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Due to the low number of patients with
SQTS, the experience with antiarrhythmic drugs is very limited. Gaita F
et al tested the effect of flecainide, sotalol, ibutilide and
hydroquinidine on the QT interval in seven patients with SQTS.
Flecainide caused a slight prolongation of the QT interval, primarily
due to the prolongation of the QRS complex, whereas sotalol and
ibutilide had no effect on the QT interval. Hydroquinidine caused QT
prolongation, which reached the normal range, varying from 263 +/- 12 ms
to 362 +/- 25 ms. The ST segment, which was almost absent at basal
recording, appeared, while the T-wave, which was tall and peaked,
increased in duration and decreased in amplitude. The ventricular ERP
was prolonged to >200 ms and ventricular fibrillation was no longer
inducible after hydroquinidine administration. We have used propafenone
in two patients with paroxysmal atrial fibrillation without recurrence
of the arrhythmia. We did not see any prolongation of the QT interval
in excess of the widening of the QRS complex6.
More
recent studies in a few patients with SQTS have suggested, that
disopyramide may be a suitable alternative to both quinidine and
propafenone
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