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.>.