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ELEVATED ENDOTHELIAL MICROPARTICLES IN ASYMPTOMATIC PATIENTS: MARKERS OF UNSTABLE PLAQUES?
  1. FL Wilkinson1,
  2. A Schiro2,3,
  3. R Weston1,
  4. JV Smyth2,
  5. F Serracino-Inglott2,3,
  6. MY Alexander1,3
  1. 1Translational Science, Healthcare Science Research Institute, Faculty of Science and Engineering, Manchester Metropolitan University, John Dalton Building, Manchester, UK
  2. 2Regional Vascular and Endovascular Unit, Manchester Royal Infirmary, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
  3. 3Cardiovascular Research Institute, Manchester Academic Health Science Centre, University of Manchester, Core Technology Facility, Manchester, UK

Abstract

There is a clinical need to develop novel biomarkers to identify patients at risk of stroke. We aim to establish a systemic signature and microparticle profile of asymptomatic patients with unstable carotid disease, for improved selection of patients for interventional surgery and stroke prevention.

Blood samples were taken from 70 patients (51 symptomatic; 19 asymptomatic), undergoing carotid endarterectomy, and 20 healthy controls. Circulating endothelial microparticles (EMPs; CD31+/Annexin V+/CD42b−), together with inflammatory markers were measured using flow cytometry and Bioplex assays respectively. Carotid plaques were graded and analysed using immunohistochemistry.

EMPs were elevated in asymptomatic and symptomatic patients, compared to healthy controls (p=<0.03). Asymptomatic patients with unstable plaques exhibited higher levels of EMPs (p=<0.01) compared to those with stable plaques, with a similar trend observed in symptomatic patients. MIG and SCGF-b were increased in asymptomatic patients with unstable, compared to stable plaques (p=<0.005). CD68-positive macrophage infiltration was detected within most plaques, with MIG and SCGF-b localised in the same vicinity, leading us to suggest the plaque macrophages may contribute to the elevation of both localised and systemic inflammation. Furthermore, the bone-related marker, osteopontin, was detected within plaques, which correlated to alizarin red-positive calcific deposits. Calcification was more apparent in asymptomatic patients (p=0.05) possibly impacting on plaque stability. Future work will aim to correlate specific systemic markers, plaque morphology and patient outcome.

These data could aid in the development of a diagnostic tool whereby EMPs, together with macrophage activity markers, could identify those patients with vulnerable plaques and stroke susceptibility.

  • CARDIAC PROCEDURES AND THERAPY

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