2001 年 27 巻 5 号 p. 495-498
Liver transplantation has become a valuable treatment for FAP and tacrolimus is highly effective for the prevention of liver allograft rejection. Recently, tacrolimus-induced sinus bradycardia and QT prolongation with ventricular tachycardia have been reported, though no relationship to the plasma concentration of tacrolimus was suggested. On the 80th day after both liver transplantation and the start of tacrolimus administration, our patient experienced syncope. An ECG taken immediately revealed an additional right bundle branch block and the QT interval prolongation (corrected QT interval was 509 msec, which had slightly increased compared to 4 days before). The next day she suffered another attack and ECG monitoring disclosed wide QRS tachycardia (240 beats/minute). On the 82nd day wide ORS tachycardia (206 beats/minute) reappeared. During the following one week she suffered two episodes of dizziness and ECG showed marked bradycardia (35 beats/minute). Sinus bradycardia or sinoatrial block was suspected. In our patient the occurrence of transient RBBB, marked bradycardia (possibly sinoatrial block) and wide QRS tachycardia were considered to possibly be due to conduction block caused by the use of tacrolimus. Because brady-and tachyarrhythmias have been newly developed after liver transplantation under the tacrolimus regimen, and the tachyarrhythmias have diminished after changing the tacrolimus administration to cyclosporin, we speculate that brady-and tachy-arrhythmias were thus possibly caused by tacrolimus. In addition, the amyloid heart in FAP might be more sensitive to the intracellular calcium accumulation effect of tacrolimus, because the administration of tacrolimus does not result in an overdose based on the doses and trough levels of tacrolimus.
