A 76-year-old woman developed Takotsubo cardiomyopathy following status epilepticus due to seronegative autoimmune encephalitis, with ejection fraction recovering from 20-25% to 50-55% after treatment.
Case Report (n=1)
Status epilepticus due to autoimmune encephalitis can trigger Takotsubo cardiomyopathy, emphasizing the need for aggressive seizure management to prevent and reverse neuro-cardiac complications.
Abstract Introduction Takotsubo cardiomyopathy (TCM) is a cardiac syndrome characterized by transient left ventricular dysfunction and mimics acute coronary syndrome (ACS) without evidence of coronary artery disease. While emotional stress is a classic precipitant, neurological insults including seizures are increasingly recognized as triggers. Here we present a case of TCM in an elderly woman with new-onset status epilepticus due to seronegative autoimmune encephalitis (SAE). Case Presentation A 76-year-old previously healthy woman presented with encephalopathy and status epilepticus following a fall. Seizures were refractory to four antiepileptic drugs (AEDs), leading to endotracheal intubation and treatment with a sedation infusion. An infectious and autoimmune work up were unrevealing and imaging was unremarkable. She developed SCAI stage C cardiogenic shock with elevated troponin and EKG changes consistent with inferolateral ischemia. Cardiac catheterization ruled out ACS and echocardiogram showed an ejection fraction (EF) of 20-25% with regional wall motion abnormalities consistent with TCM as well as an incidental LV thrombus. She was treated with anticoagulation, pulse-dose steroids for one week, and intravenous immunoglobulin (IVIG) was withheld due to thrombosis risk. Repeat echocardiogram during admission showed EF recovery to 50-55%. She was eventually discharged on optimized AEDs. Discussion TCM is a rare but serious complication of status epilepticus, occurring in about 0.1% of cases. Large registry data show that acute neurological conditions significantly increase TCM risk, with odds ratios of 4.9 and 2.1 for status epilepticus and meningoencephalitis respectively. The proposed underlying mechanism involves catecholamine excess and autonomic dysregulation triggered by prolonged seizures. Catecholamine surge results in myocardial stunning and transient systolic dysfunction. In autoimmune encephalitis, dysfunction of limbic structures like the amygdala and hippocampus may further enhance sympathetic output, even in seronegative cases. Prompt control of seizures is critical to minimizing cardiac complications. Endotracheal intubation with sedation may be required in refractory cases to reduce cerebral injury and systemic catecholamine surges. Management of SAE includes rapid initiation of immunotherapy, high-dose IV glucocorticoids, and IVIG. Most patients with neurogenic TCM recover cardiac function within days to weeks, as in this case. Conclusion This case underscores the importance of early identification and treatment of autoimmune encephalitis and aggressive management of status epilepticus to prevent neuro-cardiac complications such as TCM. Clinicians should consider endotracheal intubation with sedation when seizure burden is high and refractory to medical therapy. This abstract is funded by: None
Foster et al. (Fri,) conducted a case report in Takotsubo cardiomyopathy following status epilepticus due to seronegative autoimmune encephalitis (n=1). Anticoagulation, pulse-dose steroids, and antiepileptic drugs was evaluated. A 76-year-old woman developed Takotsubo cardiomyopathy following status epilepticus due to seronegative autoimmune encephalitis, with ejection fraction recovering from 20-25% to 50-55% after treatment.