A fresh look at reperfusion injury.

Time for primary review 25 days. In clinical therapy of evolving acute myocardial infarction, coronary reperfusion has proven to be the only way to limit infarct size, provided it occurs soon enough after coronary artery occlusion. However, there is also evidence that reperfusion is accompanied by detrimental manifestations known as ‘reperfusion injury’. Reperfusion injury refers to a causal event associated with reperfusion that had not occurred during the preceding ischemic period and can be entirely attenuated by an intervention given only at the time of reperfusion. It classically includes myocardial stunning, reperfusion arrhythmias and lethal reperfusion injury. Clearly, reperfusion arrhythmias do not represent an important problem for the clinician because their incidence is very low and they can be quite easily treated. Myocardial stunning is usually not a major clinical problem in the context of acute myocardial infarction because it disappears spontaneously and is very sensitive to inotropic agents. Myocardial stunning becomes of serious concern only if the affected portion of the myocardium is very large. Lethal reperfusion injury could be an interesting target for the clinician who is now able to promptly revascularize acutely ischemic myocardium. However, the existence of lethal reperfusion injury has been debated for years by scientists and is still controversial [1–4]. One of the problems is that the development of necrosis cannot be accurately followed in time, both in experimental animal preparations and in man. Instead, scientists have used an indirect approach to deal with this issue; the principle is to modify the nature of reperfusion and then assess whether the extent of necrosis is reduced. Numerous studies have been performed according to this general design. Unfortunately, many of them remained inconclusive, partly for technical reasons [5]. In most, actually hundreds of studies on lethal reperfusion injury, the effects of antioxidants were investigated. … * Corresponding author. Tel.: +49 (641) 994-7241; Fax: +49 (641) 994-7239.