The concept of reperfusion injury has been clearly demonstrated in many experimental stud- ies, although even in those studies data are not fully consistent.8,24,25,31,42 In contrast, in clinical
myocardial infarction, the importance of reperfusion injury has not been established. In fact, clinical studies with anti-inflammatory drugs,11,13 Na+/H+ exchange inhibitors,9 glucose-insulin-
potassium,12,43,44 and adenosine10,45 so far led to inconclusive results. This in mind, one might
raise the question that possibly treatment in clinical practice is too late to reduce reperfusion injury or that there is no (relevant) reperfusion injury in humans, and thus no clinical benefit of decreasing such injury. Similarly, the PARI-MI study did not reveal a clear benefit, and no dose-relation, even though higher dosages were studied than in the pre-clinical studies, in which ITF-1697 was shown to be beneficial. The main reason for discrepancy between animal and human findings would be the different pathophysiologic context in which the drug was tested, leaving open the hypothesis that the drug might have beneficial effects in different pathophysiological settings, more appropriate for the drug activity.
Acknowledgments
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