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Proarrhythmia in Patients with the Wolff-Parkinson-White Syndrome after Standard Doses of Intravenous Adenosine

Derek V. Exner, MD; Timothy Muzyka, MD; and Anne M. Gillis, MD
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From Foothills Hospital, Calgary, Alberta, Canada; and the Misericordia Hospital, Edmonton, Alberta, Canada. Requests for Reprints: Anne M. Gillis, MD, Department of Medicine, Health Science Centre, University of Calgary, 3330 Hospital Drive Northwest, Calgary, Alberta, T2N 4N1 Canada. Grant Support: In part by the Heart and Stroke Foundation of Alberta, Canada. Dr. Gillis is a scholar of the Alberta Heritage Foundation for Medical Research.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1995;122(5):351-352. doi:10.7326/0003-4819-122-5-199503010-00005
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Adenosine, an endogenous nucleoside, has various effects on the heart and cardiovascular system [1]. Its actions on the heart's conduction system and its ability to terminate re-entrant supraventricular arrhythmias involving the atrioventricular node have been well described [12]. The use of adenosine in the diagnosis and treatment of tachycardias that are not clearly of ventricular origin is now commonplace in many North American emergency departments. Adenosine is considered a safe diagnostic tool for distinguishing between regular wide-complex tachycardias (ventricular compared with aberrant supraventricular), including those seen in the setting of ventricular pre-excitation (the Wolff-Parkinson-White syndrome) [3].

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Figure 1.
Electrocardiographic tracings from patients after administration of 12 mg of adenosine. Top.Bottom.

Electrocardiographic (12-lead) tracing from patient 1. Rhythm strip (modified chest lead VI) from patient 2 immediately after adenosine administration. aVF = augmented V (unipolar lead), left leg; aVL = augmented V (unipolar lead), left arm; aVR = augmented V (unipolar lead), right arm; V1 to 5 = chest leads 1 to 5.

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