Petersen H H, Sandøe E
Medicinsk afdeling B, Rigshospitalet, Kobenhavn.
Ugeskr Laeger. 1996 May 6;158(19):2711-6.
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.
索他洛尔与胺碘酮一样,是最有效的抗心律失常药物。与I类抗心律失常药物相比,它的死亡率更低。然而,索他洛尔与IA类抗心律失常药物一样,可因促心律失常作用或过量用药引发危及生命的尖端扭转型室性心动过速(TdP-VT)发作。在所有接受索他洛尔治疗的患者中,TdP-VT的发生率为2%。在接受室性心动过速治疗的患者中,TdP-VT的发生率为4%。一些因素会增加TdP-VT的发生率:左心室功能降低、低钾血症、低镁血症、心动过缓、QT间期延长以及每日剂量超过320毫克。我们建议对这些诱发因素予以更多关注,以预防TdP-VT。药物诱发的TdP-VT可能会被误诊为“真正的”室性心动过速。这往往会导致索他洛尔剂量增加,从而使TdP-VT恶化。索他洛尔经肾脏排泄,在肾功能减退的患者中,使用正常剂量时也可能出现TdP-VT。QTC延长超过550毫秒或严重心动过缓表明存在TdP-VT风险,应停药或减量。本文介绍了六个病例。