Myocardial postconditioning

Myocardial postconditioning

In ischemic postconditioning repeated episodes of occlusion re-occlusion during reperfusion following a coronary occlusion reduces the ultimate infarct size and reperfusion injury. The RISK (reperfusion injury salvage kinase) pathway producing upregulation of prosurvival kinases is thought to mediate post conditioning. Post conditioning has been shown to have an antiarrhythmic effect in reducing reperfusion arrhythmias as well. Less free radical generation and less oxidant-induced injury has been demonstrated, with less superoxide generation. In experimental studies post conditioning has been shown to be attenuated by agents which block K+ATP channels, including glibenclamide 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.  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. (Tsang A et al, Am J Physiol Heart Circ Physiol 289: H2-H7, 2005)