Current concepts in the mechanisms and management of drug-induced QT prolongation and torsade de pointes

被引：259

作者：

Gupta, Akshay ^{[1
]}

Lawrence, Andrew T. ^{[1
]}

Krishnan, Kousik ^{[1
]}

Kavinsky, Clifford J. ^{[1
]}

Trohman, Richard G. ^{[1
]}

机构：

[1] Rush Univ, Med Ctr, Arrhythmia & Pacemaker Serv, Dept Internal Med,Sect Cardiol, Chicago, IL 60612 USA

来源：

AMERICAN HEART JOURNAL | 2007年 / 153卷 / 06期

关键词：

D O I：

10.1016/j.ahj.2007.01.040

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Drug-induced long QT syndrome is characterized by a prolonged corrected QT interval (QTc) and increased risk of a polymorphic ventricular tachycardia known as torsade de pointes (TdP). We review mechanisms, predispositions, culprit agents, and management of this potentially fatal phenomenon. Virtually all drugs that prolong QTc block the rapid component of the delayed rectifier current (I-kr). Some drugs prolong QTc in a dose-dependent manner, others do so at any dose. Most patients that develop drug-induced TdP have underlying risk factors. Female sex is the most common. Implicated drugs include class 1A and III antiarrhythmics, macrolide antibiotics, pentamidine, antimalarials, antipsychotics, arsenic trioxide, and methadone. Treatment for TdP includes immediate defibrillation for hemodynamic instability and intravenous magnesium sulfate. Potassium levels should be maintained in the high normal range, and all QT prolonging agents must be promptly discontinued.

引用

页码：891 / 899

页数：9

共 97 条

[1] MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia [J].