Abstract

BackgroundPlatelet count is a prognostic indicator in the general population and elderly. Thrombocytosis during acute exacerbation of COPD (AECOPD) has been associated with mortality; however, the relationship between platelet count and mortality in stable COPD is unknown.MethodsWe performed post hoc secondary analysis on a subsample of 1797 patients in the Study to Understand Mortality and Morbidity in COPD (SUMMIT) who had blood samples drawn at baseline. Participants were current or former smokers, 40–80 years old with moderate COPD and history or increased risk of cardiovascular (CV) disease. The primary outcome was on and post-treatment all-cause mortality. Secondary outcomes included first-on-treatment moderate/severe AECOPD and on-treatment CV composite event (CV death, myocardial infarction, stroke, unstable angina and transient ischemic attack). Multivariable Cox proportional hazards models were used to investigate study endpoint associations with platelet count quintile grouping, continuous platelet count utilizing two-term fractional polynomials, and categories of low, normal and high platelet count (< 150, ≥150 to < 300, ≥300 × 109/L).ResultsPatients were followed for 2.3 ± 0.9 years for vital status and 1.6 ± 1.1 years for morbidity endpoints during which 105 (5.8%) died, 651 (36.2%) experienced AECOPD (159 with severe AECOPD) and 86 (4.8%) experienced a CV event. A U-shaped association between platelet count and all-cause mortality was observed. Compared to the third quintile group (Q3) of platelet count, risk of death was increased in the lowest quintile group (Q1; hazard ratio [HR]: 1.73; 95% confidence interval [CI]: 0.93–3.23) and highest quintile group (Q5; HR: 1.66; 95%CI: 0.89–3.10), though point estimates were imprecise. Using clinical cutoffs, compared with normal platelet counts (≥150 to < 300 × 109/L), risk of all-cause mortality was nominally increased among patients with thrombocytopenia (HR: 1.46; 95%CI: 0.81–2.64) and high platelet count (HR: 1.66; 95%CI: 0.96–2.86). Compared with Q3, CV events were nominally increased for Q5 (HR: 1.71; 95%CI: 0.83–3.49) and Q1 (HR: 1.41; 95%CI: 0.70, 2.85). There was no association between platelet count and AECOPD.ConclusionsIn stable COPD platelet count demonstrated a U-shaped association with increased risk of 3-year all-cause mortality, though a platelet count level above or below which risk of mortality was increased could not be definitively identified.Trial registrationClinicalTrials.gov NCT01313676.

Highlights

  • Platelet count is a prognostic indicator in the general population and elderly

  • Using data from the Study to Understand Mortality and Morbidity in Chronic obstructive pulmonary disease (COPD) (SUMMIT), a prospective randomized controlled trial enriched for presence of CV comorbidity and containing adjudicated events, we investigated post hoc the association of platelet count measured in the stable phase of COPD with all-cause mortality, CV and respiratory outcomes

  • Study population SUMMIT was a prospective, multi-center, international randomized controlled trial to determine whether treatment with an inhaled long-acting beta-agonist (LABA) in combination with an inhaled corticosteroid (ICS), versus either component, could improve clinical outcomes in patients with moderate COPD and increased CV risk compared with placebo

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Summary

Introduction

Platelet count is a prognostic indicator in the general population and elderly. Chronic systemic inflammation in COPD has been associated with poor clinical outcomes [2, 3]. A component of a routinely measured clinical assay, remains within a relatively narrow range among healthy individuals but can be significantly altered in the setting of both acute and chronic disease [5]. A U-shaped association between platelet count and increased mortality has been recognized in the general population and the elderly [9,10,11,12,13,14], though its role in COPD remains unclear. In addition to the well documented role of platelets in cardiovascular (CV) disease, platelets are recognized as playing a role in many pathophysiologic processes such as inflammation, host defense, and tumor biology [15]

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