Abstracts

Rationale: Takotsubo cardiomyopathy describes the ballooning of the apex of the heart, transiently creating a systolic dysfunction mimicking myocardial infarction and may be a rare, potentially fatal sequela of seizures thought to contribute to sudden death in epilepsy (SUDEP). We present a patient who develops Takotsubo cardiomyopathy after status epilepticus and describe current literature on the pathophysiology and incidence of this phenomenon. Methods: Case Report: A 62-year old female with a past medical history of hypothyroidism was brought to our emergency department by ambulance after a 20-minute witnessed generalized seizure. She was given midazolam intramuscularly in the field to abort the seizure. Cardiac troponins rose to 10.89 ng/mL within 12 hours, and cardiac catheterization revealed apical ballooning without occlusive coronary artery disease. The patient's ejection fraction dropped to 20% and her blood pressure dropped to a low of 66/36, but was responsive to IV fluid bolus resuscitation. The patient's blood pressure stabilized enough for discharge after 5 days, and follow-up echocardiogram one month later showed 60% EF and normal ventricular function. Results: Takotsubo cardiomyopathy in seizure (TCS) has been attributed to massive catecholamine surges, possibly due to overstimulation of the insular cortex. Patients may not be aware of chest pain in the post-ictal state, causing this phenomenon to be overlooked. TCS may also be caused by hypersensitivity of β-adrenergic receptors in the heart due to denervation from repeated seizures, leaving it vulnerable to catecholamine surges. Compared non-epileptogenic patients, seizure patients with this condition are likely younger in age, more often male, report chest pain less, and have higher rates of cardiogenic shock and recurrence. TCS may present up to 72 hours after seizures, and may contribute to SUDEP by causing arrhythmias and shock. To date, no specific therapy or guideline has been developed to treat TCS; only serial EKG, echocardiography, and troponins in the post-ictal period can detect this phenomenon early enough for supportive therapy. Conclusions: TCS is a rare and lethal adverse effect of seizures that warrants heightened vigilance for close cardiac monitoring.