The cardioprotective effect of therapeutic hypothermia (32-34°C) has been well demonstrated in animal models of acute myocardial infarction. Beyond infarct size reduction, this protection was associated with prevention of the no-reflow phenomenon and long-term improvement in terms of left ventricular remodelling and performance. However, all these events were observed when hypothermia was induced during the ischaemic episode, and most benefits virtually vanished after reperfusion. This is consistent with clinical findings showing a lack of benefit from hypothermia in patients presenting acute myocardial infarction in most trials. In these studies, hypothermia was most often achieved too far into the reperfusion phase (i.e. possibly too late to reduce infarct size); this is supported by meta-analyses and subgroup analyses suggesting that the benefits of hypothermia could still be observed in patients with a large infarction and more rapid cooling before reperfusion. Novel strategies for ultra-fast induction of hypothermia and/or prehospital cooling might therefore be more beneficial.
Keywords: Acute myocardial infarction; Cardioprotection; Hypothermia; Hypothermie; Infarctus du myocarde; STEMI; Temperature; Température.
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