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Effects of Adenosine on Local Stimulus‐Response Latency and Induction of Atrial Fibrillation by Premature Stimuli
Author(s) -
CORBISIERO RAFFAELE,
KABELL GLENN,
COOK JAMES R.,
FITZGERALD THOMAS F.,
KIRCHHOFFER JAMES B.
Publication year - 1999
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1999.tb00632.x
Subject(s) - medicine , adenosine , atrial fibrillation , refractory period , stimulus (psychology) , cardiology , latency (audio) , anesthesia , effective refractory period , psychology , electrical engineering , psychotherapist , engineering
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 (S 2 ) at twice diastolic threshold after eight paced (S 1 ) complexes. At short coupling intervals, S 2 latency increased relative to S 1 latency. S 2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S 2 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 transient 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 ± 37 to 158 ± 38 ms (P < 0.01). Adenosine was also given to 10 patients S 2 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 S 2 in all cases. Latency for S 2 was significantly greater than S 1 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 S 2 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 S 2 falling within the relative refractory period at the site of stimulation.