Does Cool Reperfusion Limit Myocardial Infarction Injury?

In this issue of Circulation: Cardiovascular Interventions , a pilot study by Gotberg et al1 deserves notice. It may have major implications for clinicians who deal with myocardial infarction, and it suggests important insights into the poorly understood area of human reperfusion injury.Article see p 400The investigator team is to be congratulated for successfully surmounting a formidable implementation challenge. Within 30 minutes, they were able to rapidly cool patient body temperatures to an average less than the target temperature of <35°C without allowing the induction of cooling to interfere with or prolong the door-to-balloon time for percutaneous coronary intervention. To put this 30-minute speed of cooling into perspective, a 2010 investigation of human hypothermia from Australia reported a nearly 8-hour time interval to achieve temperatures <34°C in patients with cardiac arrest.2 The Gotberg pilot study goes on to describe a 38% reduction in infarct size and 43% reduction in peak troponin T release for the patients who received cooling before coronary reperfusion versus controls who received standard reperfusion within the same time period. The study raises an important clinical question that we must address: Is cool reperfusion the best reperfusion?An even more crucial scientific question lies just beneath the surface of these data: Does reperfusion injury exist in humans, and if so, does it have any relevance in terms of long-term function or tissue injury? Reperfusion injury remains controversial since its first description in the 1970s when it was observed that reoxygenation of the ischemic perfused isolated heart resulted in a large release of cardiac injury enzymes along with structural cellular damage seen extensively during reperfusion but only very minimally during the preceding ischemia.3,4 The notion of reperfusion injury suggested that some portion of cell death was caused by the conditions of …