Microparticles in acute coronary syndrome. Issue 156 (August 2017)

• Record Type: Journal Article
• Authors: Mavroudis, Chrysostomos A.; Eleftheriou, Despina; Hong, Ying; Majumder, Bikash; Koganti, Sudheer; Sapsford, Ray; North, Janet; Lowdell, Mark; Klein, Nigel; Brogan, Paul; Rakhit, Roby D.
• Is Part Of: Thrombosis research. Issue 156(2017)
• Page Start: 109
• Page End: 116
• Publication Date: 2017-08
• Subjects: Acute coronary syndrome -- Microparticles -- Inflammation -- Platelet activation -- Myocardial necrosis; Thrombosis -- Periodicals; 616.135
• DOI: 10.1016/j.thromres.2017.06.003
• Languages: English
• ISSNs: 0049-3848

Abstract

Abstract: Background: Emerging evidence supports the role of cell-derived microparticles (MPs) in the pathophysiology of acute coronary syndrome (ACS). Objectives: To explore the relationship between coronary and systemic MP levels, investigate the correlation between MPs, inflammatory markers and Troponin T in patients with ACS. Methods: Thirty seven patients with ACS scheduled for percutaneous coronary interventions (PCI) were studied. Eleven patients with stable angina (SA) were included as a control group. AnnexinV + MPs (AnV + MPs) and activated platelet-monocyte aggregates (PMA) from right atrium (RA) and culprit coronary artery (CO) distal to culprit lesion were measured using flow cytometry. High sensitivity C-reactive protein (CRP), Interleukin - 6 (IL-6), tumour necrosis factor – α (TNF-α), serum amyloid A (SAA) and Troponin T were assayed. Results: Total and cell specific AnV + MP expression were higher in the ACS group in both the CO and RA, with greater levels detected in the CO. Platelet activation showed positive correlation with Troponin-T and platelet MP in both CO and RA of the ACS group (r = 0.4 for both; p = 0.04 & p = 0.03 respectively). Inflammatory markers levels did not differ between the ACS and SA patients. Conclusions: Elevated coronary and systemic MP levels and positive correlation of platelet activation with Troponin-T and platelet MPs suggest a pathogenic role for MPs in ACS.