Severe ventricular arrhythmia following parenteral administration of vincamine. Predisposing factors in 6 cases

: Six patients developed ventricular arrhythmias with parenteral administration of vincamine. Direct intravenous injection was the mode of administration in 2 cases, intravenous infusion in 3 cases (one at very high dosage) and intramuscular injection in 1 case. The same signs of toxicity were observed in al patients:--5 patients had recorded attacks of "torsades de pointe", which recurred in 1 of them when the drug was restarted.--1 patient had syncope and, although an ECG was not recorded at the time, an ECG shortly afterwards showed a long QT interval and R/T ventricular extrasystoles. Symptoms were generally neurological in nature with syncope, cyanosis, and convulsions. Spontaneous regression was observed in 3 cases but in the others the drug had to be stopped and cardiopulmonary resuscitation instituted. None of our patients died of their arrhythmia. In some patients a predisposing factor was found:--metabolic: hypokalaemia (1 case), moderate reduction of potassium pool (1 case), severe reduction of calcium pool (1 case);--pharmacological: previous treatment with fenoxidil (1 case), thioridazine (1 case);--cardiac: congenital long QT interval (Romano-Ward) (1 case), revealed by vincamine administration. Chronic obstructive airways disease with right ventricular strain and atrial fibrillation (1 case) which might have predisposed the patient to "torsades de pointes". Three patients had no predisposing factors apart from their age. "Torsades de pointes" occurred in a pacemaker patient, but pacemaker function was normal. These six cases may be grouped with the other ten or so cases of vincamine toxicity already reported; they carry and additional warning on the use of intramuscular vincamine. Vincamine toxicity is probably a direct effect on the myocardial cells. This fact merits verification by further electrophysiological studies.