Impact of acute exacerbations on platelet reactivity in chronic obstructive pulmonary disease patients

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 antip...

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Bibliographic Details
Authors: Muñoz Esquerre, Mariana, Ferreiro, José Luis, Huertas, David, Marcano, Ana Lucrecia, López Sánchez, Marta, Roura i Ferrer, Gerard, Gómez Hospital, Joan Antoni, Dorca i Sargatal, Jordi, Cequier Fillat, Àngel R., Santos Pérez, Salud
Format: article
Status:Published version
Publication Date:2017
Country:España
Institution:Universidad de Barcelona
Repository:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/132965
Online Access:https://hdl.handle.net/2445/132965
Access Level:Open access
Keyword:Inflamació
Agregació plaquetària
Trombosi
Malalties pulmonars obstructives cròniques
Inflammation
Blood platelet aggregation
Thrombosis
Chronic obstructive pulmonary diseases
Description
Summary: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.