beat oscillations in conduction times preceded the spontaneous termination of AVRT in 10 of the 21 (48%) patients. An apparent enhance- ment in atrio-His or ventriculoatrial conduction times immediately preceded the spontaneous termination of AVRT in 11 patients (52%), while an apparent conduc- tion delay occurred in only 2 patients (10%). Moreover, signi®cant oscillations in conduction times were present in 9 of the 11 patients (82%) with enhanced conduction, but only in 1 of the 10 (10%) remaining patients (p  0:002). Conduction time oscillations, which are related to apparent enhancement in atrio-His or ventriculoatrial conduction, frequently precede the spontaneous termi- nation of reentry in humans. Key Words. accessory pathway, reentry, Wolff- Parkinson-White Syndrome Introduction Orthodromic atrioventricular (AV) reciprocating tachycardia (RT) provides a unique opportunity to study reentrant arrhythmias in humans. This macroscopic, anatomically discrete circuit is composed of an anterograde limb, with atrio-His and His-ventricular components, and a retro- grade limb with interventricular, ventriculoatrial and atrial components. Evaluation of beat-to-beat changes in conduction times within this circuit may provide insight into the mechanisms asso- ciated with the spontaneous termination of AVRT and other human reentrant tachycardias. Prerequisites for the initiation of reentry are well described [1,2]. Once initiated, maintenance of reentry depends on a delicate balance between conduction times and refractoriness of all tissues within the reentrant circuit [3]. Thus, alterations in conduction times and=or refractoriness might be anticipated to lead to the spontaneous termi- nation of reentry. A number of investigators have reported the spontaneous termination of human AVRT due to atrial or ventricular premature beats [4], AV node reentry [5], an abrupt shift in AV nodal conduc- tion [6,7], concealed penetration in the AV node [8] or alterations in sympathetic tone [9]. More- over, a larger series identi®ed that conduction slowing commonly precedes the spontaneous 231 Address for correspondence: Derek V. Exner, MD, Cardiovas- cular Research Group, University of Calgary, 3330 Hospital Drive NM, Calgary, AB Canada T2N 4N1. Phone (403) 220- 6889; Fax (403) 270-0313; E-mail: Exner@ucalgary.ca Dr. Exner is supported by the Medical Research Council of Canada. Drs.' Exner, Gillis and Duff are supported by the Alberta Heritage Foundation for Medical Research. Received 21 June 1999; accepted 2 December 1999