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Fibrinogen does not relate to cardiovascular or muscle manifestations in COPD: cross-sectional data from the ERICA study
  1. Divya Mohan1,2,
  2. Julia R Forman3,
  3. Matthew Allinder2,
  4. Carmel M McEniery3,
  5. Charlotte Emma Bolton4,
  6. John R Cockcroft5,
  7. William MacNee6,
  8. Jonathan Fuld3,
  9. Mellone Marchong3,
  10. Nichola Sian Gale5,
  11. Marie Fisk3,
  12. Sridevi Nagarajan3,
  13. Joseph Cheriyan3,
  14. David A Lomas7,
  15. Peter M A Calverley8,
  16. Bruce E Miller2,
  17. Ruth Tal-Singer2,
  18. Ian B Wilkinson3,
  19. Michael I Polkey1
  20. on behalf of the ERICA Consortium
  1. 1NIHR Respiratory Biomedical Research Unit, Royal Brompton and Harefield NHS Foundation Trust, Imperial College, London, UK
  2. 2R&D, GlaxoSmithKline King of Prussia, Philadelphia, Pennsylvania, USA
  3. 3Division of Experimental Medicine and Immunotherapeutics, Cambridge Clinical Trials Unit, Addenbrooke’s Hospital, University of Cambridge, Cambridge, UK
  4. 4Nottingham Respiratory Research Unit, NIHR Nottingham BRC, School of Medicine, City Hospital NUH Trust Campus, University of Nottingham, Nottingham, UK
  5. 5Department of Cardiology, Wales Heart Research Institute, Cardiff University, Cardiff, UK
  6. 6MRC Centre for Inflammation, University of Edinburgh, Edinburgh, UK
  7. 7Division of Medicine, UCL Respiratory, University College London, London, UK
  8. 8School of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK
  1. Correspondence to Dr Divya Mohan, R and D, GlaxoSmithKline King of Prussia, Philadelphia, PA 19406, USA; divya.x.mohan{at}gsk.com

Abstract

Cardiovascular and skeletal muscle manifestations constitute important comorbidities in COPD, with systemic inflammation proposed as a common mechanistic link. Fibrinogen has prognostic role in COPD. We aimed to determine whether aortic stiffness and quadriceps weakness are linked in COPD, and whether they are associated with the systemic inflammatory mediator—fibrinogen. Aortic pulse wave velocity (aPWV), quadriceps maximal volitional contraction (QMVC) force and fibrinogen were measured in 729 patients with stable, Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages II–IV COPD. The cardiovascular and muscular manifestations exist independently (P=0.22, χ2). Fibrinogen was not associated with aPWV or QMVC (P=0.628 and P=0.621, respectively), making inflammation, as measured by plasma fibrinogen, an unlikely common aetiological factor.

  • copd pathology

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Footnotes

  • RT-S, IBW and MIP contributed equally.

  • Contributors MIP, DM, JRF, CMM, CEB, JRC, WM, JF, NSG, MF, JRC, DAL, PMAC, BEM, RT-S and IBW all made substantial contributions to the conception and design of the work. MIP, DM, JRF, MA, CMM, CEB, JRC, WM, JF, MM, SN, NSG, MF and IBW made substantial contributions to the acquisition and analysis of data for the work. All authors contributed to the interpretation of the data, drafting and revision of the manuscript, and final approval of the version submitted for publication. All authors take accountability for all aspects of the work.

  • Funding This study was funded by a grant from Innovate UK. GlaxoSmithKline, a consortium partner, made contributions in kind towards study management. The UK Clinical Research Network contributed towards the study at all participating sites. Subjects from the Wales Heart Research Institute, Cardiff, were simultaneously recruited to the ARCADE study (ClinicalTrials.gov Identifier NCT01656421), which was funded by GSK. IBW, JRC and CMM have received funding support from the National Institute for Health Research (NIHR) Cambridge Comprehensive Biomedical Research Centre. Part of the work was undertaken at the NIHR Respiratory Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London, which part-funded DM and MIP’s salary.

  • Competing interests MIP has received payment to his institution or himself for advice on skeletal muscle weakness in COPD from GSK, Novartis, AZ, Pfizer, Lilly and Astellas. DM is an employee and shareholder of GSK. JRF, CMM, MM, SN and NSG have no conflict of interest to report. CEB reports grants from Innovate UK (formerly Technology Strategy Board (TSB) UK) during the conduct of the study; advisory board fees from GSK paid to their institution, grants from GSK and grants from MRC/ABPI outside the submitted work. JRC reports grants from TSB/MRC, during the conduct of the study; personal fees from GSK, outside the submitted work. WM received research support from GlaxoSmithKline and Pfizer, and was on advisory committees of Almirall, GlaxoSmithKline, Novartis and Pfizer; he was a speaker for AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Janssen and Novartis. JF received speaker fees from GSK. MF acknowledges receipt of an imaging fellowship award from GSK. JRC is employed full-time by Cambridge University Hospitals National Health Service Foundation Trust and is obligated to spend 50% of his time on GSK clinical trial research, representing a significant relationship; however, he receives no other benefits or compensations from GSK. DAL reports grants and personal fees from GSK, and personal fees from Grifols, outside the submitted work. PMAC has advised Boehringer Ingelheim, GSK, AstraZeneca and Takeda on the design and conduct of clinical trials, and has spoken at meetings sponsored by these companies and by Novartis; he has no stock holdings in any pharmaceutical company or connection with the tobacco industry. BEM and RT-S are shareholders and employees of GSK. IBW reports grants from TSB and GSK during the conduct of the study, and grants from GSK outside the submitted work.

  • Patient consent Obtained.

  • Ethics approval The Cambridge South Research Ethics Committee (reference 11/EE/0357) approved the study.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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