Role of Drugs in Torsade de Pointes and Triggered Activity

Abstract

Although most of the characteristic diagnostic features of ventricular tachyarrhythmias of the torsade de pointes (TDP) type (Table 1) have already been published almost 30 years ago [70, 71,194, 202, 203, 215], the arrhythmia itself, the pathophysiological and clinical circumstances of its manifestations as well as its mechanism are still a matter of discussion and debate [63, 107, 132, 139, 162, 179, 243]. TDP (Fig. 1) is a particular form of a potentially life threatening ventricular tachyarrhythmia which almost exclusively occurs in the setting of abnormal repolarization (i. e. QT prolongation, presence of U waves, QTU alternans). The association between abnormal repolarization and TDP (long QT interval syndrome, LQTS) has been subclassified into idiopathic and acquired forms. The idiopathic forms (Jervell and Lange-Nielsen syndrome [120], Romano-Ward syndrome [185, 250]) may present with a familial pattern in children and young adults. The sporadic occurrence of the syndrome without a familial pattern has also been described [197]. In contrast, the acquired form usually occurs in older patients after administration of drugs or other inverventions and circumstances capable of prolonging the QT interval and inducing repolarization abnormalities [24, 107, 116, 184]. The incidence of TDP in patients treated with quinidine ranges between o.5% and 8.8% [20, 123, 128, 176, 182]. A 1.4%–4.5% incidence of TDP has been reported during treatment with the class III antiarrhythmic agent sotalol [146].