Vinci Ramona, Pedicino Daniela, Bonanni Alice, d'Aiello Alessia, Pisano Eugenia, Ponzo Myriana, Severino Anna, Ciampi Pellegrino, Canonico Francesco, Russo Giulio, Di Sario Marianna, Vergallo Rocco, Filomia Simone, Montone Rocco Antonio, Flego Davide, Stefanini Lucia, Piacentini Roberto, Conte Cristina, Cribari Francesco, Massetti Massimo, Crea Filippo, Liuzzo Giovanna
Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.
Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Front Cardiovasc Med. 2022 Jan 25;8:741221. doi: 10.3389/fcvm.2021.741221. eCollection 2021.
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 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. 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.
尽管心血管护理领域最近有创新，但动脉粥样硬化血栓形成仍然是急性冠状动脉综合征（ACS）的主要并发症。我们通过在接受双联抗血小板治疗（DAPT）的非ST段抬高型心肌梗死（NSTEMI）患者中形成单核细胞 - 血小板（Mo - Plt）聚集体，评估CD31分子在血栓形成风险中的作用。我们招募了19名对照（CTRL）受试者、46名稳定型心绞痛（SA）患者和86名NSTEMI患者，其中，通过光学相干断层扫描（OCT）评估，16名患者为完整纤维帽（IFC），19名患者为破裂纤维帽（RFC）。测量单核细胞和血小板上CD31的表达。冠状动脉造影后，根据血栓分级（TG）评估对52例NSTEMI患者进行进一步分层。最后，一系列实验验证了CD31是否参与Mo - Plt聚集体的形成。在NSTEMI患者中，单核细胞上的CD31减少，血小板上的CD31增加，特别是与IFC病变患者相比，RFC斑块的NSTEMI患者，以及与零/低TG患者相比，高TG患者。实验记录了NSTEMI患者中Mo - Plt聚集体增加，在CD31连接后显著减少，特别是在RFC斑块患者中。在NSTEMI中，尽管有最佳治疗和DAPT，CD31仍参与Mo - Plt聚集体的形成，提示存在替代血栓形成途径，主要表现在RFC患者中。
