Volume 17, Issue 4 pp. 585-589
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Effect of Pacing Site on the Atrial Electrogram at Target Sites for Slow Pathway Ablation in Patients with Atrioventricular Nodal Reentrant Tachycardia

JOHN HUMMEL

Corresponding Author

JOHN HUMMEL

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

Address for reprints: John Hummel, M.D., University of Michigan Medical Center, Division of Cardiology, 1500 East Medicial Center Drive, Ann Arbor, MI 48109–0022. Fax: (313) 763-7390.Search for more papers by this author
S. ADAM STRICKBERGER

S. ADAM STRICKBERGER

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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STEVEN KALBELEISCH

STEVEN KALBELEISCH

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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BRIAN WILLIAMSON

BRIAN WILLIAMSON

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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K. CHING MAN

K. CHING MAN

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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VICKEN VORPERIAN

VICKEN VORPERIAN

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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ERED MORADY

ERED MORADY

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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JONATHAN LANGBERG

JONATHAN LANGBERG

Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Michigan

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First published: April 1994
Citations: 4

Abstract

Atrial electrograms recorded from target sites during radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway are often fractionated and may be associated with a late, high frequency component (the slow pathway potential). The purpose of the current study was to assess the effects of slow pathway ablation on the morphology of the atrial electrogram and to determine whether target site electrograms display direction dependent changes in morphology during atrial pacing maneuvers. Twenty-six patients with typical AV nodal reentry had electrograms recorded from target sites before and after successful ablation of the slow A V nodal path way and during pacing from the high right atrium and distal coronary sin us at cycle lengths of 500 and 300 msec. There was no significant change in the duration or degree of fractionation of the atrial electrogram as the result of slow pathway ablation. In contrast, the duration and degree of fractionation were less when pacing from the coronary sinus compared with sinus rhythms or right atrial pacing. Pacing rate did not affect electrogram morphology. These data suggest that the morphology of the slow pathway target site electrogram is dependent on the direction of atrial activation and that the “slow pathway potential” does not represent activation of an anatomically discrete pathway.

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