Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli

Premature atrial stimuli delivered during the relative refractory or "vulne rable" period exhibit increased local stimulus-response latency and may occ asionally induce atrial arrhythmias. The use of adenosine to treat supraven tricular tachycardias may also provoke atrial arrhythmias. In this study ry e investigated the effects of adenosine on the latency of premature complex es in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential ca theter was used for recording in the right atrium and introducing premature stimuli (S-2) at twice diastolic threshold after eight paced (S-1) complex es. At short coupling intervals, S-2 latency increased relative to S-1 late ncy. S-2 was delivered repeatedly at a fixed coupling interval (producing m aximal local response latency) and adenosine (6 mg) was given intravenously . Adenosine decreased St latency significantly (23 +/- 5 to 11 +/- 3 ms, P < 0.01), to values similar to S-1 latency. However, despite the decrease in S-2 latency, the combination of adenosine and S-2 more often resulted in t ransient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P < 0.05). Adenosine had no effect on S-1 latency (9 +/- 2 vs 9 +/- 2 ms) but decreased monophasic action potential duration from 202 +/- 3 7 to 258 +/- 38 ms (P < 0.02). Adenosine was also given to 10 patients with S-2 introduced at a coupling interval 40-50 ms less than the baseline effe ctive refractory period, This resulted in a decrease in atrial refractorine ss and capture of S-2 in all cases. Latency for S-2 was significantly great er than S-1 latency (21 +/- 12 vs 9 +/- ms, P < 0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S-2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreas ed latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potent ial duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S-2 falling within the relative refractory period at the site of stimulati on.