(Circulation. 1999;99:E7.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Drug-Induced Torsade de Pointes
Richard G. Trohman, MD;
Jonathan Sahu, MD
From the Section of Cardiology, Rush–Presbyterian–St
Luke's Medical Center and Rush Medical College, Chicago, Ill.
Correspondence to Richard G. Trohman, MD, Rush–Presbyterian–St Luke's Medical Center, Department of Cardiology, 1750 W Harrison St, Suite 1091 Jelke, Chicago, IL 60612.
A73-year-old man with mild coronary artery
disease and a dilated cardiomyopathy
presented to the emergency room with a
hemodynamically stable wide-QRS
tachycardia. His 12-lead ECG revealed episodes of
ventriculoatrial block, and a diagnosis of ventricular
tachycardia (VT) was made (Figure 1
). Intravenous
procainamide restored sinus rhythm. Tachycardia
recurred, and a second bolus of intravenous
procainamide again restored sinus rhythm. The patient was
started on concomitant amiodarone 800 mg/d.
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Figure 1. During presenting wide-QRS
tachycardia, there is intermittent loss of ventriculoatrial
conduction (arrows). V1, II, V5 surface ECG
leads.
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The next day, the patient had significant prolongation of the QT
interval with prominent U waves (Figure 2). He continued to have slower episodes
of monomorphic VT on combination therapy. After 5 days of
intravenous procainamide and oral
amiodarone, he developed sustained polymorphic VT (Figure 3), suffered a cardiac arrest, and
required defibrillation to restore sinus rhythm. His
procainamide and N-acetylprocainamide levels
were 5.6 µg/mL and 9.4 mg/mL near the time of the arrest.
Electrolytes, magnesium, BUN, and creatinine were all
within normal limits.
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Figure 2. A 12-lead ECG after intravenous
procainamide demonstrates sinus rhythm with QT prolongation and
prominent U waves. I, II, III, aVR, aVL, aVF, V1 through
V6 surface ECG leads.
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Figure 3. On intravenous procainamide
and oral amiodarone, increasing ventricular ectopy
was followed by ventricular fibrillation.
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Procainamide was discontinued. After arrest, the patient
continued to have short runs of polymorphic VT (compatible with
torsade de pointes, Figure 4) that
resulted in no hemodynamic compromise. These episodes
gradually diminished. Despite this apparent stability, a routine ECG 2
days after arrest revealed profound QT prolongation and dramatic T-wave
alternans (Figure 5). These changes
gradually resolved with reduction of his amiodarone dose.
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Figure 5. Dramatic QT prolongation and T-wave alternans.
These changes occurred "paradoxically" after
tachyarrhythmias stabilized and most likely reflect
complex (multitarget) electrophysiologic and
antiarrhythmic effects of amiodarone. I, II, III, aVR, aVL,
aVF, V1 through V6 surface ECG leads.
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An implantable cardioverter-defibrillator (ICD) was placed before
hospital discharge. After 10 months of follow-up, he has been
clinically stable (requiring no ICD therapies). His QT interval (and
QTc) was 460 ms.
Footnotes
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 Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
