Impact of acute exacerbations on platelet reactivity in chronic obstructive pulmonary disease patients
Authors Muñoz-Esquerre M, Ferreiro JL, Huertas D, Marcano AL, López-Sánchez M, Roura G, Gómez-Hospital JA, Dorca J, Cequier A, Santos S
Received 27 September 2017
Accepted for publication 12 November 2017
Published 28 December 2017 Volume 2018:13 Pages 141—148
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Charles Downs
Peer reviewer comments 3
Editor who approved publication: Dr Richard Russell
Mariana Muñoz-Esquerre,1 José Luis Ferreiro,2 Daniel Huertas,1,3 Ana Lucrecia Marcano,2 Marta López-Sánchez,1 Gerard Roura,2 Joan Antoni Gómez-Hospital,2 Jordi Dorca,1 Angel Cequier,2 Salud Santos1,3
1Department of Pulmonary Medicine, Bellvitge University Hospital, IDIBELL, University of Barcelona, L’Hospitalet de Llobregat, 2Heart Diseases Institute, Bellvitge University Hospital, IDIBELL, University of Barcelona, L’Hospitalet de Llobregat, 3Biomedical Research Networking Centre Consortium Respiratory Diseases, CIBERES, Barcelona, Spain
Background: A higher risk of atherothrombotic cardiovascular events, which are platelet-driven processes, has been described during acute exacerbations of chronic obstructive pulmonary disease (AECOPD). However, the relevance of platelet reactivity during AECOPD and whether this is affected by antiplatelet agents are not fully elucidated to date. This study aimed to evaluate whether platelet reactivity is augmented during an exacerbation in COPD patients with and without antiplatelet therapy and its association with systemic inflammatory parameters.
Materials and methods: Prospective, observational, ex vivo investigation was conducted in consecutive patients suffering an exacerbation of COPD. Platelet reactivity was assessed during AECOPD and at stable state. Platelet function assays included: 1) vasodilator-stimulated phosphoprotein assay expressed as P2Y12 reactivity index (PRI), 2) multiple electrode aggregometry and 3) optical aggregometry. Systemic inflammatory parameters such as leukocyte count, interleukin-6 and fibrinogen were also assessed.
Results: Higher platelet reactivity was observed during AECOPD compared to stability measured by vasodilator-stimulated phosphoprotein (PRI: 75.2%±1.9% vs 68.8%±2.4%, p=0.001). This augmented platelet aggregability was also observed in the subset of patients on antiplatelet therapy (PRI: 72.8%±3.1% vs 61.7%±7.5%, p=0.071). Consistent findings were observed with all other platelet function tests. Patients with greater enhancement of inflammatory markers during AECOPD were more likely to present a higher increase in platelet reactivity.
Conclusion: Platelet reactivity is increased during AECOPD, which may contribute to the augmented cardiovascular risk of these patients. Additionally, the increase in platelet reactivity might be associated with an increment in inflammatory markers during exacerbations.
Keywords: airflow limitation, inflammation, platelet aggregation, antiplatelets agents, thrombosis
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