Background Therapeutic hypothermia (TH) is used in neuroprotection following cardiac arrest. Accidental hypothermia has been itself known to cause prolongation of the corrected QT interval (QTc). QTc prolongation can cause polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF). The interval from the peak to the end of the T wave (TpTe) indicates myocardial transmural dispersion of repolarization (TDR) and increased TDR may create electrophysiological conditions for reentry. We investigate the effect of TH on the pattern of ventricular repolarization including the QTc and TpTe. Methods We consecutively enrolled 18 patients undergoing TH following cardiac arrest at our hospital between January 2010 and August 2011. We excluded 8 patients from the study because of atrial fibrillation, or when T waves were flat or the end of T waves were indefinite. We measured the QTc with Bazett���s formula and the TpTe in 10 patients (6 males, 4 females; 51 짹 7 years). The TpTe was also expressed as relative to the duration of QTe ([TpTe/QTe]x100%), and the corrected value for heart rate (TpTe/���RR). These parameters were obtained from all the 12-leads of ECG on arrival at the hospital, during TH, and after rewarming to the normal temperature. Results The only one case showed non-sustained ventricular tachycardia during rewarming. The QTc became prolonged in all cases during TH and recovered to near baseline after cessation of TH (baseline: 464 짹 25 ms, TH: 533 짹 49 ms, rewarmed: 481 짹 113 ms; p=0.007). While the change of the TpTe/���RR (cTpTe) was not significant (baseline: 103 짹 14 ms, TH: 105 짹 22 ms, rewarmed: 88 짹 14 ms; p=0.074), the [TpTe/QTe] x 100(%) was significantly decreased during TH and rewarming relative to baseline measurement (baseline: 22 짹 3%, TH: 19 짹 4%, rewarming: 18 짹 3%; P=0.019). Conclusion In present study, although the TDR was not increased during TH, delay of repolarization was demonstrated with the QTc prolongation. If recurrent ventricular arrhythmia is occurred, the early afterdepolarization (triggered activity) might be the more important mechanism of ventricular arrhythmia during TH than the reentry. As the QTc prolongation per se carries potential for refibrillation, close ECG monitoring is needed during TH. Since the QTc and the [TpTe/QTe] x 100(%) showed statistically significant decrease after cessation of TH, the risk of refibrillation may be attenuated during rewarming.