Platelet degranulation is associated with respiratory morbidity in COPD

<bold>Background:</bold> Elevated urine 11-dehydro-thromboxane B2 is associated with worse respiratory outcomes in COPD, suggesting a role for platelet activation. <bold>Question:</bold> Are specific platelet activation pathways associated with COPD morbidity? <bold>Methods:</bold> Multicolor flow cytometry was used to measure platelet surface expression of P-selectin, CD40L, CD63, and activated glycoprotein IIb/IIIa (PAC1) in platelet rich plasma and platelet-monocyte and platelet-neutrophil conjugates in whole blood of 40 former smokers with COPD without cardiovascular disease (CVD) and low coronary calcium. Multivariable linear regression adjusted for age, sex, aspirin use, platelet count, and FEV1% evaluated the association of platelet surface markers, platelet-monocyte and platelet-neutrophil conjugates (% positive) with clinical outcomes. <bold>Results:</bold> Greater platelet surface expression of α-granule constituents P-selectin and CD40L and dense granule constituent CD63 was associated with higher CAT, SGRQ, and CCQ scores. There were no consistent associations between PAC1 expression (platelet-endothelial interaction), platelet-monocyte, or platelet-neutrophil conjugates with respiratory morbidity. <bold>Conclusions:</bold> Among former smokers with COPD without CVD, <italic>in vivo</italic> platelet degranulation is associated with more severe respiratory symptoms, worse health status, and quality of life. Whether cytokines and chemokines released from platelet granules impact COPD morbidity remains unknown. <fig><object-id>erj;64/suppl_68/PA3090/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>