Case Presentation: A 68-year old female with a history of uncomplicated alcohol dependence was brought in by ambulance after a witnessed seizure at home characterized by myoclonus for several minutes and prolonged post-ictal confusion. Upon presentation, she was altered, hypertensive to 183/118, and had a supraventricular tachycardia to the 160s broken with adenosine. The patient then went into hypoxic respiratory failure, requiring intubation, with plain film findings concerning for pulmonary edema vs. consolidation. EKG was notable for new T wave inversions in V4 and V5 associated with a rising troponin peaking at 13.6. Acute Coronary Syndrome protocol was initiated and the patient was transferred to the CCU out of concern for cardiogenic shock requiring phenylephrine drip to support her blood pressure. TTE showed a newly depressed ejection fraction of 30%, marked left ventricle apical hypokinesis and ballooning, and LV basal hypokinesis. Cardiac catheterization showed no significant coronary artery disease. Her hemodynamics and volume status improved with diuretics and phenylephrine drip, and, eventually, the patient was weaned from the ventilator, but remained persistently altered. Video EEG was obtained and showed epileptiform activity within the left frontotemporal region, with subsequent MRI demonstrated asymmetric volume loss and increased signal in the left hippocampus compatible with mesial temporal sclerosis. She was initiated on levetiracetam with good response. She was discharged on a new heart failure regimen and antiepileptics. She is scheduled for a follow-up TTE in several months to evaluate for recovery of systolic function.

Discussion: The above case describes a woman who developed new-onset non-ischemic heart failure in the setting of newly diagnosed epilepsy with echocardiographic findings consistent with Takotsubo cardiomyopathy. Takotsubo cardiomyopathy (TCM), or stress cardiomyopathy, is a syndrome of transient systolic dysfunction that presents with signs and symptoms that closely mimic those of acute coronary syndrome with no obstructive coronary artery disease.  The pathogenesis of TCM is not well understood, but predominantly centers of the release of excess catecholamines in times physical or emotional stress causing myocardial stunning or damage.  In regards to the patient presented above, her new-onset seizure disorder likely caused stress-related catecholamine release, triggering TCM with associated myocardial stunning and demand ischemia. After subarachnoid hemorrhage, seizures are the most frequent central nervous disorder associated with the development of TCM. Cardiac conduction and rhythm abnormalities can often be seen during and after seizures. Post-ictal troponin elevation can be observed in a small but significant percentage of patients with status epilepticus.

Conclusions: Our case demonstrates the importance of considering the association and treating potentially fatal cardiac complications from seizures, such as Takotsubo cardiomyopathy, even in patients without any previous significant cardiac history or risk factors.