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Neutrophil-derived microparticles are released into the coronary circulation following percutaneous coronary intervention in acute coronary syndrome patients

Identifieur interne : 000741 ( Main/Exploration ); précédent : 000740; suivant : 000742

Neutrophil-derived microparticles are released into the coronary circulation following percutaneous coronary intervention in acute coronary syndrome patients

Auteurs : Gonzalo J. Martínez [Australie, Chili] ; Jennifer Y. Barraclough [Australie] ; Shirley Nakhla [Australie] ; Vivian Kienzle [Australie] ; Stacy Robertson [Australie] ; Ziad Mallat [France, Royaume-Uni] ; David S. Celermajer [Australie] ; Sanjay Patel [Australie]

Source :

RBID : PMC:5240586

Abstract

To evaluate (i) local coronary and systemic levels of microparticles (MP) in acute coronary syndrome (ACS) and stable angina pectoris (SAP) patients and (ii) their release after plaque disruption with percutaneous coronary intervention (PCI). MP are small vesicles originating from plasma membranes of cells after activation or apoptosis and are implicated in the pathogenesis of atherosclerosis. Neutrophils play a role in plaque destabilization and shed neutrophil-derived MP that have the potential to drive significant proinflammatory and thrombotic downstream effects. Eight ACS and eight SAP patients were included. Coronary sinus (CS) samples pre-intervention (CS1), 45 s following balloon angioplasty (CS2) and at 45 s intervals following stent deployment (CS3, CS4 and CS5), together with peripheral vein samples, pre- and post-PCI were analysed for neutrophil-derived (CD66b+), endothelial-derived (CD144+), platelet-derived (CD41a+), monocyte-derived (CD14+) and apoptotic (Annexin V+) MP. ELISA for interleukin (IL)-6, myeloperoxidase (MPO) and P-selectin was also performed. CD66b+ MP levels were similar in both groups pre-intervention. Post-PCI, CS levels rose significantly in ACS but not SAP patients (ACS area under the curve (AUC): 549 ± 83, SAP AUC: 24 ± 29, P<0.01). CS CD41a+, CD144+, CD14+ and Annexin V+ MP levels did not differ between groups. Acute neutrophil-derived MP release post-PCI occurs in ACS compared with stable patients, likely to be reflective of plaque MP content in vulnerable lesions.


Url:
DOI: 10.1042/BSR20160430
PubMed: 27913753
PubMed Central: 5240586


Affiliations:


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Le document en format XML

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<name sortKey="Robertson, Stacy" sort="Robertson, Stacy" uniqKey="Robertson S" first="Stacy" last="Robertson">Stacy Robertson</name>
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<wicri:regionArea>Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke’s Hospital, Cambridge</wicri:regionArea>
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<name sortKey="Celermajer, David S" sort="Celermajer, David S" uniqKey="Celermajer D" first="David S." last="Celermajer">David S. Celermajer</name>
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<nlm:aff id="A1">Department of Cardiology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia</nlm:aff>
<country xml:lang="fr">Australie</country>
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<name sortKey="Patel, Sanjay" sort="Patel, Sanjay" uniqKey="Patel S" first="Sanjay" last="Patel">Sanjay Patel</name>
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<nlm:aff id="A1">Department of Cardiology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia</nlm:aff>
<country xml:lang="fr">Australie</country>
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<nlm:aff id="A2">Sydney Medical School, The University of Sydney, New South Wales, Australia</nlm:aff>
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<orgName type="university">Université de Sydney</orgName>
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<series>
<title level="j">Bioscience Reports</title>
<idno type="ISSN">0144-8463</idno>
<idno type="eISSN">1573-4935</idno>
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<date when="2017">2017</date>
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<div type="abstract" xml:lang="en">
<p>To evaluate (i) local coronary and systemic levels of microparticles (MP) in acute coronary syndrome (ACS) and stable angina pectoris (SAP) patients and (ii) their release after plaque disruption with percutaneous coronary intervention (PCI). MP are small vesicles originating from plasma membranes of cells after activation or apoptosis and are implicated in the pathogenesis of atherosclerosis. Neutrophils play a role in plaque destabilization and shed neutrophil-derived MP that have the potential to drive significant proinflammatory and thrombotic downstream effects. Eight ACS and eight SAP patients were included. Coronary sinus (CS) samples pre-intervention (CS1), 45 s following balloon angioplasty (CS2) and at 45 s intervals following stent deployment (CS3, CS4 and CS5), together with peripheral vein samples, pre- and post-PCI were analysed for neutrophil-derived (CD66b+), endothelial-derived (CD144+), platelet-derived (CD41a+), monocyte-derived (CD14+) and apoptotic (Annexin V+) MP. ELISA for interleukin (IL)-6, myeloperoxidase (MPO) and P-selectin was also performed. CD66b+ MP levels were similar in both groups pre-intervention. Post-PCI, CS levels rose significantly in ACS but not SAP patients (ACS area under the curve (AUC): 549 ± 83, SAP AUC: 24 ± 29,
<italic>P</italic>
<0.01). CS CD41a+, CD144+, CD14+ and Annexin V+ MP levels did not differ between groups. Acute neutrophil-derived MP release post-PCI occurs in ACS compared with stable patients, likely to be reflective of plaque MP content in vulnerable lesions.</p>
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<name sortKey="Patel, Sanjay" sort="Patel, Sanjay" uniqKey="Patel S" first="Sanjay" last="Patel">Sanjay Patel</name>
<name sortKey="Robertson, Stacy" sort="Robertson, Stacy" uniqKey="Robertson S" first="Stacy" last="Robertson">Stacy Robertson</name>
<name sortKey="Robertson, Stacy" sort="Robertson, Stacy" uniqKey="Robertson S" first="Stacy" last="Robertson">Stacy Robertson</name>
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<country name="Chili">
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<name sortKey="Martinez, Gonzalo J" sort="Martinez, Gonzalo J" uniqKey="Martinez G" first="Gonzalo J." last="Martínez">Gonzalo J. Martínez</name>
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<country name="France">
<region name="Île-de-France">
<name sortKey="Mallat, Ziad" sort="Mallat, Ziad" uniqKey="Mallat Z" first="Ziad" last="Mallat">Ziad Mallat</name>
</region>
</country>
<country name="Royaume-Uni">
<region name="Angleterre">
<name sortKey="Mallat, Ziad" sort="Mallat, Ziad" uniqKey="Mallat Z" first="Ziad" last="Mallat">Ziad Mallat</name>
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</country>
</tree>
</affiliations>
</record>

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