Circulation, Vol 74, 1037-1043, Copyright © 1986 by American Heart Association
FE Marchlinski, AE Buxton, JM Miller, JA Vassallo, BT Flores and ME Josephson
Induction of rapid ventricular tachycardia or fibrillation during therapy
with amiodarone is associated with an increased risk of sudden death. To
determine whether the addition of a type IA antiarrhythmic agent to therapy
would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a
cycle length less than 350 msec was induced after 14 +/- 2 days of
amiodarone were randomly assigned to therapy with amiodarone alone (group
1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients).
Type IA therapy consisted of procainamide in 13 patients and quinidine in
four procainamide-intolerant patients. To assess the short-term effects of
a type IA agent on inducibility of ventricular tachyarrhythmia, cycle
length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all
patients in group 2 underwent repeat programmed stimulation after the
intravenous administration of procainamide during amiodarone therapy (mean
procainamide serum concentration 7.2 +/- 2.0 micrograms/ml). Procainamide
prevented induction of sustained arrhythmia in only two of 33 patients.
Procainamide increased the cycle length of induced ventricular tachycardia
from 283 +/- 30 to 352 +/- 46 msec (p less than .001). After the addition
of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone
had an induced arrhythmia that was tolerated hemodynamically (p less than
.05). There were no differences between groups 1 and 2 with respect to
patient or arrhythmia characteristics, response to short-term procainamide,
or duration of follow-up. The mean follow-up for all patients was 14 +/- 10
months.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Amiodarone versus amiodarone and a type IA agent for treatment of patients with rapid ventricular tachycardia
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