In patients with malignant ventricular anrhythmias, antiarrhythmic the
rapy is known to carry a substantial risk of proarrhythmia. This risk
is usually considered to be low when supraventricular arrhythmias or b
enign ventricular arrhythmias are considered. We were able to collect
data on four patients without a history of life-threatening arrhythmia
s, in whom anti-arrhythmic therapy was used and resulted in documented
ventricular fibrillation or torsade de pointes. In Cases No. 1 and 2,
atrial fibrillation was treated with either quinidine or quinidine an
d sotalol in combination. In both patients Holter monitoring, 4-12 h a
fter conversion to sinus rhythm, documented the spontaneous occurrence
of torsade de pointes degenerating into ventricular fibrillation and
requiring DC shock for termination. In Case No. 3, atrial fibrillation
was treated with sotalol and amiodarone for 2 months when incessant e
pisodes of torsade de pointes were documented. In Case No. 4, frequent
but unsustained ventricular arrhythmias were treated with amiodarone
in a patient suffering dilative cardiomyopathy After 6 days of treatme
nt at a heart rate of 54 beats/min, a marked QT increase was associate
d with the occurrence of repetitive episodes of polymorphic ventricula
r tachycardia degenerating into ventricular fibrillation. None of the
patients presented significant electrolyte abnormalities in the labora
tory. A pathologic increase of the QTc-time was documented in Cases No
. 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn af
ter the proarrhythmic event and the patient became free of malignant t
achyarrhythmias. Antiarrhythmic therapy also carries a considerable ri
sk of proarrhythmia when ''benign'' cardiac arrhythmias are treated. T
he risk seems to be lower than in patients with malignant arrhythmias,
however it includes the occurrence of lethal tachyarrhythmias. Specia
l attention should be paid to the selection of antiarrhythmic agents w
hen used in combination.