Protective ischaemia in patients: preconditioning and postconditioning.
Infarct size can be limited by reducing the determinants of infarct size or increasing collateral blood flow by treatment initiated before the ischaemic event. Reperfusion is the definitive treatment for permanently reducing infarct size and restoring some degree of contractile function to the affected myocardium. Innate survival mechanisms in the heart can be stimulated by short, non-lethal periods of ischaemia and reperfusion, applied either before or after the ischaemic event. Preconditioning, a series of transient intervals of ischaemia and reperfusion applied before the lethal 'index' ischaemic event, sets in motion molecular and cellular mechanisms that increase cardiomyocyte survival to a degree that had not hitherto been seen before. The cardioprotective ischaemic-reperfusion protocol applied at onset of reperfusion, termed 'postconditioning' (Postcon), is also associated with significant cardioprotection that can be applied at the point of reperfusion treatment in the catheterization laboratory or operating room. Both preconditioning and Postcon have been successfully applied to the clinical setting and have been found to reduce infarct size and other attributes of post-ischaemic injury. This review will summarize the physiological preclinical data on preconditioning and Postcon that are relevant to their translation to clinical therapeutics and treatment.
Granfeldt
Asger
A
Department of Anesthesiology and Critical Care, Aarhus University, Aarhus, Denmark.
Lefer
David J
DJ
Vinten-Johansen
Jakob
J
D000818:Animals; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D002470:Cell Survival; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000150:complications / Q000473:pathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology*; D016896:Treatment Outcome
D002317:Cardiovascular Agents