Monocyte-platelet aggregates affect local inflammation in patients with acute myocardial infarction

Abstract The local inflammatory response following acute myocardial infarction (AMI) is increasingly being recognized as a central factor determining infarct healing. Myocardial inflammation can be visualized in patients using fasting 18 F-FDG PET/MRI. Although this novel biosignal correlates with long-term functional outcome, the corresponding cellular substrate is not well understood. Here we present a retrospective analysis of 29 patients with AMI who underwent revascularization, suggesting a connection between post infarction myocardial fasting 18 F-FDG uptake, monocyte platelet aggregates (MPA), and P2Y 12 inhibition. In detail, patients with high MPA percentages of CD14 high CD16 + and CD14 low CD16 + monocytes had significantly higher local 18 F-FDG uptake (SUV mean ) in the infarcted myocardium than patients with low MPA ( p p high monocyte subpopulations than Clopidogrel ( p p Taken together, the findings from this analysis suggest that platelet aggregability may affect monocyte extravasation into the infarcted myocardium and influence long-term functional outcome. P2Y 12 inhibition may intervene in this pathophysiologic process. Prospective studies are needed to further examine this important relationship.