Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical
Ramona Vinci1,2, Daniela Pedicino1,2, Alice Bonanni1,2
1Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.
Insights
CD31 molecule involvement in atherothrombosis was studied in acute coronary syndromes (ACS) patients. CD31 plays a role in monocyte-platelet aggregate formation, even with dual anti-platelet therapy, suggesting alternative pathways in ruptured fibrous cap lesions.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Molecular Biology
Background:
- Atherothrombosis remains a significant complication of acute coronary syndromes (ACS) despite advances in cardiovascular care.
- Understanding the mechanisms of thrombotic risk is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the role of the CD31 molecule in the formation of monocyte-platelet (Mo-Plt) aggregates in patients with no-ST-segment elevation myocardial infarction (NSTEMI).
- To assess CD31 expression and its impact on thrombotic risk in NSTEMI patients, particularly those with different plaque characteristics and thrombus grades.
Main Methods:
- Cross-sectional study involving control subjects, stable angina (SA) patients, and NSTEMI patients.
- Optical Coherence Tomography (OCT) to assess plaque characteristics (Intact Fibrous Cap - IFC, Ruptured Fibrous Cap - RFC).
- Measurement of CD31 expression on monocytes and platelets, and ex vivo experiments to evaluate Mo-Plt aggregate formation.
Main Results:
- CD31 expression was altered in NSTEMI patients: reduced on monocytes and increased on platelets.
- These alterations were more pronounced in NSTEMI patients with RFC plaques compared to IFC lesions.
- Ex vivo studies confirmed CD31's participation in Mo-Plt aggregate formation, which decreased upon CD31 ligation, especially in RFC cases.
Conclusions:
- CD31 is implicated in monocyte-platelet aggregate formation in NSTEMI patients, irrespective of dual anti-platelet therapy (DAPT).
- This suggests alternative thrombotic pathways, particularly evident in patients with ruptured fibrous cap lesions.
- Targeting CD31 pathways may offer new therapeutic strategies for managing atherothrombosis in high-risk ACS patients.
Abstract:
Despite the recent innovations in cardiovascular care, atherothrombosis is still a major complication of acute coronary syndromes (ACS). We evaluated the involvement of the CD31 molecule in thrombotic risk through the formation of monocyte-platelet (Mo-Plt) aggregates in patients with ACS with no-ST-segment elevation myocardial infarction (NSTEMI) on top of dual anti-platelet therapy (DAPT). We enrolled 19 control (CTRL) subjects, 46 stable angina (SA), and 86 patients with NSTEMI, of which, 16 with Intact Fibrous Cap (IFC) and 19 with Ruptured Fibrous Cap (RFC) as assessed by the Optical Coherence Tomography (OCT). The expression of CD31 on monocytes and platelets was measured. Following the coronary angiography, 52 NSTEMIs were further stratified according to thrombus grade (TG) evaluation. Finally, a series of ex vivo experiments verified whether the CD31 participates in Mo-Plt aggregate formation. In patients with NSTEMI, CD31 was reduced on monocytes and was increased on platelets, especially in NSTEMI presented with RFC plaques compared to those with IFC lesions, and in patients with high TG compared to those with zero/low TG. Ex vivo experiments documented an increase in Mo-Plt aggregates among NSTEMI, which significantly decreased after the CD31 ligation, particularly in patients with RFC plaques. In NSTEMI, CD31 participates in Mo-Plt aggregate formation in spite of optimal therapy and DAPT, suggesting the existence of alternative thrombotic pathways, as predominantly displayed in patients with RFC.
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