| Abstract
| - QT interval prolongation is a risk factor in a number of cardiovascular as well as non-cardiovascular diseases. Apart from this, abnormal, i.e. excessive, QT prolongation is typical for patients with acquired as well as congenital 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 induced 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 genetic analysis revealed a familial form. In order to prevent an unwanted exposure to risk, physicians prescribing agents that may prolong repolarization need to be aware of their potential to cause excessive QT prolongation and TdP. A clearer delineation of the factors 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.
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