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Local vessel injury following PCI does not promote early mobilisation of endothelial progenitor cells in the absence of myocardial necrosis
  1. Honey E Thomas (h.e.thomas{at}ncl.ac.uk)
  1. University of Newcastle, United Kingdom
    1. Peter Avery
    1. University of Newcastle, United Kingdom
      1. Javed Ahmed
      1. Freeman Hospital, Newcastle upon Tyne, United Kingdom
        1. Richard Edwards
        1. Freeman Hospital, Newcastle upon Tyne, United Kingdom
          1. Ian Purcell
          1. Freeman Hospital, Newcastle upon Tyne, United Kingdom
            1. Azfar Zaman
            1. Freeman Hospital, Newcastle upon Tyne, United Kingdom
              1. Helen Arthur
              1. University of Newcastle, United Kingdom
                1. Bernard Keavney (b.d.keavney{at}ncl.ac.uk)
                1. Newcastle University, United Kingdom

                  Abstract

                  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 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 six hours following PCI was significant and its relation to early post-PCI complications such as stent thrombosis requires further exploration.

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