<p><b><i>Background:</i></b> Chronic obstructive pulmonary disease
(COPD) is well known for its cardiovascular co-morbidities. Increased
platelet-monocyte interaction is found in COPD and may reflect altered
platelet function and a potential role for anti-platelet therapy. <b><i>Objectives:</i></b>
The objectives were to investigate platelet-monocyte interaction,
platelet activation and reactivity and plasmatic coagulation in stable
COPD. <b><i>Methods:</i></b> Platelet-monocyte interaction and platelet
activation were determined by flow cytometry in 30 stable COPD patients
and 25 controls. Platelet activation was measured by binding of
fibrinogen to the activated fibrinogen receptor and platelet P-selectin
expression at baseline and after platelet stimulation with platelet
agonists. Plasmatic coagulation was measured by D-dimer and thrombin
generation. <b><i>Results:</i></b> Platelet-monocyte interaction was
increased in stable COPD (median fluorescence intensity of platelet CD61
was 19.8 [IQR 14.0-33.2] vs. 10.0 [IQR 8.7-16.7], <i>p</i> = 0.002). In
contrast, platelet activation and reactivity, reflected by fibrinogen
binding and P-selectin expression, were the same in both groups. Plasma
P-selectin and interleukin-6 were increased in COPD (<i>p</i> = 0.01 and <i>p</i> = 0.02, respectively), whereas soluble fibrinogen, D-dimer and thrombin generation were similar. <b><i>Conclusions:</i></b>
Increased platelet-monocyte interaction was found in the absence of
platelet hyper-reactivity and activation of plasmatic coagulation in
stable COPD. Future clinical evaluation of the effects of different
anti-platelet drugs in COPD is warranted, as anti-platelet therapy may
interfere with platelet-monocyte interaction.</p