Long-term myocardial toxicity in a patient with tizanidine and etizolam overdose.

Tizanidine hydrochloride, α2-receptor stimulant, is a central muscle relaxant. Etizolam is a benzodiazepine-based anti-anxiety agent. Both drugs are widely used for the treatment of a variety of muscle pain and frequently used together in Japan. We experienced a case of complicating prolonged myocardial dysfunction in a 56-year-old woman. Six hours after overdose of 48 mg tizanidine and 24 mg etizolam, she showed sinus bradycardia and peripheral vascular resistance decreasing shock. At that time new ST-T depressions were recognized in electrocardiography (ECG); however, structural heart diseases were interpreted as negative by other examinations. Intravenous norepinephrine infusion was useful to maintain the hemodynamic stability. ECG reversed to normal findings on day 14; however, the cardiac nuclear medicine studies on day 30 showed severe fatty metabolic disorder and sympathetic denervation. Non-sustained ventricular tachycardia was detected. Complete recovery of the myocardium damage required one year. For one mechanism, it was suggested that over-stimulation of α2-receptor by tizanidine inhibited the norepinephrine secretion and reuptake at pre-synaptic surface of adipose cell and cardiac sympathetic nerve. We want to suggest that the cardiologist should consider the risk of fatal arrhythmia and long-term myocardium toxicity as the poisoning of the central muscle relaxant and benzodiazepine agent. <Learning objective: We experienced a case of complicating prolonged myocardial dysfunction in a 56-year-old woman. Six hours after overdose of 48 mg tizanidine and 24 mg etizolam, she showed sinus bradycardia and peripheral vascular resistance decreasing shock. The cardiac nuclear medicine studies on day 30 showed severe fatty metabolic disorder and sympathetic denervation. Non-sustained ventricular tachycardia was detected. Complete recovery of the myocardium damage required one year.>.