QT interval prolongation is a risk factor in a number of cardiovascular as
well as non-cardiovascular diseases. Apart from this, abnormal, i.e. excess
ive, QT prolongation is typical for patients with acquired as well as conge
nital long QT syndrome. In these syndromes, prolongation of repolarization
is often associated with severe, potentially life-threatening, ventricular
tachyarrhythmias of the type torsade de pointes (TdP). While the congenital
long QT syndrome has recently been identified as an ion channelopathy, the
mechanisms underlying acquired long QT syndrome, which is most often induc
ed by drugs prolonging myocardial repolarization, are far from understood.
Recent studies have yielded only a small number of individual cases in whom
the clinical setting has suggested an acquired form of the syndrome and ge
netic analysis revealed a familial form.
In order to prevent an unwanted exposure to risk, physicians prescribing ag
ents that may prolong repolarization need to be aware of their potential to
cause excessive QT prolongation and TdP. A clearer delineation of the fact
ors predisposing to abnormal prolongation of repolarization and TdP, and a
more precise quantification of the torsadogenic potency of individual drugs
appear mandatory in order to prevent, or at least minimize, the incidence
of this potentially fatal adverse effect of certain drugs. (Eur Heart J Sup
plements 2001; 3 (Suppl K): K81-K88) (C) 2001 The European Society of Cardi
ology.