Reprinted with permission from JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 12, No. 6, June 2001 Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418
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Polymorphic Ventricular Tachycardia and Torsades de Pointes: Beyond Etymology NABIL EL-SHERIF, M.D. From the Cardiology Division, Department of Medicine, SUNY–Downstate Medical Center, and NY Harbor VA Medical Center, Brooklyn, New York
Editorial Comment Poly(pleo)morphic ventricular tachycardia (PVT) is a VT with continuously varying QRS morphology in any recorded ECG lead. Sometimes, simultaneous recording of more than one ECG lead is necessary to detect the changes in beat-to-beat QRS morphology. Compared with sustained monomorphic VT, PVT usually is viewed as having a more ominous prognosis. Although many prolonged episodes of fast PVT ($200 beats/min) are associated with hemodynamic collapse and usually degenerate into ventricular brillation, a majority of episodes of PVT terminate spontaneously.1 Torsades de pointes (TdP) is an ear-pleasing term that describes an eye-catching form of PVT. The term was rst coined by Dessertennes,2 who described its ECG pattern of continuously changing morphology of the QRS complexes that seem to twist around an imaginary baseline. The quasi-musical term and the intriguing ECG pattern have caught the attention of electrophysiologists for years and, to some extent, have been a driving force behind the recent focused interest in the role of genetics and ion channelopathy in cardiac arrhythmias in general. More importantly, it is helping to refocus attention on the role of dispersion of ventricular repolarization in the genesis of malignant ventricular tachyarrhythmias. PVT can be seen in the presence or absence of organic heart disease. One way to classify PVT is whether it is associated with normal or prolonged QT (or QTU) segment. It has been suggested that the term TdP should be reserved for use with the long QT syndrome (LQTS). However, a minority of PVTs in patients with LQTS have a characteristic TdP con guration, and this classic con guration can be seen without a prolonged QT interval or even structural heart disease, for example, in the Brugada syndrome.3 There is more than one electrophysiologic mechanism for PVT, and understanding these mechanisms can be of valuable help in the proper management of individual patients. PVT can be caused by multifocal discharge, reentrant excitation, or a combination thereof. In electrophysiologic parlance, ectopic discharge can be due to normal or abnormal automaticity and early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs). In a clinical report more than a quarter of a century ago,4 a number of patients with advanced cardiac disease were described to have polymorphic rhythms and/or PVT that were explained on the basis of concurrent multifocal (parasystolic) discharge using what was fashionable at the time, i.e., deductive analysis of the ECG. The majority of those patients died of terminal J Cardiovasc Electrophysiol, Vol. 12, pp. 695-696, June 2001. Address for correspondence: Nabil El-Sherif, M.D., SUNY–Downstate Medical Center, Cardiology Division, 450 Clarkson Avenue, Box 1199, Brooklyn, NY 11203. Fax: 718-630-3740; E-mail:
[email protected]
heart failure; none died suddenly. Therefore, it was concluded that this type of PVT (usually , 120 beats/min) has a rather benign electrophysiologic consequence. It is possible nowadays to suggest that these rhythms are due to multifocal DAD-triggered activity, probably secondary to increased intracellular calcium of cardiac cells in the failing heart. This is essentially the same mechanism for spontaneous PVT seen in the rst 48 hours after infarction in both the experimental model and in man.5 On the other hand, the majority of “fast” PVT is due to reentrant excitation. To be more exact, in PVTs seen in ischemic heart disease, both the initiating and subsequent beats can all be based on reentrant excitation. The same is true for all PVTs induced by programmed electrical stimulation in the electrophysiology laboratory.1 On the other hand, in PVT in LQTS, the initiating one or two beats are EAD-triggered beats that arise predominantly from the Purkinje network and infringe on an underlying substrate of spatial nonhomogeneous repolarization to initiate continuously varying tridimensional circulating wavefronts (scrolls).6 In this issue of the Journal, Dr. Andrew Wit’ s group revisited the electrophysiologic mechanism of PVT that resembles TdP in the canine experimental model of myocardial infarction.7 In an elegant study, they showed that the predominant mechanism for the change in QRS morphology was a shift in the exit point of the circulating wavefront (initially con ned to the epicardial surviving layer in this model) to activate the ventricles. Such shifts resulted from small changes in conduction velocity of the reentrant circuit, either speeding or slowing, that modi ed the length of the lines (arcs) of functional conduction block. The study nicely con rms similar conclusions reported two decades earlier using the same experimental model (see reference 5, Figs. 8 and 9). It should be emphasized that the mechanism for transition of the QRS con guration of TdP in LQTS is somewhat different from that described above. The transition is attributed to bifurcation of a single circulating wavefront into two simultaneous independent wavefronts, followed by termination (extinction) of one of the wavefronts.8 A period of transitional complexes covering more than one cycle is associated with a gradual dominance of 1 of the 2 circulating wavefronts before termination of the other wavefront. The initiating mechanism for bifurcation of the single wavefront is similar to what was described above, i.e., the development of new arcs of functional conduction block associated with subtle changes in the conduction velocity of the circulating scroll. To summarize, previous studies recon rmed by the present one seem to indicate the following. (1) PVT is due to beat-to-beat variation in the tridimensional ventricular activation pattern (a classic tautology). (2) The change in
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activation pattern is due to subtle (or not so subtle) changes in the adaptation of the tridimensional spatial repolarization pattern. The latter can result in the creation of new arcs of functional conduction block, as well as the disappearance of old ones associated with acceleration or slowing of intramyocardial conduction in different regions of the ventricles. Such a pattern also could be complicated by faster conduction in the Purkinje system. (3) If this process results in fractionation of stable gure-of-eight two synchronous wavefronts into three or more asynchronous wavefronts or in bifurcation of a single tridimensional rotor into two or more asynchronous rotors, a pre brillatory state could develop. However, recoalescence or extinction of some of these wavefronts can result in reestablishment of a stable reentrant activation that can self-terminate. Although it is easy to theorize that development of a pre brillatory state and its possible reversal in the course of PVT is due to dynamic adaptation of spatial refractoriness and conduction in successive cycles, the underlying exact electrophysiologic rules still are not well understood. Thus, at present, no one can predict which PVT will self-terminate and which will degenerate into ventricular brillation. Given this state of affairs, it is reasonable to conclude by quoting Ludwig Wittgenstein9 : “Whereof one cannot speak (to explain), thereof one must be silent.”
References 1. El-Sherif N: Polymorphic ventricular tachycardia. In Podrid PJ, Kowey PR, eds: Cardiac Arrhythmias: Mechanisms, Diagnosis, and Management. Williams & Wilkins, Baltimore, 1995, pp. 936-950. 2. Dessertennes F: La tachycardie ventriculaire a deux foyers opposes variables. Arch Mal Coeur 1966;59:263-272. 3. El-Sherif N, Turitto G: The long QT syndrome and torsade de pointes. PACE 1999;22:91-110. 4. El-Sherif N, Samet P: Multiform ventricular ectopic rhythms. Evidence for multiple parasystolic activity. Circulation 1975;51:492-505. 5. El-Sherif N, Mehra R, Gough WB, Zeiler RH: Ventricular activation patterns of spontaneous and induced ventricular rhythms in canine one-day-old myocardial infarction. Evidence for focal and reentrant mechanisms. Circ Res 1982;51:152-166. 6. El-Sherif N, Caref EB, Yin H, Restivo M: The electrophysiological mechanisms of ventricular tachyarrhythmias in the long QT syndrome: Tridimensional mapping of activation and recovery patterns. Circ Res 1996;79:474-492. 7. Schmitt H, Cabo C, Costeas C, Coromilas J, Wit AL: Mechanisms for spontaneous change in QRS morphology sometimes resembling torsades de pointes during reentrant ventricular tachycardia in a canine infarct model. J Cardiovasc Electrophysiol 2001;12:686-694. 8. El-Sherif N, Chinushi M, Caref EB, Restivo M: Electrophysiological mechanisms of the characteristic electrocardiographic morphology of torsade de pointes tachyarrhythmias in the long QT syndrome. Detailed analysis of ventricular tridimensional activation patterns. Circulation 1997;96:4392-4399. 9. Wittgenstein L: Tractatus Logico-Philosophicus. The Humanities Press, New York, 1961 (Pears DF, McGuinness BF, trans).
