Therapeutic hypothermia to reduce infarct size in STEMI: time to give it the cold shoulder?

Timely reperfusion of the infarct-related coronary artery in acute ST-segment elevation myocardial infarction (STEMI) patients using primary percutaneous coronary intervention (PCI) is the gold-standard therapy for limiting myocardial infarct (MI) size1. However, the process of restoring coronary blood flow can, in itself, induce further cardiomyocyte death due to the detrimental effects of acute ischaemia/reperfusion injury (IRI) which include mitochondrial dysfunction, oxidative stress, calcium overload, inflammation and microvascular obstruction1. As such, there is still a need for new cardioprotective treatments to reduce MI size and prevent the onset of heart failure in STEMI patients treated by primary PCI.

Although a large number of cardioprotective strategies have been reported to reduce MI size in animal models of acute IRI, their translation into the clinical setting for patient benefit has been largely disappointing. The potential reasons for this failed translation of cardioprotection are multiple and include limitations with the preclinical animal IRI models, which do not accurately recapitulate the clinical setting, and issues with clinical study design, including the following: the testing of cardioprotective interventions which failed in preclinical studies, poor selection...