Effects of Adenosine on Local Stimulus‐Response Latency and Induction of Atrial Fibrillation by Premature Stimuli

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Abstract
Premature atrial stimuli delivered during the relative refractory or “vulnerable” period exhibit increased local stimulus‐response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23 ± 5 to 11 ± 3 ms, P < 0.01), to values similar to S1 latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P < 0.05). Adenosine had no effect on S1 latency (9 ± 2 vs 9 ± 2 ms) but decreased monophasic action potential duration from 202 ± 37 to 158 ± 38 ms (P < 0.01). Adenosine was also given to 10 patients S2 introduced at a coupling interval 40–50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than S1 latency (21 ± 12 vs 9 ± 2 ms, P < 0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus–response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine‐mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.