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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{at}olvz-aalst.be

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.

Footnotes

*The first 2 authors contributed equally to this work.

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rivero-Ayerza, M. Articles by Brugada, P. Search for Related Content PubMed PubMed Citation Articles by Rivero-Ayerza, M. Articles by Brugada, P. Related Collections Arrhythmias, clinical electrophysiology, drugs Other heart failure Electrocardiology Pacemaker