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Remote Ischemic Preconditioning: A Complex Question with an Even More Complex Answer.

The concept of ischemic preconditioning dates back to the 1980s, when it was discovered that brief periods of ischemia slow rates of adenosine triphosphate (ATP) depletion during subsequent episodes of ischemia and that intermittent reperfusion during ischemic periods can flush out accumulated catabolites. 1 Given that applying ischemia directly to target organs – such as the heart, brain, or kidneys – is impractical outside of an experimental setting, attention turned to the application of remote ischemia – that is, applying an ischemic stimulus in an area away from target organs. 2 Over the next several years, continued experimentation with remote ischemic preconditioning (RIPC) led to the discovery that even brief induced limb ischemia can reduce myocardial infarct size and prevent endothelial dysfunction. 3, 4 It is believed that RIPC works by to limit ischemia-reperfusion injury, which is tissue damage induced by an ischemic insult and the subsequent injury that occurs with repercussion of those tissues. 5 In for attenuation regard 6–8 In their manuscript, “Remote Ischemic Preconditioning in High-risk Cardiovascular Surgery Patients: A Randomized-controlled Trial,” the authors present a valiant attempt to elucidate the complex of complex process. The authors report their results of a double-blind trial in which patients undergoing high risk cardiac or vascular surgery procedures were randomized to undergo RIPC or a sham-RIPC treatment (control) prior to their planned surgical intervention. Assuming an event rate of 30%, type I error equal to 0.05, power equal to 0.80, and relative risk reduction of 40% with RIPC, their study was well-powered to detect a difference