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Ann Thorac Surg 2004;78:969
© 2004 The Society of Thoracic Surgeons
Department of Surgery, University of Kentucky College of Medicine, Room MN 276, Chandler Medical Center, 800 Rose St, Lexington, KY 40536–0298, USA
rlasley{at}uky.edu
The study by Halkos and colleagues addressed the hypothesis that the combination of ischemic preconditioning and ischemic postconditioning exerts greater cardioprotection than either agent alone. This is an intriguing question from both a basic science standpoint and in terms of clinical relevance. Ischemic preconditioning has been shown to reduce numerous metabolic and ionic perturbations that occur during prolonged ischemia. Thus ischemic preconditioning appears to delay the onset of irreversible ischemic injury. Ischemic postconditioning, on the other hand, exerts no effects on ischemic injury, but exerts its beneficial infarct-reducing effect by modulating early reperfusion injury. Given these fundamental differences the authors' hypothesis was relatively straightforward.
At first perusal then the results that the combination of ischemic preconditioning and postconditioning did not exert additive protection would appear to be unexpected. However, as the authors pointed out, one of the limitations of their study was the fact that the protection exerted by both ischemic preconditioning and ischemic postconditioning in the present model (
10% infarct size) may have been maximal. To fully address this issue the prolonged ischemia time should have been extended to produce more injury or the ischemic area at risk enlarged. This study and the authors' original report of the phenomenon of ischemic postconditioning [1] do provide some evidence for both decreased neutrophil infiltration and reduced reactive oxygen species formation. However, whether these are the mechanisms or results of the protection have yet to be determined. Furthermore whether ischemic postconditioning produces infarct reduction following prolonged reperfusion (
24 hours), as does ischemic preconditioning, remains unknown.
Despite the limitations of the study by Halkos and colleagues, the major strength of this study is the further confirmation that modulation of the reperfusion process can result in significant cardioprotection. This may seem a trivial point, particularly to cardiac surgeons who have been using various reperfusion interventions for years, but just over a decade ago, the significance of reperfusion injury was still being debated [2]. Although the combination of ischemic preconditioning and postconditioning did not exert additive protection in the above report, this study does address the important issue of investigating the combination of both preischemic and reperfusion therapies to maximize cardioprotection during both on-pump and off-pump cardiac surgery.
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