TY - JOUR
T1 - Recurrent ventricular tachycardia in man
T2 - Evaluation of disopyramide therapy by intracardiac electrical stimulation
AU - Benditt, D. G.
AU - Pritchett, E. L C
AU - Wallace, A. G.
AU - Gallagher, J. J.
PY - 1979/1/1
Y1 - 1979/1/1
N2 - Effectiveness of disopyramide phosphate therapy was examined on 12 patients with recurrent ventricular tachycardia (VT) resistant to standard antiarrhythmic agents. Prior to initiation of treatment with disopyramide, a control electrophysiological study demonstrated that reproducible initiation of VT was possible in 10/12 patients by programmed intracardiac electrical stimulation. In 1 other patient frequent episodes of VT were induced only once. In 8/12 patients the effects of intravenously administered disopyramide on VT were examined during the study. VT slowed in 6/8 patients, accelerated in 1 patient and was unchanged in 1. 5 patients tolerated VT sufficiently to undergo drug infusion during ongoing arrhythmia, and in 4/5 patients tachycardia was terminated. Subsequently successive dose levels of disopyramide were administered orally to all 12 patients. In 7/10 patients with reproducible VT in the laboratory, drug effectiveness was tested at 2 or more oral drug levels by attempting to reinduce arrhythmia using intracardiac stimulation. In 3 patients only 1 restudy was carried out during oral treatment. During follow-up (18±9 mth), 4/5 patients in whom disopyramide therapy prevented reinduction of VT in the laboratory remain arrhythmia-free, while 1 patient had a single recurrence. Of 6 patients in whom prevention of induced VT was not demonstrated, 1 is arrhythmia free, 3 had recurrence and 2 died. In 1 patient disopyramide failed to control VT in-hospital, and this patient died.
AB - Effectiveness of disopyramide phosphate therapy was examined on 12 patients with recurrent ventricular tachycardia (VT) resistant to standard antiarrhythmic agents. Prior to initiation of treatment with disopyramide, a control electrophysiological study demonstrated that reproducible initiation of VT was possible in 10/12 patients by programmed intracardiac electrical stimulation. In 1 other patient frequent episodes of VT were induced only once. In 8/12 patients the effects of intravenously administered disopyramide on VT were examined during the study. VT slowed in 6/8 patients, accelerated in 1 patient and was unchanged in 1. 5 patients tolerated VT sufficiently to undergo drug infusion during ongoing arrhythmia, and in 4/5 patients tachycardia was terminated. Subsequently successive dose levels of disopyramide were administered orally to all 12 patients. In 7/10 patients with reproducible VT in the laboratory, drug effectiveness was tested at 2 or more oral drug levels by attempting to reinduce arrhythmia using intracardiac stimulation. In 3 patients only 1 restudy was carried out during oral treatment. During follow-up (18±9 mth), 4/5 patients in whom disopyramide therapy prevented reinduction of VT in the laboratory remain arrhythmia-free, while 1 patient had a single recurrence. Of 6 patients in whom prevention of induced VT was not demonstrated, 1 is arrhythmia free, 3 had recurrence and 2 died. In 1 patient disopyramide failed to control VT in-hospital, and this patient died.
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M3 - Article
C2 - 428417
AN - SCOPUS:0018351732
SN - 0301-4711
VL - 9
SP - 255
EP - 276
JO - European journal of cardiology
JF - European journal of cardiology
IS - 4
ER -