The Pattern of Ventricular Repolarization during Therapeutic Hypothermia

Abstract

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. We investigate 63 patients undergoing TH following cardiac arrest at our hospital between January 2009 and October 2011. We excluded 43patients 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 20 patients (15 males, 5 females; 50.7 ± 11.4years). The TpTe was also expressed as relative to the duration of QT ([TpTe/QT]x100%), and the corrected value for heart rate (TpTe/√RR). These parameters were obtained from the precordial lead V4 and V6 of ECG on arrival at the hospital, during TH, and after rewarming to the normal temperature. The QTc became prolonged in all cases during TH and recovered to near baseline after cessation of TH (baseline: 459 ± 30 ms, TH: 539 ± 50 ms, rewarmed: 467 ± 86 ms; p<0.001). While the change of the TpTe/√RR (cTpTe) was not significant at lead V4 (baseline: 127 ± 28 ms, TH: 125 ± 36 ms; p=0.970) and V6 (baseline: 116 ± 20 ms, TH: 113 ± 33 ms; p=0.601), the [TpTe/QTe] x 100(%) was significantly decreased during TH relative to baseline measurement at lead V4 (baseline: 27 ± 5%, TH: 23 ± 5%; p=0.013) and lead V4 (baseline: 25 ± 4%, TH: 21 ± 4%; p=0.009). 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.