Key result
Mild hypothermia significantly delayed the onset of stone heart to 52 ± 4 minutes compared to 29 ± 3 minutes in normothermic swine during untreated sustained ventricular fibrillation.
Why the study?
Does mild hypothermia delay the development of stone heart in a swine model of untreated sustained ventricular fibrillation?
RCT (n=14)
Single-blind
Randomized
No
Does mild hypothermia delay the development of stone heart in a swine model of untreated sustained ventricular fibrillation?
Effect estimate: 81% delay
Absolute Event Rate: 52% vs 29%
p-value: p=<0.001
In a swine model of untreated ventricular fibrillation, pre-arrest mild hypothermia significantly delayed the onset of ischemic myocardial contracture (stone heart), suggesting a direct cardioprotective mechanism that extends the morphologic limit of resuscitability.
Does not support clinical adoption; leaves open whether mild hypothermia extends resuscitability in human VF.
BACKGROUND: 'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart. METHODS: Fourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n=6) or hypothermia groups (group II; n=8). Mild hypothermia (34 ± 2 °C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point. RESULTS: In group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p<0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P<0.001). CONCLUSIONS: In this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability.
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Sorrell et al. (2011) conducted an RCT in Untreated sustained ventricular fibrillation (n=14). Mild hypothermia vs. Normothermia was evaluated on Time to development of stone heart (LV volume <1/3 of baseline) (81% delay, p=<0.001). Mild hypothermia significantly delayed the onset of stone heart to 52 ± 4 minutes compared to 29 ± 3 minutes in normothermic swine during untreated sustained ventricular fibrillation.
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