Torsade de pointes is a particular form of polymorphic ventricular tac
hycardia causing few haemodynamic symptoms, but carries a poor prognos
is because of recurrence and sudden death in up to 31% of patients. A
wide range of agents have been shown to aggravate and even to cause to
rsade de pointes by prolonging the QT interval or increasing QT disper
sion. For the majority of substances the incidence of torsade de point
es remains unclear, but is of the order of 3 to 15% for a wide range o
f agents. Elicitation of proarrhythmia by drug-induced QT prolongation
is mainly based on increased cellular excitability and/or abnormal di
spersion of ventricular repolarisation. Torsade de pointes has been sh
own to be related to bradycardia-dependent early after-depolarisations
and/or increased dispersion of repolarisation. Clinically, patients w
ith predisposing factors prior to medication should be considered at r
isk of drug-mediated proarrhythmic therapy. During this phase, QT inte
rval measurement and assessment of the QTc time should be performed fr
equently. Phases of bradycardia or occurrence of ventricular extra bea
ts with a long coupling interval may be of help to identify patients a
t high risk of proarrhythmic events. As a first attempt in managing th
is arrhythmia, magnesium sulphate has been shown to be effective in ma
ny patients. In case of recurrence of torsade de pointes, the use of a
temporary pacemaker with pacing at about 100 to 120 beats/min is the
therapy of choice until the causative agent has been completely elimin
ated.