Reduction of infarct size by ischaemic post-conditioning in humans: fact or fiction?

This editorial refers to ‘Ischaemic postconditioning revisited: lack of effects on infarct size following primary percutaneous coronary intervention’ by X. Freixa et al. , doi:10.1093/eurheartj/ehr297 Acute myocardial infarction continues to be a major cause of mortality and morbidity, and infarct size is the major determinant of patients' prognosis. The only way to reduce infarct size is to restore coronary blood flow; however, reperfusion not only salvages myocardium from infarction, but also brings about additional ‘reperfusion injury’. Ischaemic post-conditioning, i.e. the repeated mechanical brief interruption of coronary blood flow during early reperfusion, attenuates reperfusion injury and reduces the ultimate infarct size.1,2 Ischaemic post-conditioning was first characterized in dogs3 and confirmed in all species tested so far, provided they were young and healthy.4 Staat et al. in a landmark proof-of-concept study translated the experimental finding to a small cohort of select patients with acute myocardial infarction; the cumulative creatine kinase (CK) release during reperfusion was reduced by a protocol of four cycles of 1 min angioplasty balloon inflation/1 min deflation before full reperfusion. The cumulative CK release vs. the area at risk, as determined using ventriculography before reperfusion from the abnormally contracting myocardium, was also reduced.5 Reduction of infarct size by ischaemic post-conditioning in patients with acute myocardial infarction was subsequently confirmed in a number of small studies, using as endpoints CK6–9 or troponin release,9 ECG ST-segment resolution, …