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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Monocyte-platelet aggregates affect local inflammation in patients with acute myocardial infarction.
International Journal of Cardiology 2019 July 16
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 P2Y12 inhibition. In detail, patients with high MPA percentages of CD14high CD16+ and CD14low CD16+ monocytes had significantly higher local 18 F-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 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 CD14high 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.
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