Disulfiram-ethanol reactions may sometimes be accompanied by some serious cardiocirculatory complications, including tachycardia and profound hypotension. Life-threatening cardiac arrhythmias are infrequent and cardiac manifestations are usually limited in time. We describe a recent case with unexpected electrocardiographic findings and cardiac arrhythmias during the course of a disulfiram-ethanol reaction.

A 57-year-old man, chronic ethanol abuser, was brought by the relatives to the Emergency Department (ED). Fifteen hours before hospital admission, he had ingested one litre of whisky together with 20 grams of disulfiram. His chronic medications also included prothipendyl and citalopram. An electrocardiogram (ECG) performed one year before had showed a QTc interval < 450msec. The patient had no personal or familial history of serious cardiac events. He rapidly developed during the night symptoms consisting with a disulfiram/ethanol reaction (facial flush, nausea, vomiting, diarrhea…) and that were still present on ED arrival. Admission heart rate was 126/min, with arterial blood pressure 179/107mm Hg. Initial ECG showed atrial fibrillation with high ventricular response (126/min), and QTc 435msec. The admission troponin-I concentration was 0.01ng/ml (<0.08). Toxicological analysis showed: ethanol serum level 0,6g/l, prothipendyl and citalopram < 5ng/ml. Routine laboratory investigations showed normal potassium, magnesium and calcium serum concentrations. The patient was transferred to the observation unit for further ECG monitoring during the night. No specific treatment was applied. After spontaneous return to sinus rhythm, he became progressively bradycardic (HR < 50/min), but arterial blood pressure was well preserved. By the next morning (> 34 hours after exposure to disulfiram), the ECG revealed sinus rhythm (39/min) with a QTc interval at 588msec and a few minutes later, the patient presented “torsades de pointe” and ventricular fibrillation. He was successfully resuscitated by electric counter shock. The troponin-I concentration was slightly increased (0.26ng/ml), no electrolytes disorders were observed. Coronary angiography was normal. The QTc interval remained > 500msec during the hospital stay. The patient was observed one month later, with a normal QTc interval on the ECG.

Sinus tachycardia with ischemic-like ST segment changes is a usual feature of disulfiram-ethanol reaction. The onset of an acute prolongation of the QT interval in the context of drug poisoning raises a concern about a causative link between both factors. A direct effect of disulfiram alone or in combination with ethanol on the QT interval seems, however, unlikely. Indeed, despite the wide use of disulfiram, the drug has not been reported to modify the QT interval. Moreover, as the disulfiram-ethanol reaction appears usually soon after ingestion, the first ECG (15h postingestion) did not reveal QT prolongation. The role of the autonomic nervous system and genetic predispositions has to be kept in mind. QTc prolongation may be absent on routine ECG and may be only revealed when several co-factors are present. Ionic disturbances were ruled out in the present case. It was supposed that the intense stimulation of the autonomic nervous system due to the disulfiram-ethanol reaction may have influenced the QT interval in a patient who could be an asymptomatic carrier of an ion channel mutation responsible of a latent congenital long QT syndrome.