Why the study?
Does rapid myocardial cooling terminate ventricular fibrillation in Langendorff-perfused rabbit hearts?
Does rapid myocardial cooling terminate ventricular fibrillation in Langendorff-perfused rabbit hearts?
Rapid myocardial cooling to <20°C effectively terminates ventricular fibrillation by significantly depressing myocardial conduction in a preclinical rabbit model.
Rapid cooling terminates VF in rabbit hearts via conduction slowing; leaves open clinical translation to human VF management.
Because of its electrophysiological effects, hypothermia can influence the mechanisms that intervene in the sustaining of ventricular fibrillation. We hypothesized that a rapid and profound reduction of myocardial temperature impedes the maintenance of ventricular fibrillation, leading to termination of the arrhythmia. High-resolution epicardial mapping (series 1; n = 11) and transmural recordings of ventricular activation (series 2; n = 10) were used to analyze ventricular fibrillation modification during rapid myocardial cooling in Langendorff-perfused rabbit hearts. Myocardial cooling was produced by the injection of cold Tyrode into the left ventricle after induction of ventricular fibrillation. Temperature and ventricular fibrillation dominant frequency decay fit an exponential model to arrhythmia termination in all experiments, and both parameters were significantly correlated (r = 0.70, P < 0.0001). Termination of the arrhythmia occurred preferentially in the left ventricle and was associated with a reduction in conduction velocity (-60% in left ventricle and -54% in right ventricle; P < 0.0001) and with activation maps predominantly exhibiting a single wave front, with evidence of wave front extinction. We conclude that a rapid reduction of temperature to <20 degrees C terminates ventricular fibrillation after producing an important depression in myocardial conduction.
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Chorro et al. (2002) studied this question.
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