Association of Systemic Endothelial-Derived and Platelet-Derived Microparticles With Clinical Outcomes in Chronic Obstructive Pulmonary Disease

Purpose: Endothelial and platelet microparticles (eMPs and pMPs), markers of cellular activation, dysfunction, or apoptosis, have been associated with multiple cardiovascular conditions. Chronic obstructive pulmonary disease (COPD) is associated with cardiovascular comorbidities and platelet/endothelial dysfunction. We analyzed whether eMPs and pMPs are associated with COPD status and/or severity. Patients and Methods: A total of 58 COPD patients and 19 controls were enrolled and followed for an average of 1.17 years. Characterization of COPD included lung function, Body mass index-airflow ObstructionDyspnea-Exercise (BODE) scores, health-related quality of life, exacerbations, comorbidities, and mortality. Plasma collection to measure eMPs and pMPs via flow cytometry was performed at enrollment as well as during acute exacerbation in 17 participants. We measured pMPs (CD31(+), CD41(+)31(+), CD 62P(+)), eMPs (ULEX lectin(+), CD51(+), CD54(+), CD62E(+)), the apoptotic CD62E(+)/CD31(+) ratio, and Annexin V MP. Results: As a group, COPD participants had no difference in all MP levels studied compared with controls. No significant correlations with diffusion capacity for carbon monoxide, quality of life, and exacerbation status were found in all MPs studied. However, the eMP ULEX and the pMP CD 62P(+) were higher among COPD Global initiative for chronic Obstructive Lung Disease (GOLD) stage 3 patients compared to controls. The CD62E(+)/CD31(+) ratio was lower in controls and GOLD stage 1 COPD participants compared with GOLD stage 2/3 COPD participants, suggesting increased apoptosis. eMP ULEX lectin(+) decreased during acute exacerbations and pMP41(+)31(+) significantly increased as BODE score increased. Conclusion: After adjusting for comorbidities, most eMPs and pMPs studied do not correlate significantly with COPD status or severity.