RT Journal Article
SR Electronic
T1 Increased platelet activation in patients with stable and acute exacerbation of COPD
JF Thorax
JO Thorax
FD BMJ Publishing Group Ltd and British Thoracic Society
SP 769
OP 774
DO 10.1136/thx.2010.157529
VO 66
IS 9
A1 John D Maclay
A1 David A McAllister
A1 Shonna Johnston
A1 Jennifer Raftis
A1 Catherine McGuinnes
A1 Andrew Deans
A1 David E Newby
A1 Nicholas L Mills
A1 William MacNee
YR 2011
UL http://thorax.bmj.com/content/66/9/769.abstract
AB 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.