Coronary microembolization during early reperfusion: infarct extension, but protection by ischaemic postconditioning.

Abstract

Reperfusion injury following acute myocardial infarction impacts not only on the myocardium but also on the coronary microcirculation, and microembolization from the culprit lesion contributes to microvascular obstruction. Prior experimental studies have not accounted for microembolization in ischaemia/reperfusion injury and not considered microembolization as a confounder and target of protection by ischaemic postconditioning. We therefore investigated the impact of microembolization during reperfusion on infarct size and cardioprotection by postconditioning. Anaesthetized, open-chest pigs were subjected to 90 min low-flow ischaemia. Immediate full reperfusion (n = 8) served as the control. Microembolization was induced by intracoronary infusion of 42 µm microspheres with the onset of reperfusion (n = 8). In a second step, postconditioning was induced by six cycles of 20s reperfusion/20s re-occlusion without (n = 8) and with superimposed microembolization (n = 8). Transmural blood flow and area at risk were determined by radioactive microspheres, infarct size by triphenyl tetrazolium chloride staining. Area at risk and transmural blood flow were not different between groups. Microembolization increased infarct size from 32 ± 3% of the area at risk to 47 ± 3% (P < 0.05). Embolizing particles were re-distributed away from the central infarcted area and accumulated in the infarct border, thus contributing to infarct extension. Postconditioning reduced infarct size without (21 ± 3%; P < 0.05 vs. immediate full reperfusion) and also with additional microembolization (26 ± 5%; P < 0.05 vs. immediate full reperfusion and microembolization); embolizing particles did not accumulate in the infarct border. Microembolization at reperfusion augments infarct size, but postconditioning in the presence of microembolization still reduces infarct size and attenuates infarct expansion.