Seizure-related takotsubo cardiomyopathy in a patient with recurrent malignant meningioma

Takotsubo cardiomyopathy (TTC) is an acute and reversible cardiomyopathy commonly precipitated by emotional or physical stress. The clinical presentation is similar to the acute coronary syndrome, manifesting as chest pain in association with mild cardiac enzyme elevation and electrocardiographic (EKG) changes in the absence of obstructive lesions on coronary angiography [1, 2]. Increasingly, cases are being described in the setting of acute neurological illnesses, including malignancy, and seizures [3–6]. Compared with typical TTC, seizure-induced TTC confers a higher mortality, thus necessitating prompt recognition and investigation [7]. A 76-year-old female with recurrent malignant meningioma presented to the emergency department following a generalized tonic–clonic seizure (GTCS). The patient’s history was significant for multiple cranial resections (the most recent one-month prior), two previous seizures, hypercholesterolemia, hypertension and chronic bradycardia. On admission, the patient received intravenous lorazepam 1 mg and dexamethasone 10 mg. She was hemodynamically stable and blood glucose was 147 mg/dl. A noncontrast CT-brain revealed bilateral vasogenic edema corresponding to previous resection sites. EEG demonstrated sharp waves in the right parietal region with associated diffuse generalized slowing. Following admission, the patient had witnessed a 30 s GTCS and was admitted to the neurosurgical intensive care unit and administered dexamethasone. Here she reported chest pain, despite post-ictal confusion. Subsequent troponin was 2.7 ng/ml, peaking at 2.9 ng/ml (n \ 0.1 ng/ml), and an EKG showed ST-changes concerning for ischemia. Given a diagnosis of non-STsegment elevation myocardial infarction (NSTEMI), aspirin, clopidogrel and atorvastatin were promptly initiated. Coronary angiography was performed but revealed no culprit lesion. Left ventriculography demonstrated an impaired left ventricular ejection fraction (25 %) and a hyperkinetic base with severe hypokinesis of the anterolateral, diaphragmatic and apical segments, consistent with a diagnosis of TTC. This was confirmed on echocardiography (Fig. 1). The patient was commenced on lisinopril and carvedilol, and clopidogrel was ceased. Once stable, she was discharged home with scheduled cardiac followup. At 1 month, repeat EKG and echocardiogram were performed, revealing resolution of ischemic and structural changes. We describe the case of a 76-year-old woman suffering from seizure-related TTC. This case is remarkable for the patient’s symptomatic presentation, history of multiple brain surgeries, and the absence of the classical echocardiographic finding of apical ballooning. A number of mechanisms have been proposed to explain the relationship between seizures and TTC. The level of circulating catecholamines has been demonstrated to spike in the 30-minutes following a GTCS [8]. This excessive release of catecholamines can cause damage to cardiac muscle, leading to ventricular dysfunction [3, 7, 9]. In addition, the circulatory complications of seizures, including ventricular arrhythmias, metabolic disturbances and hemodynamic compromise, can provide sufficient physical stress to precipitate TTC in certain patients [7, J. Warren U. Baber B. Mohanty S. K. Sharma A. Kini R. Mehran (&) Mount Sinai Medical Center, 1 Gustave L. Levy Place, Box 1030, New York, NY 10029, USA e-mail: roxana.mehran@mountsinai.org