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.>.