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(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.

View larger version (24K): [in this window] [in a new window]   Figure 1. During presenting wide-QRS tachycardia, there is intermittent loss of ventriculoatrial conduction (arrows). V1, II, V5 surface ECG leads.

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.

View larger version (23K): [in this window] [in a new window]   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.

View larger version (11K): [in this window] [in a new window]   Figure 3. On intravenous procainamide and oral amiodarone, increasing ventricular ectopy was followed by ventricular fibrillation.

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 . . . [Full Text of this Article]