We thank Drs Rai, Cronin, Kluger, and LaSala for their interest in our study and for their thorough discussion of the possible mechanisms for prolonged systolic duration during therapeutic hypothermia.

As they point out, we showed in our figures a prolonged QT interval during hypothermia, although we did not comment specifically on this. Prolonged duration of the QT interval during hypothermia has been demonstrated since the earliest experiments on cardiac function during hypothermia. It is a frequent finding in hypothermic patients and is considered a hallmark of hypothermic effects on cardiac function. The prolongation of the QT interval could be due to prolonged depolarization and repolarization of the cardiomyocytes but could also be caused by delayed conduction properties and dyssynchrony in the left ventricle.

Recent studies in patients with long-QT syndrome have demonstrated prolonged duration of contraction and greater variation in contraction duration of the ventricle. These variations also appear to be transmural. What we can see from our findings is that the prolonged QT interval coincides with the prolonged mechanical systole, not only in global left ventricle recordings but also in regional recordings. This indicates that the prolonged QT interval is caused by prolongation of the duration of systole. The effect from eventual delayed conduction velocity or dyssynchrony in the hypothermic left ventricle is uncertain and warrants further studies.

In conclusion, we agree with Rai et al . that the prolonged systolic duration could be due to a change in electrical properties resulting in a prolongation of the QT interval. We appreciate their attention to this important aspect of the hypothermic effects on cardiac function.