From the Division of Cardiology, Department of Medicine, National
Yang-Ming University School of Medicine (S.-H.L.), and Veterans General
Hospital-Taipei, Taipei, Taiwan.
Correspondence to Shih-Ann Chen, MD, Division of Cardiology, Veterans General Hospital-Taipei, 201 Sec 2, Shih-Pai Rd, Taipei, Taiwan. E-mail sachen{at}vghtpe.gov.tw
Background—Atrial fibrillation (AF)
has been shown to shorten the atrial effective refractory period (ERP)
and make the atrium more vulnerable to AF. This study investigated the
effect of atrial rate and antiarrhythmic drugs on ERP shortening
induced by tachycardia.
Methods and Results—Seventy adult patients without structural
heart disease were included. For the first part of the study, right
atrial ERP was measured with a drive cycle length of 500 ms before and
after 10 minutes of rapid atrial pacing using five pacing cycle lengths
(450, 400, 350, 300, and 250 ms) in 10 patients. For the second part of
the study, the remaining 60 patients were included to study the effects
of antiarrhythmic drugs on changes in atrial ERP induced by AF. Atrial
ERP was measured with a drive cycle of 500 ms before and after an
episode of pacing-induced AF. After the patients were randomized to
receive one of six antiarrhythmic drugs (procainamide,
propafenone, propranolol, dl-sotalol,
amiodarone, and verapamil), atrial ERP was measured
before and after another episode of pacing-induced AF. In the first
part of the study, atrial ERP shortened significantly after 10 minutes
of rapid atrial pacing, and the degree of shortening was correlated
with pacing cycle length. The second part of the study showed that
atrial ERP shortened after conversion of AF (172±15 versus 202±14 ms,
P<0.0001) and that ERP shortening was attenuated after
verapamil infusion (-4.6±1.2% versus -15.1±3.4%,
P<0.001) but was unchanged after infusion of the other
antiarrhythmic drugs. Furthermore, all of these antiarrhythmic drugs
could decrease the incidence and duration of secondary AF.
Conclusions—The atrial ERP shortening induced by
tachycardia was a rate-dependent response.
Verapamil, but not other antiarrhythmic drugs, could
markedly attenuate this effect. However, verapamil and the
other drugs could decrease the incidence and duration of secondary AF.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Tachycardia-Induced Change of Atrial Refractory Period in Humans
Rate Dependency and Effects of Antiarrhythmic Drugs
Key Words: antiarrhythmia agents • atrium • fibrillation • electrophysiology
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