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[Sotalol and torsades de pointes ventricular tachycardia].

H H Petersen, Erik Sandøe

Open publisher page 2 citations

Abstract

Sotalol is together with amiodarone the most effective antiarrhythmic. Compared to class I antiarrhythmics it has less mortality. However, sotalol can, like class IA antiarrhythmics, release life-threatening attacks of torsade de pointes ventricular tachycardia (TdP-VT), as proarrhythmia or by overdosing. TdP-VT appears in 2% of all patients treated with sotalol. In patients treated for ventricular tachycardias TdP-VT appears in 4%. Some factors increase the incidence of TdP-VT: reduced left ventricular function, hypokalaemia, hypomagnesiaemia, bradycardia, extended QT-interval and daily doses exceeding 320 mg. We recommend increased attention to these predisposing factors so as to prevent TdP-VT. Pharmacologically induced TdP-VT may be misdiagnosed as "genuine" ventricular tachycardia. This often results in increased doses of sotalol, which worsen the TdP-VT. Sotalol is renally excreted and TdP-VT can appear in patients with reduced renal function where normal doses are used. QTC prolongation above 550 ms. or severe bradycardia indicates risk of TdP-VT and should result in end of treatment or dose-reduction. Six case-stories are presented.

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What this paper is about

Sotalol is together with amiodarone the most effective antiarrhythmic. Compared to class I antiarrhythmics it has less mortality. However, sotalol can, like class IA antiarrhythmics, release life-threatening attacks of torsade de pointes ventricular tachycardia (TdP-VT), as proarrhythmia or by overdosing. TdP-VT appears in 2% of all patients treated with sotalol. In patients treated for ventricular tachycardias TdP-VT appears in 4%. Some factors increase the incidence of TdP-VT: reduced left ventricular function, hypokalaemia, hypomagnesiaemia, bradycardia, extended QT-interval and daily doses exceeding 320 mg. We recommend increased attention to these predisposing factors so as to prevent TdP-VT. Pharmacologically induced TdP-VT may be misdiagnosed as "genuine" ventricular tachycardia. This often results in increased doses of sotalol, which worsen the TdP-VT. Sotalol is renally excreted and TdP-VT can appear in patients with reduced renal function where normal doses are used. QTC prolongation above 550 ms. or severe bradycardia indicates risk of TdP-VT and should result in end of treatment or dose-reduction. Six case-stories are presented.

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Available abstract

Sotalol is together with amiodarone the most effective antiarrhythmic. Compared to class I antiarrhythmics it has less mortality. However, sotalol can, like class IA antiarrhythmics, release life-threatening attacks of torsade de pointes ventricular tachycardia (TdP-VT), as proarrhythmia or by overdosing. TdP-VT appears in 2% of all patients treated with sotalol. In patients treated for ventricular tachycardias TdP-VT appears in 4%. Some factors increase the incidence of TdP-VT: reduced left ventricular function, hypokalaemia, hypomagnesiaemia, bradycardia, extended QT-interval and daily doses exceeding 320 mg. We recommend increased attention to these predisposing factors so as to prevent TdP-VT. Pharmacologically induced TdP-VT may be misdiagnosed as "genuine" ventricular tachycardia. This often results in increased doses of sotalol, which worsen the TdP-VT. Sotalol is renally excreted and TdP-VT can appear in patients with reduced renal function where normal doses are used. QTC prolongation above 550 ms. or severe bradycardia indicates risk of TdP-VT and should result in end of treatment or dose-reduction. Six case-stories are presented.

Key concepts: Sotalol, Proarrhythmia, Torsades de pointes, Medicine, Amiodarone, Ventricular tachycardia, Cardiology, QT interval

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