Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical Implications in Plaque Rupture
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...
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| Published in | Frontiers in cardiovascular medicine Vol. 8; p. 741221 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
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| Language | English |
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25.01.2022
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| 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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| AbstractList | 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. 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. 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. 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.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. |
| Author | Montone, Rocco Antonio Bonanni, Alice Severino, Anna Liuzzo, Giovanna Pedicino, Daniela Flego, Davide Vinci, Ramona Filomia, Simone d'Aiello, Alessia Russo, Giulio Crea, Filippo Cribari, Francesco Massetti, Massimo Ciampi, Pellegrino Canonico, Francesco Pisano, Eugenia Di Sario, Marianna Piacentini, Roberto Ponzo, Myriana Vergallo, Rocco Stefanini, Lucia Conte, Cristina |
| AuthorAffiliation | 2 Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS , Rome , Italy 1 Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore , Rome , Italy 3 Department of Internal Medicine and Medical Specialties, Sapienza University of Rome , Rome , Italy 4 Department of Neuroscience, Università Cattolica del Sacro Cuore , Rome , Italy 5 Fondazione Policlinico Universitario A. Gemelli IRCCS , Rome , Italy |
| AuthorAffiliation_xml | – name: 1 Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore , Rome , Italy – name: 2 Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS , Rome , Italy – name: 3 Department of Internal Medicine and Medical Specialties, Sapienza University of Rome , Rome , Italy – name: 5 Fondazione Policlinico Universitario A. Gemelli IRCCS , Rome , Italy – name: 4 Department of Neuroscience, Università Cattolica del Sacro Cuore , Rome , Italy |
| Author_xml | – sequence: 1 givenname: Ramona surname: Vinci fullname: Vinci, Ramona – sequence: 2 givenname: Daniela surname: Pedicino fullname: Pedicino, Daniela – sequence: 3 givenname: Alice surname: Bonanni fullname: Bonanni, Alice – sequence: 4 givenname: Alessia surname: d'Aiello fullname: d'Aiello, Alessia – sequence: 5 givenname: Eugenia surname: Pisano fullname: Pisano, Eugenia – sequence: 6 givenname: Myriana surname: Ponzo fullname: Ponzo, Myriana – sequence: 7 givenname: Anna surname: Severino fullname: Severino, Anna – sequence: 8 givenname: Pellegrino surname: Ciampi fullname: Ciampi, Pellegrino – sequence: 9 givenname: Francesco surname: Canonico fullname: Canonico, Francesco – sequence: 10 givenname: Giulio surname: Russo fullname: Russo, Giulio – sequence: 11 givenname: Marianna surname: Di Sario fullname: Di Sario, Marianna – sequence: 12 givenname: Rocco surname: Vergallo fullname: Vergallo, Rocco – sequence: 13 givenname: Simone surname: Filomia fullname: Filomia, Simone – sequence: 14 givenname: Rocco Antonio surname: Montone fullname: Montone, Rocco Antonio – sequence: 15 givenname: Davide surname: Flego fullname: Flego, Davide – sequence: 16 givenname: Lucia surname: Stefanini fullname: Stefanini, Lucia – sequence: 17 givenname: Roberto surname: Piacentini fullname: Piacentini, Roberto – sequence: 18 givenname: Cristina surname: Conte fullname: Conte, Cristina – sequence: 19 givenname: Francesco surname: Cribari fullname: Cribari, Francesco – sequence: 20 givenname: Massimo surname: Massetti fullname: Massetti, Massimo – sequence: 21 givenname: Filippo surname: Crea fullname: Crea, Filippo – sequence: 22 givenname: Giovanna surname: Liuzzo fullname: Liuzzo, Giovanna |
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| Copyright | Copyright © 2022 Vinci, Pedicino, Bonanni, d'Aiello, Pisano, Ponzo, Severino, Ciampi, Canonico, Russo, Di Sario, Vergallo, Filomia, Montone, Flego, Stefanini, Piacentini, Conte, Cribari, Massetti, Crea and Liuzzo. Copyright © 2022 Vinci, Pedicino, Bonanni, d'Aiello, Pisano, Ponzo, Severino, Ciampi, Canonico, Russo, Di Sario, Vergallo, Filomia, Montone, Flego, Stefanini, Piacentini, Conte, Cribari, Massetti, Crea and Liuzzo. 2022 Vinci, Pedicino, Bonanni, d'Aiello, Pisano, Ponzo, Severino, Ciampi, Canonico, Russo, Di Sario, Vergallo, Filomia, Montone, Flego, Stefanini, Piacentini, Conte, Cribari, Massetti, Crea and Liuzzo |
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| Keywords | CD31 monocyte-platelet aggregates thrombus burden unstable plaque plaque rupture precision medicine acute coronary syndromes |
| Language | English |
| License | Copyright © 2022 Vinci, Pedicino, Bonanni, d'Aiello, Pisano, Ponzo, Severino, Ciampi, Canonico, Russo, Di Sario, Vergallo, Filomia, Montone, Flego, Stefanini, Piacentini, Conte, Cribari, Massetti, Crea and Liuzzo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Daiju Fukuda, Tokushima University, Japan This article was submitted to Atherosclerosis and Vascular Medicine, a section of the journal Frontiers in Cardiovascular Medicine These authors have contributed equally to this work and share first authorship These authors have contributed equally to this work and share last authorship Reviewed by: Kenichiro Otsuka, Massachusetts General Hospital, United States; Junnan Tang, First Affiliated Hospital of Zhengzhou University, China |
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| Title | Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical Implications in Plaque Rupture |
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