Key result
Intravenous adenosine triphosphate terminated supraventricular wide QRS tachycardia and triggered-activity ventricular tachycardia, but had no effect on pre-excited atrial fibrillation or flutter, or reentry ventricular tachycardia.
Why the study?
Does intravenous adenosine triphosphate terminate wide QRS tachycardia in patients with QRS width > 120 msec and rate >= 150 beats/min?
Observational (n=18)
No
Does intravenous adenosine triphosphate terminate wide QRS tachycardia in patients with QRS width > 120 msec and rate >= 150 beats/min?
ATP is useful for both terminating triggered-activity wide QRS tachycardias and diagnosing their underlying mechanisms.
May aid termination of triggered wide QRS tachycardias in select cases; hypothesis-generating for mechanism diagnosis, needs validation.
A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.
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Hina et al. (1996) conducted an observational in Wide QRS tachycardia (n=18). Adenosine Triphosphate (ATP) was evaluated on Termination of tachycardia. Intravenous adenosine triphosphate terminated supraventricular wide QRS tachycardia and triggered-activity ventricular tachycardia, but had no effect on pre-excited atrial fibrillation or flutter, or reentry ventricular tachycardia.
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