An increased platelet–leukocytes interaction at the culprit site of coronary artery occlusion in acute myocardial infarction: A pathogenic role for “no-reflow” phenomenon?

Abstract

Background Distal protection devices have been shown to reduce the incidence of “no flow” phenomenon during primary percutaneous coronary intervention (PCI). So far, it has not been well clarified which mechanism is mainly involved in distal coronary protection. Aim To investigate the activation state of leukocytes and platelets locally present within the blood from the site of coronary occlusion. Methods Ten patients with acute myocardial infarction (AMI) underwent primary PCI with an embolization protection device and aspiration catheter (PercuSurge GuardWire) were included. The following functional parameters: a) monocyte and neutrophils surface molecules; b) platelet surface activatory antigens; c) leukocytes–platelet conjugates were studied by flow cytometry in blood obtained from the site of coronary occlusion and from peripheral femoral artery. Results The leukocyte–platelet adhesion index was significantly higher in the aspirated blood at the site of coronary occlusion than in the peripheral arterial blood for both monocytes (0.226 ± 0.04 vs. 0.084 ± 0.01; p = 0.004) and neutrophils (1.372 ± 0.3 vs. 0.524 ± 0.1; p = 0.02). Moreover, the volume of coaggregates exhibited a significant increase in coronary blood for both populations ( p = 0.02 for monocytes and for neutrophils). Interestingly, a significant up-regulation of the adhesive molecule CD18 was observed in coronary blood respect to systemic circulation either in monocytes ( p = 0.01) than in neutrophils ( p = 0.003). A significant up-regulation of monocyte (HLA-DR) and neutrophil (CD66b) activatory molecules expression was also observed in the aspirated coronary compared to peripheral artery blood ( p = 0.02 and p = 0.03 for HLA-DR and CD66b, respectively). Conclusions These data indicate an increased leukocyte–platelet functional interaction in AMI at the site of plaque rupture relative to the systemic circulation, which may be one of the pathogenetic mechanisms responsible for myocardial “no-reflow” phenomenon.