Published online Oct 26, 2015. doi: 10.4330/wjc.v7.i10.621
Peer-review started: May 20, 2015
First decision: June 24, 2015
Revised: July 21, 2015
Accepted: August 13, 2015
Article in press: August 14, 2015
Published online: October 26, 2015
Processing time: 168 Days and 7.5 Hours
In remote ischemic conditioning (RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site (remote ischemic preconditioning), during the ischemic insult (remote ischemic perconditioning) or at the onset of reperfusion (remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy.
Core tip: Remote ischemic conditioning (RIC) is a safe, non-invasive, and inexpensive technique that has the potential to protect the heart against the ischemia-reperfusion injury. Its cardioprotective efficacy is currently being evaluated, and diverging results are emerging. It is thus worth resuming current understanding of RIC pathophysiology and clinical efficacy.