Key result
Advanced hypothermia at 28 °C enhanced arrhythmogenic potential, with ventricular fibrillation induced in 5 of 11 porcine hearts compared to 1 of 11 at both 37 °C and 32 °C.
Why the study?
Therapy-resistant ventricular arrhythmias can occur during accidental advanced hypothermia, but the arrhythmogenic substrate developing under hypothermic conditions required further clarification.
Does advanced hypothermia increase the inducibility and therapy-resistance of ventricular arrhythmias compared to mild hypothermia or normothermia in a porcine ventricular wedge model?
Does advanced hypothermia increase the inducibility and therapy-resistance of ventricular arrhythmias compared to mild hypothermia or normothermia in a porcine ventricular wedge model?
Advanced hypothermia (28°C) enhances the arrhythmogenic substrate characterized by slowed conduction and prolonged repolarization, leading to more frequent and therapy-resistant ventricular fibrillation compared to mild hypothermia (32°C).
Suggests caution with 28°C hypothermia in arrhythmia-prone settings; leaves open translation to human therapeutic protocols.
Therapy-resistant ventricular arrhythmias can occur during accidental advanced hypothermic conditions. On the other hand, hypothermic therapy using mild cooling has been successfully accomplished with infrequent ventricular arrhythmia events.To further clarify the therapeutic-resistant arrhythmogenic substrate which develops in hypothermic conditions, an experimental study was performed using a perfusion wedge preparation model of porcine ventricle, and electrophysiological characteristics, inducibility of ventricular arrhythmias, and effects of therapeutic interventions were assessed at 3 target temperatures (37, 32 and 28°C).As the myocardial temperature decreased, myocardial contractions and the number of spontaneous beats deceased. Depolarization (QRS width, stimulus-QRS interval) and repolarization (QT interval, ERP) parameters progressively increased, and dispersion of the ventricular repolarization increased. At 28°C, VF tended to be inducible more frequently (1/11 at 37°C, 1/11 at 32°C, and 5/11 hearts at 28°C), and some VFs at 28°C required greater defibrillation energy to resume basic rhythm.An advanced but not a mild hypothermic condition had an enhanced arrhythmogenic potential in our model. In the advanced hypothermic condition, VF with relatively prolonged F-F intervals and a greater defibrillation energy were occasionally inducible based on the arrhythmogenic substrate characterized as slowed conduction and prolonged repolarization of the ventricle.
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Saitoh et al. (2019) studied Hypothermia-induced ventricular arrhythmias (n=11). Advanced hypothermia (28 °C) vs. Normal temperature (37 °C) and mild hypothermia (32 °C) was evaluated on Inducibility of ventricular fibrillation. Advanced hypothermia at 28 °C enhanced arrhythmogenic potential, with ventricular fibrillation induced in 5 of 11 porcine hearts compared to 1 of 11 at both 37 °C and 32 °C.
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