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Department of Cardiology (Miyai, Kawaski, Sugihara) Department of Anesthesiology; Matsushita Memorial Hospital; Osaka, Japan; js-k{at}wf6.so-net.ne.jp (Kayo)
To the Editor:
Droperidol has been scrutinized for its potential arrhythmogenicity (1). This report describes a case of coronary artery spasm as a possible cause of droperidol-induced ventricular fibrillation.
A 60-yr-old man with no history of cardiac disease underwent ileocecectomy to treat ileocecal lymphoma. He was receiving no medications, and was healthy other than the lymphoma. His preoperative 12-lead electrocardiogram showed QT prolongation with a QTc of 452 ms.
Anesthesia was induced with 4.0 mg midazolam, 0.5 mg atropine, 200 µg fentanyl citrate, and 12 mg vecuronium bromide, and maintained with 50% NO2. One and a half hours after the start of surgery, we administered droperidol of 1.0 mg IV as prophylaxis for postoperative nausea and vomiting. Within a few minutes, the patient developed ventricular fibrillation (Fig. 1) with a torsade de pointes pattern, which subsided after electrical cardioversion at 200 J. Subsequent monitoring showed ST segment depression. Twelve-lead electrocardiogram approximately 5 min after defibrillation showed slight ST segment elevation in the inferior limb leads, and increased QTc of 463 ms. The ST segment elevation returned to baseline in several minutes. His electrolytes were normal: sodium 142 mEq/L, potassium 3.7 mEq/L, and calcium 7.8 mg/dL. The surgery was completed without complication, using IV lidocaine hydrochloride.
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On postoperative day 5 the patient underwent cardiac catheterization. Coronary angiograms showed no significant stenosis, but intracoronary injection of 10 µg ergonovine maleate provoked total obstruction of the middle right coronary artery segment (Fig. 2), accompanied by inferior ST segment elevations and polymorphic premature ventricular contractions.
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Torsade de pointes was temporally associated with droperidol, but was it caused by droperidol? Myocardial ischemia due to coronary artery spasm likely played a role in inducing ventricular fibrillation (2). Droperidol has been reported to enhance the effect of dopamine by blocking 
-aminobutyric acid receptors on the postsynaptic membrane (3). Dopamine may provoke coronary artery spasm (4), as does ergonovine maleate. Crea et al. (4) administered dopamine to 18 patients with active vasospastic angina. Half of the subjects developed angina and ischemic electrocardiographic changes suggestive of coronary spasm. Thus, one mechanism might be droperidol enhancement of coronary artery spasm.
QT prolongation has been considered to be a risk factor for the development of the life-threatening ventricular arrhythmias (5), especially in the case of droperidol administration (1). Our patient showed a mild QT prolongation before surgery and after defibrillation. QTc was not measured strictly immediately after droperidol administration. Lischke et al. (6) studied serial electrocardiograms after injection of droperidol, demonstrating dose-dependent increase in QTc intervals. In isolated guinea pig ventricular myocytes, droperidol lengthened cardiac repolarization by blocking the rapid component of the delayed rectifier potassium current (7). In rabbit Purkinje fibers, droperidol induced early depolarizations and triggered activity (8). Thus, the heart may have been rendered more susceptible to arrhythmia from the coronary spasm, and thus more prone to droperidol-induced torsade.
There are two mechanisms that potentially link the administration of droperidol to the onset of ventricular fibrillation with a torsade de pointes pattern. However, we cannot know whether the temporal association was causal or just coincidental.
REFERENCES
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