Ischemic preconditioning is now well known, but post conditioning is a relatively new concept. In ischemic preconditioning, repeated episodes of ischemia preceding a coronary occlusion conditions the myocardium so that the infarct size is lesser. In ischemic post conditioning repeated episodes of occlusion re-occlusion during reperfusion following a coronary occlusion reduces the ultimate infarct size and reperfusion injury. In a dog model with occlusion of left anterior descending artery occlusion for 60 minutes followed by reperfusion, cyclical re-perfusion / re-occlusion of 30 seconds, for three cycles reduced the infarct size by 44%. The RISK (reperfusion injury salvage kinase) pathway producing upregulation of prosurvival kinases is thought to mediate post conditioning. PI3K-Akt and MEK 1/2-p42/44 kinases have been considered to be components of these cell survival pathways.  Post conditioning has been shown to have an anti-arrhythmic effect in reducing reperfusion arrhythmias as well. Less free radical generation less oxidant-induced injury has been deomonstrated, with less superoxide generation. In experimental studies post conditioning has been shown to be attenuated byagents which block K+ATP channels, including glibenclimide which is a nonselective K+ATP blocker.

“Pharmacological postconditioning”  with agents that activate the RISK pathway and mediate the protective effects of postconditioning is an option to be investigated.  Insulin, atorvastatin, bradykinin, TGF-beta and glucagon-like peptide1 (GLP-1) may be potential adjuvants to conventional reperfusion strategies which could be investigated. Physical occlusion /re-occlusion cycles during percutaneous intervention or coronary bypass grafting may not be considered due to the potential for other damages like plaque disruption and thrombus formation.

Ref: Tsang A et al, Am J Physiol Heart Circ Physiol 289: H2-H7, 2005