To the Editors: I read with great interest the excellent review article published recently by Surges et al. in Epilepsia (Surges et al., 2010). The authors reviewed the abnormal cardiac repolarization in patients with epilepsy and discussed the potential role of pathologic cardiac repolarization in sudden unexpected death in epilepsy (SUDEP). They have appropriately described in detail the role of QTc prolongation, QTc shortening, and QT dispersion in causing cardiac arrhythmias. They also have pointed out in the article that SUDEP is probably caused by periictal cardiorespiratory alterations such as central apnea, bradyarrhythmia, and neurogenic pulmonary edema. However, one important increasingly recognized cardiac disease entity, which can be triggered by an epileptic seizure and may be a potential cause of abnormal cardiac repolarization resulting in QTc prolongation in periictal period, was not mentioned. This relatively new cardiac clinical entity is called Takotsubo syndrome (TS) (Kawai et al., 2000), also known as neurogenic stunned myocardium or broken heart syndrome. The syndrome has a clinical presentation resembling that of acute coronary syndrome. It causes a characteristic regional ventricular wall motion abnormality affecting all the walls of the left ventricle circumferentially causing a peculiar balloon-like appearance of the ventricle during systole. The ventricular wall motion abnormality is transient and resolves completely within days to weeks. Coronary angiography usually reveals no identifiable lesions explaining the observed ventricular wall motion abnormality. The disease is usually preceded by an emotional or a physical stressor (Sharkey et al., 2010). A variety of critical neurologic illnesses and events, status epilepticus, and recurrent seizure activities may precipitate TS (Lemke et al., 2008). Recurrent episodes of TS triggered by convulsive status epilepticus have been reported (Legriel et al., 2008). During the last few years, many case reports of TS induced by epilepsy have been published. Among the most important electrocardiographic (ECG) findings in TS is evolving QTc prolongation besides ST-segment elevation and T-wave inversion (Kurisu et al., 2004). Certain ECG changes may last for weeks or months. Torsades de pointes and other malignant ventricular arrhythmia and sudden death have been reported as complications of TS. Denney et al. reported a case of TS with QT-interval prolongation in a young man who developed torsades de pointes and experienced aborted sudden cardiac death (Denney et al., 2005). Torsade de pointes associated with bradycardia and TS have been reported (Kurisu et al., 2008). The authors in the review article (Surges et al., 2010) have pointed out that sympathetic stimulation is among the potential mechanisms of periictal QTc prolongation. Cardiac sympathetic overactivation with excessive catecholamine production and intracardiac norepinephrine spill over is also among the discussed pathomechanisms of TS. A 12-lead ECG should be recommended in all patients after an epileptic seizure. If the above-mentioned ECG changes are detected, further investigation with myocardial biomarker control and performance of echocardiography will be necessary. Although specific treatments for TS have not yet been established, accurate diagnosis of the disease is indispensable in order to avoid unnecessary treatments as fibrinolysis. Furthermore, patients with TS may develop other serious complications besides life-threatening arrhythmias during the acute stage of illness as heart failure, pulmonary edema, cardiogenic shock, cardiovascular thromboembolism, and ventricular rupture with cardiac tamponade. The author has no conflict of interest to disclose. I confirm that I have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.