Key result
Inhaled xenon plus hypothermia significantly reduces 72-hour troponin-T release vs hypothermia alone after OHCA.
Why the study?
Inhaled xenon combined with hypothermia was previously reported to attenuate brain white matter injury in comatose survivors of OHCA, and its effect on myocardial ischemic damage in the same population remained to be assessed.
Does inhaled xenon combined with hypothermia reduce myocardial ischemic damage (troponin-T release) compared to hypothermia alone in comatose survivors of out-of-hospital cardiac arrest?
RCT (n=110)
Randomized
Yes
Does inhaled xenon combined with hypothermia reduce myocardial ischemic damage (troponin-T release) compared to hypothermia alone in comatose survivors of out-of-hospital cardiac arrest?
In comatose survivors of out-of-hospital cardiac arrest, adding inhaled xenon to hypothermia significantly attenuates myocardial injury as evidenced by reduced 72-hour troponin-T release compared to hypothermia alone.
Answers are grounded in this paper and cite their sources.
Xenon shows no clear myocardial benefit in OHCA; leaves open its role beyond neuroprotection in larger trials.
Background The authors previously reported that inhaled xenon combined with hypothermia attenuates brain white matter injury in comatose survivors of out-of-hospital cardiac arrest (OHCA). Objectives A pre-defined secondary objective was to assess the effect of inhaled xenon on myocardial ischemic damage in the same study population. Methods A total of 110 comatose patients who had experienced OHCA from a cardiac cause were randomized to receive either inhaled xenon (40% end-tidal concentration) combined with hypothermia (33°C) for 24 h (n = 55; xenon group) or hypothermia treatment alone (n = 55; control group). Troponin-T levels were measured at hospital admission, and at 24 h, 48 h, and 72 h post-cardiac arrest. All available cases were analyzed for troponin-T release. Results Troponin-T measurements were available from 54 xenon patients and 54 control patients. The baseline characteristics did not differ significantly between the groups. After adjustments for age, sex, study site, primary coronary percutaneous intervention (PCI), and norepinephrine dose, the mean ± SD post-arrival incremental change of the ln-transformed troponin-T at 72 h was 0.79 ± 1.54 in the xenon group and 1.56 ± 1.38 in the control group (adjusted mean difference -0.66; 95% confidence interval: -1.16 to -0.16; p = 0.01). The effect of xenon on the change in the troponin-T values did not differ in patients with or without PCI or in those with a diagnosis of ST-segment elevation myocardial infarction (group by PCI or ST-segment elevation myocardial infarction interaction effect; p = 0.86 and p = 0.71, respectively). Conclusions Among comatose survivors of OHCA, in comparison with hypothermia alone, inhaled xenon combined with hypothermia suggested a less severe myocardial injury as demonstrated by the significantly reduced release of troponin-T.
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Arola et al. (2017) conducted an RCT in Comatose survivors of out-of-hospital cardiac arrest from a cardiac cause (n=110). Inhaled xenon combined with hypothermia (33°C) vs. Hypothermia treatment alone (33°C) was evaluated on Post-arrival incremental change of ln-transformed troponin-T at 72 hours (MD -0.66, 95% CI -1.16 to -0.16, p=0.01). Inhaled xenon plus hypothermia reduced 72-h ln-transformed troponin-T release vs hypothermia alone in comatose OHCA survivors.
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