Electrophysiologic Effects of Adenosine in Patients with SVT
ABSTRACT & COMMENTARY
Synopsis: The response to adenosine for tachycardia termination is of only limited value for defining either the mechanism of supraventricular tachycardia or the anatomic location of the arrhythmia in patients with atrial tachycardia.
Source: Glatter KA, et al. Circulation 1999;99: 1034-1040.
In this paper, glatter and colleagues from the electrophysiology section at the University of California-San Francisco report the results of a retrospective analysis of the use of adenosine during electrophysiologic studies for supraventricular tachycardia (SVT) at their institution. Patients with atrial fibrillation, atrial flutter, and automatic junctional tachycardia were not included in the study. Two hundred twenty-nine patients with other forms of supraventricular arrhythmia received adenosine during the period reviewed. The principal diagnoses were as follows: typical AV nodal reentrant tachycardia (AVNRT)—82 patients; atrioventricular reentry (AVRT)—59 patients; atypical AVNRT—13 patients; permanent form of junctional reciprocating tachycardia—12 patients; atrial tachycardia—53 patients; and inappropriate sinus tachycardia—10 patients. Patients received the usual clinical doses of adenosine (6 mg or 12 mg) as a rapid bolus injection via peripheral vein during running tachycardia. Glatter et al then cataloged responses as either tachycardia termination, tachycardia suppression, AV block without effect on tachycardia, or no effect.
All patients with both AVRT and AVNRT had their tachycardias terminated after adenosine. The pattern of termination was somewhat variable. The most common pattern was block during anterograde conduction in the AV node. Block during retrograde conduction and termination of the tachycardia with premature complexes, however, were also seen. The latter was not usually a reproducible finding. Adenosine administration led to initiation of atrial fibrillation in nine of 59 patients with AVRT but in no patient with AVNRT.
In the atypical form of AVNRT, tachycardia termination usually occurred during retrograde conduction over the slow AV nodal pathway, but two tachycardias terminated in the fast pathway. In patients with permanent junctional reciprocating tachycardia (PJRT), three of 11 showed tachycardia termination in the AV node and eight in the retrograde pathway. No patient with atypical AVNRT developed atrial fibrillation, while two of 12 patients with PJRT developed atrial fibrillation. Responses to adenosine during atrial tachycardias were more variable. Fourteen of 24 automatic tachycardias were transiently suppressed by adenosine. Six of 20 tachycardias thought to be either triggered or reentrant were suppressed or terminated by adenosine. Site of origin did not determine response. All 10 patients with inappropriate sinus tachycardia showed an increase in sinus cycle length and three of these also had high-grade AV block. Among the patients with atrial tachycardia whose tachycardias were neither suppressed nor terminated, AV block was the observed response.
Glatter et al conclude that there are multiple possible effects of adenosine in patients with SVT. Therefore, they believe that the response to adenosine for tachycardia termination is of only limited value for defining either the mechanism of the SVT or the anatomic location of the arrhythmia in patients with atrial tachycardia.
Comment by John P. DiMarco, MD, PhD
When adenosine was first introduced, it was hoped that it might be a highly specific pharmacologic tool for evaluating the mechanisms of various arrhythmias. In supraventricular tissues, adenosine’s primary effect is to increase the outward potassium current, which leads to hyperpolarization of the atrial cell, shortening of the atrial refractory period, and block of AV nodal conduction. In addition, adenosine has indirect anti-adrenergic effects to lower the intracellular levels of cyclic AMP produced in response to beta adrenergic stimulation.
During its development, it was hoped that since adenosine had such a short period of effect after intravenous injection, it could provide a specific probe for differentiating the mechanisms of arrhythmias. As shown by Glatter et al, there are significant limitations to the diagnostic uses of adenosine due to heterogeneity in both the substrate for arrhythmias and multiple effects of the agent itself.
Adenosine will continue to have some diagnostic role. Its diagnostic value will be most valuable in those situations where it produces a definite change. Increase in pre-excitation due to AV nodal block and production of AV block during ongoing tachycardia will continue to be useful diagnostic findings. Occasionally, it can be useful in patients with wide complex tachycardia in whom a supraventricular mechanism is strongly suspected. In most other situations, responses to adenosine will only provide mechanistic information of limited value.
It is also important to remember that use of adenosine is not without hazards. Glatter et al report a significant incidence of atrial fibrillation after adenosine injection. It appears that the incidence of atrial fibrillation is higher when it is administered during electrophysiologic studies than during clinical use, but other clinical reports of atrial fibrillation during treatment of SVT have appeared. Other potential pro-arrhythmic effects of adenosine include AV block and production of bradycardia-dependent polymorphic ventricular tachycardia under appropriate circumstances. Therefore, anyone planning to use adenosine infusions for diagnostic purposes should be prepared for these consequences and should recognize that the response observed will rarely be definitive.
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