Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical Implications in Plaque Rupture.

Ramona Vinci,Massimo Massetti,Daniela Pedicino,Francesco Canonico,Rocco Vergallo,Roberto Piacentini,Lucia Stefanini,Giovanna Liuzzo,Giulio Russo,Myriana Ponzo,Alice Bonanni,Pellegrino Ciampi,Filippo Crea,Francesco Cribari,Simone Filomia,Anna Severino,Davide Flego,Rocco Antonio Montone,Cristina Conte,Eugenia Pisano,Marianna Di Sario,Alessia D’aiello

doi:10.3389/fcvm.2021.741221

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.

Highlights

Despite the advances in medical treatments and interventional innovations, the prevalence of acute coronary syndromes (ACS) is still high [1]
This study investigates the following: [1] the expression of CD31 on monocytes and platelets in ACS patients, patients with stable angina (SA), and control (CTRL) subjects; [2] the different role of CD31 in patients with ACS presented with ruptured fibrous cap (RFC) and intact fibrous cap (IFC)
Our population included a total of 151 individuals: [1] 86 patients with Acute Coronary Syndrome (ACS) admitted to our Coronary Care Unit (CCU) with a diagnosis of NonST Elevation Myocardial Infarction (NSTEMI) confirmed at coronary angiography [37]; [2] 46 patients with Stable Angina (SA) with symptoms of stable effort angina lasting more than 1 year, angiographically confirmed coronary artery disease, with any precedent acute coronary events, and any evident ischemic episodes during the last 48 h [38]; [3] 19 Control (CTRL) subjects without apparent clinical sign of coronary artery disease screened during their cardiovascular prevention medical examination

Summary

Introduction

Despite the advances in medical treatments and interventional innovations, the prevalence of acute coronary syndromes (ACS) is still high [1]. The rupture of a lipid-rich plaque, with the consequent release of highly thrombotic elements, characterizes at least 50% of patients with ACS [8]. Each plaque phenotype may be associated with a different thrombotic burden and this may be due to alternative pathogenic mechanisms [12,13,14,15,16,17]. Intracoronary imaging using optical coherence tomography (OCT) allows us to distinguish between a ruptured fibrous cap (RFC) and an intact fibrous cap (IFC) lesion. Histological analysis of thrombus aspirates from patients with ACS revealed a reduced thrombotic burden in patients with IFC, compared with those with RFC, which was enriched by inflammatory infiltrates [18]

Methods

Results

Conclusion