Electrophysiologic studies [3, 4] in patients with the Wolff-Parkinson-White syndrome have suggested that the risk that adenosine will cause hemodynamic compromise or that atrial flutter or atrial fibrillation will convert to ventricular fibrillation is small. We describe two patients with the Wolff-Parkinson-White syndrome who had hemodynamically unstable proarrhythmia after the administration of standard doses of adenosine.

Case Reports

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Patient 1

A 43-year-old man had intermittent, brief episodes of regular palpitations for 12 years. He had not previously sought medical attention or undergone electrocardiographic study. He was otherwise healthy and was not receiving any medications. The morning of presentation he awoke with palpitations and the sensation of a heavy chest. According to physicians' notes, when he arrived at our emergency department, the monitor showed a regular wide-complex rhythm at 200 beats/min and a blood pressure of 140/90 mm Hg. The initial diagnosis was supraventricular tachycardia, and a 6-mg bolus of intravenous adenosine was given without any effect. A 12-mg bolus of adenosine was then administered, resulting in presyncope, an increase in heart rate to 280 beats/min, and a decrease in blood pressure to 90/40 mm Hg. Because a 12-lead electrocardiogram was immediately available, prompt intervention was not delayed.

Electrocardiographic results showed atrial fibrillation with ventricular pre-excitation (Figure 1, top), and the patient was electrically cardioverted to sinus rhythm and given intravenous procainamide. His physical examination was normal, and his electrocardiogram in sinus rhythm showed ventricular pre-excitation. An electrophysiologic study confirmed the presence of a left lateral accessory pathway. Atrial fibrillation induced during the study was associated with a rapid ventricular response (260 beats/min) and with syncope requiring electrical cardioversion. The accessory pathway was subsequently ablated without complication.

View larger version (38K): [in this window] [in a new window]   Figure 1. Electrocardiographic tracings from patients after administration of 12 mg of adenosine. Top. Electrocardiographic (12-lead) tracing from patient 1. Bottom. 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.

Patient 2

His electrocardiogram showed an irregular wide-complex tachycardia not recognized as atrial fibrillation with accessory pathway conduction. He was given 6 mg of intravenous adenosine without any effect. While the Valsalva maneuver was being done, he was given a 12-mg bolus of adenosine. Ventricular fibrillation developed immediately (Figure 1, bottom). He was defibrillated and treated with intravenous procainamide. His physical examination was normal. He was subsequently referred to our center for an ablation procedure.

Discussion

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These cases highlight the potential danger associated with the use of standard doses of adenosine in patients with the Wolff-Parkinson-White syndrome. Acceleration of atrial flutter in patients without the syndrome has been recently reported in a middle-aged man with no underlying structural heart disease after he received 6 mg of adenosine [5] and in a child with congenital heart disease [6] who received 28 mg of adenosine. Another patient with the Wolff-Parkinson-White syndrome who was receiving flecainide therapy had acceleration of atrial flutter with resultant hemodynamic compromise after receiving 50 mg of adenosine [7].

The reason our patients were adversely affected by standard doses of adenosine is probably multifactorial. At electrophysiologic study, both patients had atrial fibrillation with rapid ventricular responses. Our second patient was clearly having atrial fibrillation at the time of hemodynamic compromise, whereas our first patient had accelerated arrhythmia that was subsequently identified as atrial fibrillation. Adenosine blocks the atrioventricular node while accelerating conduction through the accessory pathway; this probably caused the observed hemodynamic deterioration [3, 4]. Recent research [8] has also shown that standard doses of adenosine result in shortening of atrial refractoriness and a predisposition toward atrial fibrillation.

Adenosine has been advocated as a safe and effective treatment of tachyarrhythmias in patients with the Wolff-Parkinson-White syndrome in various settings, including pregnancy [9]. However, as shown in patient 2, even transient atrioventricular block can precipitate ventricular fibrillation in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation. These cases also show that atrial fibrillation may not be recognized when ventricular rates are rapid. Intravenous procainamide or synchronized electrical cardioversion remains the treatment of choice for the short-term management of patients with wide QRS complex tachycardias in the setting of known or suspected ventricular pre-excitation [10].