A 67-year-old woman, with no remarkable medical history, was admitted to emergency for a first time generalised seizure. Her physical examination was normal. The electroencephalogram (EEG) performed 12 h later revealed a generalised slowing pattern. Cerebral magnetic resonance imaging (MRI) revealed an old ischaemia localised in the left centrum semiovale, which probably explained for the seizure. The initial electrocardiogram (ECG) showed a slight ST segment elevation in leads V2 and V3. Control of the ECG 24 h later showed a T wave inversion in leads V2 to V6 (fig 1). No cardiovascular risk factors or chest pain were noted. The troponin concentration increased to 0.2 μg/l (normal <0.04 μg/l) at admission and did not increase thereafter. Transthoracic echocardiography revealed a septo-apical hypokinesia with left ventricular systolic dysfunction (ejection fraction 40%). Angiography (fig 2) revealed mild coronary artery disease without significant stenosis, an akinesis of the apical and mild left ventricular segments with hyperkinesis of the basal segment, which is typical of takotsubo cardiomyopathy. Five days later a complete recovery was noted on echocardiography, despite a persistent T wave inversion in leads V2 and VL on the ECG.
Takotsubo cardiomyopathy is a reversible neuromyocardial failure classically occurring in postmenopausal women,1 and is supposed to be related to acute catecholamines toxicity. Typical triggers are sudden psychological or physically stressful events, including electroconvulsive therapy.2 In the literature, only 11 case reports of takotsubo cardiomyopathy triggered by epilepsy have been published.1–3 Because the mortality rate is between 1–3.2%,3 and is mostly due to cardiac instability, an ECG should be carried out after any seizure, to detect a takotsubo cardiomyopathy.