Abstract
Torsades de pointes associated with the administration of quinidine or other class 1A antiarrhythmic agents, phenothiazines, or tricyclic antidepressants is a very distinctive and unusual ventricular tachyarrhythmia. It occurs in the setting of pronounced QTU interval prolongation and has a characteristic pause-related pattern of initiation [1–6]. The incidence of this arrhythmia does not seem to increase with increasing severity of ventricular disease, and may occur in patients with seemingly normal hearts [6–8]. Similarly, the incidence does not seem to increase with increasing drug dose. Torsades de pointes typically occurs at usual or low doses and serum drug levels [3–5, 9–14], and may occur after months of uncomplicated drug therapy without the appearance of other known inciting factors, such as hypokalemia and hypomagnesemia [5, 6, 15]. Susceptible patients have a high risk of recurrence of this arrhythmia upon exposure to any of the other drugs which broaden the T wave and enhance the U wave [5, 14, 16–21], whereas the majority of patients will not develop torsades de pointes regardless of the number of agents tried.
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© 1987 Martinus Nijhoff Publishers, Dordrecht
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Jackman, W.M., Friday, K.J., Szabo, B., Patterson, E., Aliot, E.M., Lazzara, R. (1987). Drug-induced torsades de pointes: clinical and experimental observations bearing on mechanism. In: Aliot, E., Lazzara, R. (eds) Ventricular Tachycardias. Developments in Cardiovascular Medicine, vol 71. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3323-1_12
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DOI: https://doi.org/10.1007/978-94-009-3323-1_12
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