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尖端扭转型室性心动过速:临床考量

Torsade de pointes: the clinical considerations.

作者信息

Gowda Ramesh M, Khan Ijaz A, Wilbur Sabrina L, Vasavada Balendu C, Sacchi Terrence J

机构信息

Division of Cardiology, Long Island College Hospital, Brooklyn, NY, USA.

出版信息

Int J Cardiol. 2004 Jul;96(1):1-6. doi: 10.1016/j.ijcard.2003.04.055.

Abstract

Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram. Congenital causes of prolonged QT interval occur in individuals with genetic mutations in genes that control expression of potassium and sodium channels and acquired causes are numerous, predominantly drugs causing prolonged QT interval by blockade of potassium channels. Among the drugs, antiarrhythmic agents most notably quinidine, sotalol, dofetilide and ibutilide have the potential to induce the fatal torsade de pointes. Many non-antiarrhythmic drugs can also cause torsade de pointes. Although it is important to distinguish between the congenital and the acquired forms of long QT syndrome as the later can often be reversed by correction of the underlying disorder or discontinuation of the offending drug, both forms are not mutually exclusive. Clinical considerations and management of torsade de pointes are described.

摘要

尖端扭转型室性心动过速是一种多形性室性心动过速,发生于体表心电图QT间期延长的情况下。QT间期延长的先天性原因见于控制钾通道和钠通道表达的基因突变个体,获得性原因众多,主要是通过阻断钾通道导致QT间期延长的药物。在这些药物中,抗心律失常药物尤其是奎尼丁、索他洛尔、多非利特和伊布利特具有诱发致命性尖端扭转型室性心动过速的可能性。许多非抗心律失常药物也可导致尖端扭转型室性心动过速。虽然区分先天性和获得性长QT综合征很重要,因为后者通常可通过纠正潜在疾病或停用致病药物而逆转,但这两种形式并非相互排斥。本文描述了尖端扭转型室性心动过速的临床考虑因素和管理方法。

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