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 F-18-FDG PET/MRI. Although this novel biosignal correlateswith long-termfunctional 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 F-18-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 F-18-FDG uptake (SUVmean) in the infarcted myocardium than patients with low MPA (p < 0.05). Furthermore, there was an association of high MPA percentage in all monocyte subpopulations with deteriorating Delta LV-EF after 6 months (p < 0.01), which was confirmed in an extended analysis with additional 29 patients without PET/MRI data available. In this analysis, administration of Ticagrelor was associated with lower MPA percentage of CD14(high) monocyte subpopulations than Clopidogrel (p < 0.01) or Prasugrel (p < 0.05).
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. (c) 2019 Elsevier B.V. All rights reserved.
I. Medizinische Klinik und Poliklinik (Kardiologie); III. Medizinische Klinik und Poliklinik (Hämatologie / Onkologie); Klinik für Herz- und Kreislauferkrankungen im Erwachsenenalter (Prof. Schunkert); Klinik und Poliklinik für Nuklearmedizin