Torsade de pointes is a particular form of polymorphic
ventricular tachycardia causing few haemodynamic symptoms, but carries a poor prognosis 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
torsade de pointes by prolonging the QT interval or increasing QT dispersion. For the majority of substances the incidence of
torsade de pointes remains unclear, but is of the order of 3 to 15% for a wide range of agents. Elicitation of proarrhythmia by
drug-induced QT prolongation is mainly based on increased cellular excitability and/or abnormal dispersion of ventricular repolarisation.
Torsade de pointes has been shown to be related to
bradycardia-dependent early after-depolarisations and/or increased dispersion of repolarisation. Clinically, patients with predisposing factors prior to medication should be considered at risk of
drug-mediated proarrhythmia. Typically,
torsade de pointes occurs during the first days of antiarrhythmic
therapy. During this phase, QT interval measurement and assessment of the QTc time should be performed frequently. Phases of
bradycardia or occurrence of ventricular extra beats with a long coupling interval may be of help to identify patients at high risk of proarrhythmic events. As a first attempt in managing this
arrhythmia,
magnesium sulphate has been shown to be effective in many 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 eliminated.