Yasumura Kaori, Sera Fusako, Akazawa Yasuhiro, Ohtani Tomohito, Sakata Yasushi
Department of Cardiovascular Medicine, The University of Osaka Graduate School of Medicine, 2-15 Yamadaoka, Suita 565-0871, Japan.
Eur Heart J Case Rep. 2025 Apr 28;9(5):ytaf213. doi: 10.1093/ehjcr/ytaf213. eCollection 2025 May.
Cardiac sympathetic hyperactivity may be implicated in the pathogenesis of Takotsubo syndrome (TTS). With complete denervation of a transplanted heart, the recipient heart is less susceptible to sympathetic hyperactivity. We report a rare case of recurrent TTS in a heart transplant recipient from a donor with TTS. Iodine-123 meta-iodobenzylguanidine (I-MIBG) scintigraphy results for evaluating sympathetic activity are presented.
A 46-year-old woman underwent heart transplantation for dilated phase of hypertrophic cardiomyopathy following recurrent cerebral haemorrhage complications after left ventricular assist device therapy 2 years prior. The donor heart exhibited a transient mildly reduced left ventricular ejection fraction suggestive of TTS. Four years post-transplantation, she was admitted with difficulty breathing, and echocardiography showed decreased biventricular apical wall motion. During her treatment course, wall motion improved spontaneously, and giant negative T waves were observed on electrocardiography (ECG). Coronary computed tomography and endomyocardial biopsy findings were normal, and a diagnosis of TTS was made. Approximately 5 years post-transplantation, she was readmitted with difficulty breathing, and echocardiography showed akinesis of the mid-to-apical biventricular wall. Wall motion normalized within a few days, and ECG showed typical giant negative T waves, consistent with TTS. I-MIBG scintigraphy taken prior to discharge and 6 months later showed minimal myocardial uptake in the basal anterior wall, indicating insufficient sympathetic reinnervation.
Recurrent TTS in a denervated heart suggests the possibility of other underlying mechanisms besides cardiac sympathetic hyperactivity. This case highlights potential TTS development in transplant recipients from donors with TTS, underlining the need for close monitoring.
心脏交感神经过度活跃可能与应激性心肌病(TTS)的发病机制有关。由于移植心脏完全去神经支配,受者心脏对交感神经过度活跃的敏感性较低。我们报告了一例心脏移植受者罕见的复发性TTS病例,供者患有TTS。本文展示了用于评估交感神经活动的碘-123间碘苄胍(I-MIBG)闪烁扫描结果。
一名46岁女性,因肥厚型心肌病扩张期在2年前接受左心室辅助装置治疗后出现复发性脑出血并发症,而行心脏移植。供者心脏表现出短暂的轻度左心室射血分数降低,提示TTS。移植后4年,她因呼吸困难入院,超声心动图显示双心室心尖壁运动减弱。在治疗过程中,壁运动自发改善,心电图(ECG)上观察到巨大负向T波。冠状动脉计算机断层扫描和心内膜活检结果正常,诊断为TTS。移植后约5年,她因呼吸困难再次入院,超声心动图显示双心室中至心尖壁运动消失。壁运动在几天内恢复正常,ECG显示典型的巨大负向T波,符合TTS。出院前及6个月后进行的I-MIBG闪烁扫描显示基底前壁心肌摄取极少,表明交感神经再支配不足。
去神经心脏中的复发性TTS提示除心脏交感神经过度活跃外,还存在其他潜在机制。该病例突出了来自患有TTS供者的移植受者发生TTS的可能性,强调了密切监测的必要性。