Yamamoto Yasutoshi, Matsushita Akihiro, Watanabe Sanae, Tanaka Katsuji
Pediatrics, Nishinomiya-Sunago Medical and Welfare Center, Nishinomiya, JPN.
Cureus. 2024 Oct 16;16(10):e71662. doi: 10.7759/cureus.71662. eCollection 2024 Oct.
Status epilepticus (SE)-induced Takotsubo cardiomyopathy (TTC) frequently manifests as a hemodynamic compromise, including shock, despite heart failure therapy. This can result in life-threatening events that pose significant diagnostic challenges. We report the case of a 57-year-old woman who was successfully diagnosed with TTC, without hemodynamic compromise, and treated. Two years prior to TTC onset, the patient had exacerbated gastroesophageal reflux disease (GERD) due to recurrent hiatal hernia, accompanied by electrocardiogram (ECG) changes. On the day of TTC onset, the patient developed SE, as well as a high fever due to pneumonia. The SE was resolved by diazepam, and the patient received fluid therapy and antibiotics for the pneumonia. High creatine kinase (CK) and N-terminal pro-brain natriuretic peptide (NT-pro BNP) levels, along with ECG findings (ST elevation in left precordial leads), transthoracic echocardiogram findings (typical apical ballooning), and coronary computed tomography angiography findings (absence of culprit region), confirmed the TTC diagnosis. Although transient mild left ventricular outflow tract stenosis was observed on day 14, it disappeared on day 21. During the course of the disease, the patient received conservative management, with careful monitoring and follow-up imaging, and signs of hemodynamic compromise, such as shock, hypotension, or heart failure, were not observed. The condition was triggered by SE and pneumonia following exacerbation of GERD. The extremely high NT-pro BNP level indicated that the CK elevation was due to myocardial damage rather than SE, facilitating early diagnosis. TTC should be considered when a patient presents with SE and pneumonia following GERD exacerbation and expresses remarkable NT-pro BNP elevation.
癫痫持续状态(SE)诱发的应激性心肌病(TTC)常表现为血流动力学障碍,包括休克,即便进行了心力衰竭治疗。这可能导致危及生命的事件,带来重大的诊断挑战。我们报告一例57岁女性病例,该患者成功诊断为TTC,未出现血流动力学障碍并接受了治疗。在TTC发病前两年,患者因复发性食管裂孔疝导致胃食管反流病(GERD)加重,并伴有心电图(ECG)改变。在TTC发病当天,患者出现了SE,同时因肺炎出现高热。地西泮使SE得到缓解,患者接受了针对肺炎的液体治疗和抗生素治疗。高肌酸激酶(CK)和N末端脑钠肽前体(NT-pro BNP)水平,以及心电图表现(左胸前导联ST段抬高)、经胸超声心动图表现(典型的心尖部气球样改变)和冠状动脉计算机断层扫描血管造影表现(无罪犯血管区域),证实了TTC的诊断。尽管在第14天观察到短暂的轻度左心室流出道狭窄,但在第21天消失。在疾病过程中,患者接受了保守治疗,进行了仔细的监测和随访影像学检查,未观察到休克、低血压或心力衰竭等血流动力学障碍的迹象。该病情由GERD加重后的SE和肺炎引发。极高的NT-pro BNP水平表明CK升高是由于心肌损伤而非SE,有助于早期诊断。当患者在GERD加重后出现SE和肺炎且NT-pro BNP显著升高时,应考虑TTC的诊断。