Abstract
Remote ischemic conditioning has been investigated for cardioprotection to attenuate myocardial ischemia/reperfusion injury. In this review, we provide a comprehensive overview of the current knowledge of the signal transduction pathways of remote ischemic conditioning according to three stages: Remote stimulus from source organ; protective signal transfer through neuronal and humoral factors; and target organ response, including myocardial response and coronary vascular response. The neuronal and humoral factors interact on three levels, including stimulus, systemic, and target levels. Subsequently, we reviewed the clinical studies evaluating the cardioprotective effect of remote ischemic conditioning. While clinical studies of percutaneous coronary intervention showed relatively consistent protective effects, the majority of multicenter studies of cardiac surgery reported neutral results although there have been several promising initial trials. Failure to translate the protective effects of remote ischemic conditioning into cardiac surgery may be due to the multifactorial etiology of myocardial injury, potential confounding factors of patient age, comorbidities including diabetes, concomitant medications, and the coadministered cardioprotective general anesthetic agents. Given the complexity of signal transfer pathways and confounding factors, further studies should evaluate the multitarget strategies with optimal measures of composite outcomes.
Highlights
Myocardial infarction results in tissue damage as a consequence of both ischemia and subsequent reperfusion injury [1]
A brief episode of myocardial ischemia and reperfusion can protect the myocardium from prolonged ischemia/reperfusion by activating the molecular defense mechanisms [2]
Remote conditioning is possible through brief episodes of ischemia/reperfusion of a distant limb: This transfer of protection is called remote ischemic conditioning
Summary
Myocardial infarction results in tissue damage as a consequence of both ischemia and subsequent reperfusion injury [1]. In the original animal studies, repeated brief preceding cycles of occlusion/reperfusion of the left circumflex artery reduced the size of a subsequent myocardial infarct in the left anterior descending artery territory [3]. This effect was regarded as an incidental finding. RIPC was shown to provide protection against acute kidney injury in patients undergoing cardiac surgery [15] These promising studies elicited many subsequent clinical trials to reproduce the protective effects and laboratory studies to elucidate the mechanism of transfer of protection
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