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(Circulation. 2002;106:814.)
© 2002 American Heart Association, Inc.

Clinical Investigation and Reports

Electrophysiological Response of the Right Atrium to Ibutilide During Typical Atrial Flutter

Jie Cheng, MD, PhD; Kathryn Glatter, MD; Yanfei Yang, MD; Shulong Zhang, MD; Randall Lee, MD; Melvin M. Scheinman, MD

From the Section of Cardiac Electrophysiology, University of California San Francisco, San Francisco, Calif. Dr Cheng is presently with Michigan State University, College of Human Medicine, East Lansing, Mich.

Correspondence to Melvin M. Scheinman, MD, Cardiac Electrophysiology UCSF, 500 Parnassus Ave, MU East 4S, Box 1354, San Francisco, CA 94143-1354. E-mail scheinman{at}ep4.ucsf.edu

Background— The efficacy of ibutilide in conversion of atrial fibrillation and flutter (AFL) has been demonstrated. However, its electrophysiological effects on human atria have not been fully studied.

Methods and Results— Twelve patients with typical AFL were studied. Electrograms were recorded from the anterolateral right atrium, His bundle position, and coronary sinus. During AFL, we measured the conduction time, CTi, through the isthmus between the tricuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the right atrium. Resetting response curves and atrial effective refractory periods were determined with single extrastimuli delivered in the tricuspid annulus–eustachian ridge isthmus. After infusion of ibutilide (2 mg over 15 minutes), AFL cycle length (CL) increased from 260±30 to 295±39 ms (P<0.0003) because of an increase in either CTi, CTni, or both. Effective refractory periods increased from 149±16 to 208±26 ms (P<0.001). AFL CL variability increased, with a rightward shift of the resetting response curves and loss of full excitability. In 8 patients, AFL was terminated by atrial overdrive pacing after ibutilide at CLs equal to or longer than those that were not effective at baseline, which was caused by orthodromic block in the tricuspid annulus–eustachian ridge isthmus or was associated with development of transient rapid rhythms around newly formed sites of intra-atrial conduction block.

Conclusions— Ibutilide causes prolongation of AFL CL and increased CL variability by abolishment of a fully excitable gap. Ibutilide may facilitate pace termination of AFL by development of new short-lived reentry around functional blocks.

Key Words: atrial flutter • electrophysiology • antiarrhythmic agents

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