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Increased platelet activation in patients with stable and acute exacerbation of COPD
  1. John D Maclay1,
  2. David A McAllister1,2,
  3. Shonna Johnston1,
  4. Jennifer Raftis1,
  5. Catherine McGuinnes1,
  6. Andrew Deans1,
  7. David E Newby3,
  8. Nicholas L Mills3,
  9. William MacNee1
  1. 1ELEGI/Colt Laboratories, Centre for Inflammation Research, Edinburgh University, Edinburgh, UK
  2. 2Department of Pubic Health, NHS Fife, Leven, UK
  3. 3Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK
  1. Correspondence to Dr William MacNee, ELEGI Colt Laboratory, Queen's Medical Research Institute, The University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; w.macnee{at}


Rationale Chronic obstructive pulmonary disease (COPD) is associated with systemic inflammation and cardiovascular disease. Interaction between inflammatory cells and activated platelets is important in the pathogenesis of atherothrombosis and may contribute to cardiovascular risk in patients with COPD.

Objectives To assess platelet-monocyte aggregation in patients with COPD and matched controls, and in patients with an acute exacerbation of COPD.

Methods 18 men with COPD and 16 male controls matched for age and cigarette smoke exposure were recruited. A further 12 patients were investigated during and at least 2 weeks after hospitalisation for an acute exacerbation. Platelet-monocyte aggregation and platelet P-selectin expression were determined using flow cytometry.

Results Patients with COPD had increased circulating platelet-monocyte aggregates compared with controls (mean (SD) 25.3 (8.3)% vs 19.5 (4.0)%, p=0.01). Platelet-monocyte aggregation was further increased during an acute exacerbation compared with convalescence (32.0 (11.0)% vs 25.5 (6.4)%, p=0.03). Platelet P-selectin expression and soluble P-selectin did not differ between groups.

Conclusions Patients with stable COPD have increased circulating platelet-monocyte aggregates compared with well-matched controls. Platelet activation is further increased in patients with COPD during an acute exacerbation. These findings identify a novel mechanism to explain the increased cardiovascular risk in COPD and suggest platelet inhibition as a plausible therapeutic target.

  • COPD
  • cardiovascular disease
  • platelet activation
  • inflammation
  • COPD mechanisms
  • COPD exacerbations
  • systemic disease and lungs

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  • See Editorial, p 745

  • Linked articles 155333, 153122.

  • Funding This research was funded primarily by a Chief Scientist Office Project Grant (CZB/4/424). DAMc is supported by a Chest, Heart and Stroke Scotland Research Fellowship (R40329). NLM is supported by a British Heart Foundation Intermediate Clinical Research Fellowship (FS/10/024). JR is supported by a Department of Health Policy Research Program Grant (PR-NT-0208-10025).

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the Lothian regional ethics committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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