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

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 ¹⁸F-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 ¹⁸F-FDG uptake, monocyte platelet aggregates (MPA), and P2Y₁₂ inhibition. In detail, patients with high MPA percentages of CD14^highCD16⁺ and CD14^lowCD16⁺ monocytes had significantly higher local ¹⁸F-FDG uptake (SUV_mean) 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 ΔLV-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. P2Y₁₂ inhibition may intervene in this pathophysiologic process. Prospective studies are needed to further examine this important relationship.