Torsades de pointes: Arrhythmia, syndrome, or chimera? A perspective in the light of the Lambeth Conventions

Abstract

What is torsades de pointes? Is it an arrhythmia or a syndrome? The distinction is critical. In this article I have attempted to explain why this is so. Both from the clinical and nonclinical standpoint, it is of overriding importance that torsades de pointes be amenable to measurement and quantification. This is the fundamental prerequisite for any variable to be of value as an endpoint in an investigation. Measurement and quantification require that a variable has an objective definition that is both inclusive and exclusive. In his seminal work, Dessertenne coined the term torsades de pointes to describe an arrhythmia with unusual features. However, torsades de pointes has been reinterpreted and redefined by Dessertenne's successors. It was originally described as occurring in certain settings (e.g., hypokalemia). However, this has been reinterpreted to mean that a specific set of antecedent conditions (such as hypokalemia) are part of the definition of torsades de pointes. If this is the case, then torsades de pointes is a syndrome, not an arrhythmia. For those more concerned with arrhythmias than with syndromes, the key issue to be determined is what to call the arrhythmia that is part of the syndrome. I have put forward some suggestions with the objective of answering this question, using the Lambeth Conventions as a guide. I believe that there is strong case for ventricular tachyarrhythmias to be classified simply as tachycardia or fibrillation, with the optional use of the term delayed repolarization syndrome in cases where a long QT interval is present. The latter term should be used as one might use the term acute myocardial ischemia, i.e., to denote an underlying condition; it should not be used to define the arrhythmia itself. Twenty-four years after its introduction, the term torsades de pointes has now become a chimera and is best abandoned.

Selective IK blockade as an antiarrhythmic mechanism: effects of UK66,914 on ischaemia and reperfusion arrhythmias in rat and rabbit hearts

“…172.8 ± 14.0 193.6 ± 8.8 232.8 ± 18.2* 10.2 ± 0.6 11.0 ± 0.3 Curtis, 1991a). Torsades de pointes was originally described by Dessertenne (1966) as a type of ventricular tachyarrhythmia intermediate between VT and VF, although it may better be described as a syndrome (Curtis, 1991a).…”

“…The low baseline incidence of ischaemia-induced VF in rabbits means that if the drug were to have had proarrhythmic effects then there would have been scope for such effects to be revealed. Class III antiarrhythmics have long been associated with proarrhythmia, especially torsades de pointes (McKibben et al, 1984;Curtis, 1991a). Torsades de pointes was originally described by Dessertenne (1966) as a type of ventricular tachyarrhythmia intermediate between VT and VF, although it may better be described as a syndrome (Curtis, 1991a).…”

“…Class III antiarrhythmics have long been associated with proarrhythmia, especially torsades de pointes (McKibben et al, 1984;Curtis, 1991a). Torsades de pointes was originally described by Dessertenne (1966) as a type of ventricular tachyarrhythmia intermediate between VT and VF, although it may better be described as a syndrome (Curtis, 1991a). Rabbit hearts are unusually susceptible to torsades de pointes when exposed to Class III agents in the presence of al-adenoceptor agonists (Carlsson et al, 1991).…”

Pharmacology of a Methanesulfonamide IK Blocker, UK66,914

“…Class HI antiarrhythmics have long been associated with proarrhythmia, especially torsades de pointes (17,33). Agents which share UK66,914's property to block I,, such as sotalol, are known to be associated with torsades de pointes.…”

Focal and Reentrant Mechanisms of Torsades de Pointes: EAD, Reentry, or Chimera?

“…5) As the term TdP became prevalent, some people inadvertently used the term of TdP to call an episode of polymorphic VT without careful consideration to QT prolongation or to abnormal ventricular repolarization. 6) Although a pile of evidence confirmed the ionic current abnormalities in long QT syndrome, 7) clinical diagnosis of TdP basically depends on the standard surface ECG. Consequently, it is important to know the details of ventricular activation sequences at the onset and during the continuation of this particular QRS complex to obtain an insight into electrophysiologic and therapeutic aspects of TdP.…”