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(Circulation. 2004;109:2924-2925.)
© 2004 American Heart Association, Inc.

Images in Cardiovascular Medicine

Polymorphic Ventricular Tachycardia Induced by Left Ventricular Pacing

Máximo Rivero-Ayerza, MD^*; Marc Vanderheyden, MD^*; Sofie Verstreken, MD; Marc de Zutter, RN; Peter Geelen, MD; Pedro Brugada, MD

From the Cardiovascular Center, Onze Lieve Vrouw (OLV) Ziekenhuis, Aalst, Belgium.

Correspondence to Marc Vanderheyden, MD, Cardiovascular Center, OLV Ziekenhuis, Moorselbaan 164, 9300 Aalst, Belgium. E-mail marc.vanderheyden@olvz-aalst.be

An extract of the first 250 words of the full text is provided, because this article has no abstract.

A 67-year-old woman with advanced heart failure accompanying idiopathic dilated cardiomyopathy had a broad QRS complex on the ECG and significant inter- and intraventricular asynchrony as shown by tissue Doppler echocardiography. She had no history of syncope, no documentation of any ventricular arrhythmias, and no metabolic or electrolyte abnormalities. Implantation of a biventricular pacemaker was indicated. When left ventricular stimulation was started, she developed multiple polymorphic ventricular extrasystoles (Figure 1) and polymorphic ventricular tachycardias. During the left ventricular lead threshold testing, the first noncaptured stimulus generated a "long-short"–like sequence that triggered a sustained episode of torsade de pointes that required electrical cardioversion (Figure 2). No ventricular arrhythmias were induced when the right ventricle or both ventricles were paced simultaneously.

View larger version (34K): [in this window] [in a new window]   Figure 1. Initiation of left ventricular pacing immediately generates ventricular extrasystoles and nonsustained polymorphic ventricular tachycardia. Top panel, ECG lead I. Bottom panel, Arterial pressure monitoring. Vertical lines mark 2-second intervals.

View larger version (27K): [in this window] [in a new window]   Figure 2. Left ventricular pacing during threshold testing. Note that a single noncaptured stimulus generates a long-short–like sequence that triggers a sustained episode of torsade de pointes. Organization is as in Figure 1.

Heterogeneity within the ventricular wall is a major mechanism of ventricular arrhythmias in primary electrical disorders such as Brugada syndrome and the long-QT syndrome. But acquired forms also exist, such as drug-induced torsade de pointes, drug-induced Brugada syndrome, and the entity shown here, left ventricular pacing–induced polymorphic ventricular tachycardia.

*The first 2 authors contributed equally to this work.

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