Local vessel injury following percutaneous coronary intervention does not promote early mobilisation of endothelial progenitor cells in the absence of myocardial necrosis

  1. Lookup NU author(s)
  2. Dr Honey Thomas
  3. Dr Peter Avery
  4. Dr Javed Ahmed
  5. Dr Richard Edwards
  6. Professor Azfar Zaman
  7. Professor Helen Arthur
  8. Professor Bernard Keavney
Author(s)Thomas HE, Avery PJ, Ahmed JM, Edwards R, Purcell I, Zaman AG, Arthur HM, Keavney BD
Publication type Article
ISSN (print)1355-6037
ISSN (electronic)1468-201X
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Background/objectives: Endothelial progenitor cells (EPCs) are circulating mononuclear cells that are released from the bone marrow in response to injury and participate in vascular repair. Some previous studies have suggested an early mobilisation of EPCs following percutaneous coronary intervention (PCI) that could modulate the subsequent risk of restenosis or stent thrombosis. However, those studies did not discriminate between vascular injury caused by PCI and any associated myocardial injury. Myocardial injury alone can influence EPC mobilisation in a non-specific manner, and could therefore confound any association with risk. We investigated the effect of local endothelial trauma following PCI on EPC mobilisation in the absence of myocyte necrosis. Design: We quantified circulating EPCs from 20 patients immediately before, 6 hours and 24 hours following elective PCI in patients without a 24-hour troponin rise. Absolute counts of EPCs expressing combinations of CD45, CD34, CD133 and kinase domain receptor (KDR) were recorded using flow cytometry. Results: There was a fall of 7–15% in EPC numbers between baseline and 6 hours post procedure and a subsequent rise (5–18%) from 6 hours to 24 hours. At 24 hours EPC levels were similar to baseline. Conclusions: The specific localised vascular injury induced by PCI did not lead to early mobilisation of EPCs. However, the fall in EPCs 6 hours after PCI was significant and its relation to early post-PCI complications such as stent thrombosis requires further exploration.
PublisherBritish Medical Journal
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