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

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 [1, 2]. 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]. 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 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. Figure 1. Electrocardiographic tracings from patients after administration of 12 mg of adenosine. Top. Bottom. Patient 2 A 23-year-old man had had the Wolff-Parkinson-White syndrome and palpitations since 1988. In 1988, an electrophysiologic study done elsewhere had shown a left posteroseptal accessory pathway and a rapid ventricular response (280 beats/min) after induction of atrial fibrillation. Because ablation procedures were not done at that center in 1988, the patient was discharged and received empiric disopyramide SR (250 mg twice daily). However, he was not compliant with the therapy. While playing basketball, he developed palpitations and was taken to a local emergency department. 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 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].