[Acquired long QT syndrome: a dominant problem?]

QT prolongation is essentially of pharmacologic origin. It is principally linked to a block of the outward potassium current Ikr, with as a consequence a prolongation of the repolarisation causing early after potentials and re-entry. The term "repolarisation reserve" expresses the variable risk of arrhythmia among individuals under the same drug blocking Ikr. This reserve can be altered under various pathologic or genetic conditions. A series of risk factors (bradycar-Torsades de pointes} were described in 1966 by Dessertenne. They are due to a perturbation of ventricular repolarisation causing QT prolongation on surface ECG. Acquired dia, electrolytic disorders, cardiac disease, neurologic disorders, nutrition troubles, female gender) can play a role as well as the metabolic processing of pharmacological agents by Cytochrome P450 and various inhibitors or inductors of this system which can influence the half life of drugs. The list of drugs involved is continuously increasing: antiarrhythmics, antihistamines, psychotropics, anti-infectious are the main categories involved. Risk prediction is difficult particularly for non cardiovascular drugs and a low risk incidence. An other risk is to exclude patients from the benefit of an efficient drug for a serious but not frequent risk, at last an industrial risk for the manufacturer when a drug is withdrawn lately when important quantities of money have already been invested for its development. The diagnosis of torsades is easy on standard ECG although QT measurement and its heart rate variation remain uneasy. The treatment of the arrhythmias is based on heart rate acceleration by Isoprenaline or intravenous pacing and on intravenous administration of magnesium.