Torsades de pointes (TdP) is a characteristic polymorphic ventricular arrhythmia associated with delayed ventricular repolarization as evidenced on the surface electrocardiogram by QT interval prolongation. It typically occurs in self-limiting bursts, causing dizziness and syncope, but may occasionally progress to ventricular fibrillation and sudden death. Acquired long QT syndromes are mainly caused by cardiac disease, electrolyte abnormalities or exposure to drugs that block rectifying potassium channels, especially IKr. Management of TdP or marked QT prolongation includes removal or correction of precipitants, including discontinuation of culprit drugs and institution of cardiac monitoring. Electrolyte abnormalities and hypoxia should be corrected, with potassium concentrations maintained in the high normal range. Immediate treatment of TdP is by intravenous administration of magnesium sulphate, terminating prolonged episodes using electrical cardioversion. In refractory cases of recurrent TdP, the arrhythmia can be suppressed by increasing the underlying heart rate using isoproterenol (isoprenaline) or transvenous pacing. Other interventions are rarely needed, but there are case reports of successful use of lidocaine or phenytoin. Anti-arrhythmic drugs that prolong ventricular repolarization should be avoided. Some episodes of TdP could be avoided by careful prescribing of QT prolonging drugs, including an individualized assessment of risks and benefits before use, performing baseline and periodic electrocardiograms and measurement of electrolytes, especially during acute illnesses, using the lowest effective dose for the shortest possible time and avoiding potential drug interactions. These steps are particularly important in those with underlying repolarization abnormalities and those who have previously experienced drug-induced TdP.

Pharmacological treatment of acquired QT prolongation and torsades de pointes.

Some recent clinical studies indicate that hypokalemia is characteristic for acute psychotic patients at the time of emergency admission. As hypokalemia is one of the major causes for prolonged QT interval, it was hypothesized that acute psychotic patients could show prolonged QT interval. Sixty-seven drug-free, acute psychotic patients were evaluated for corrected QT (QTc) interval, as well as demographic and clinical characteristics at the time of emergency admission. The mean QTc interval of psychiatric emergency patients was prolonged, and the mean QTc interval of psychiatric emergency patients was longer than that of psychiatric outpatients ( t =5.20, P P

Prolonged QT interval in acute psychotic patients

One of the most feared potential adverse effects of many drugs is life threatening or fatal arrhythmia--particularly torsade de pointes (TdP) ventricular tachycardia in conjunction with QT prolongation. To fully understand the implications of QT prolongation, it is essential to have an understanding of the ion currents that comprise repolarization and their relation to electrophysiological abnormalities associated with TdP. Also, the QT interval is subject to patient-specific and sometimes idiosyncratic variability. The following questions are addressed: How close is the relationship between QT prolongation and proarrhythmia? How accurately do QT-interval measurements reflect cardiac repolarization? How representative is a single QT measurement with respect to the QT response to a drug? The presumed relationship between the QT interval and myocardial repolarization will be deconstructed, demonstrating that most of the important aspects of repolarization, and subsequent arrhythmogenesis, cannot be understood only through the simple numerical measurement of the QT interval. Repolarization reserve is also discussed. Suggestions for refining the understanding of drug-induced QT prolongation, TdP, and shortcomings of some current definitions are outlined. We speculate on possible future developments in understanding this relationship.

Drug-induced QT prolongation and proarrhythmia: an inevitable link?

Prolongation of the QTc interval on the surface electrocardiogram (ECG) reflects a delay in ventricular repolarization, and, when drug-induced, it is almost always a result of inhibition of the rapid component of the delayed rectifier potassium current (IKr). The other current that is infrequently inhibited is its slow component (IKs). Drug-induced prolongation of the QTc interval, when excessive in the right setting, can be pro-arrhythmic and degenerate into torsade de pointes (TdP), a potentially fatal and unique form of polymorphic ventricular tachycardia. One review in 1993 concluded, “At present, our knowledge base about the relation of the QT interval and torsades de pointes is grossly incomplete” (1). Unfortunately, despite extensive research for more than a decade since, this still remains the case today. It is therefore not surprising that more than any other drug-induced adverse reaction, it has been responsible in recent times for the withdrawal of many drugs from the market.

Interpretation of Clinical ECG Data

QT Interval Revisited —Not Just the Matter of “Interval,” but “Dynamics, Variability and Morphology” Matter!—

Torsades de pointes associated with acquired long QT syndrome: observation of 7 cases.

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Torsades de pointes associated with acquired long QT syndrome: observation of 7 cases.