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.
Highlights
Microparticles (MP) are small vesicles (0.1–1 μm) originating from plasma membranes of cells
Ex vivo studies in human carotid plaque correlated the presence of leucocyte MP with plaque instability [6], whereas peripheral levels of endothelial-derived MP have been shown to be elevated in acute coronary syndrome (ACS) compared in patients with stable angina pectoris (SAP) [7]
Within the ACS group, four patients presented with an non-ST elevation myocardial infarction (NSTEMI), two with ST elevation myocardial infarction (STEMI) with delayed revascularization and two with unstable angina pectoris (UAP)
Summary
Microparticles (MP) are small vesicles (0.1–1 μm) originating from plasma membranes of cells. MP are most commonly derived from endothelial cells, platelets, leucocytes [1] and erythrocytes after activation or during early apoptosis [2,3]. They express surface antigens derived from their cell of origin, allowing for identification of subtype, and the majority (80%) of circulating MP are derived from platelets, with leucocyte-derived MP accounting for
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