EHRA EDUCATION COMMITTEE
Case of polymorphic ventricular tachycardia after stroke necessitating defibrillation
1 Department of Cardiology, Thoraxcenter, University Medical Center Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands; 2 Interuniversity Cardiology Institute Netherlands, Utrecht, The Netherlands; 3 Institute of Cardiology, University of Bologna, Bologna, Italy; 4 Department of Cardiology, Royal Brompton Hospital, London, UK; 5 Department of Cardiology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium; 6 Department di Biotecnologie e Bioscienze, University of Milano-Bicocca, Milano, Italy; 7 Division of Cardiology, Helsinki University Central Hospital, Helsinki, Finland; 8 Eskisehir Osmangazi University, Eskisehir, Turkey; 9 Department of Cardiology, University Hospital Uppsala, Uppsala, Sweden
Manuscript submitted 19 November 2007. Accepted after revision 23 November 2007.
* Corresponding author. Tel: + 31 50 3612355; fax: + 31 50 3614391. E-mail address: i.c.van.gelder{at}thorax.umcg.nl
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Answers to the case presented at page 77.
The tachycardia depicted in Figures 1 and 3 is a torsades de pointes. Note the prolonged QT interval with a prominent U wave (black arrows) in the 12-lead electrocardiogram in .
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Torsades de pointes is defined as a ventricular tachycardia with undulating peaks of sequential QRS complexes and T waves, occurring in the setting of QT prolongation. Almost always torsades de pointes is preceded by short–long–short RR sequences and pause dependent TU wave changes. Note, that in the present case the torsades de pointes started after a pause induced by a premature ventricular beat. The sinus beat has a prolonged QT interval with a prominent U wave (black arrow Figure 4). The first beat of the torsades de pointes has a comparable configuration as the previous ventricular premature beat (dotted arrows in Figure 3). The first ventricular tachycardia beat emerges out of the final part of the T wave.
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The patient was not treated with drugs that are known to prolong the QT interval. Laboratory tests essential to perform are potassium and magnesium plasma levels. These were 3.8 and 0.67 mmol/L, respectively. An echocardiogram was performed during sinus rhythm after two defibrillations. This revealed a globally depressed cardiac function with an assessed left ventricular ejection fraction of 45%.
Extra potassium and magnesium i.v. were given but short runs of self-terminating torsades de pointes recurred. Isoproterenol i.v. was started to increase the sinus rate and to suppress the torsades de pointes. At a sinus rate of 110 bpm the short runs of torsades de pointes completely disappeared and the QT interval normalized (QTc 430 ms). The patient was treated with isoproterenol i.v. for 48 h. After gradual discontinuation of isoproterenol i.v. no tachycardias recurred. The QT interval normalized.
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The arrhythmogenic mechanisms of torsades de pointes include early after depolarizations inducing triggered activity and, probably, increased dispersion of refractoriness. The occurrence of QT prolongation during the acute course of SAH is well known. The occurrence of torsades de pointes is a relatively rare phenomenon. Thorough evaluation afterwards did not reveal any other cause for the QT prolongation with torsades de pointes in the present patient. Neither a congenital long QT syndrome, nor treatment with drugs that may prolong the QT segment (e.g. class III antiarrhythmic drugs, tri/tetracyclic antidepressants), nor severe hypopotassaemia, nor a hypomagnesiumia. It was concluded that the cause of the torsades de pointes in the present patient was the SAH.
It is important to recognize this type of arrhythmia as antiarrhythmic therapy in these patients is completely different from ventricular tachyarrhythmias not caused by a prolonged QT syndrome.
Increase of the heart rate either by isoproterenol or by cardiac pacing may prevent recurrent torsades de pointes. The role of additional beta blockade (in combination with pacing) in these patients is unsettled. Obviously, the rationale for beta-blockers on top of cardiac pacing may be the prevention of calcium overload dependent after depolarizations, as was recently discussed by Tan et al.1
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[1] Tan HL, Bardai A, Shimizu W, Moss AJ, Schulze-Bahr E, Noda T, Wilde AAM. Genotype-specific onset of arrhythmias in congenital long-QT syndrome. Circulation (2006) 114:2096–2103.
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