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  • S51 Circulating Desmosine Relates To Cardiovascular Comorbidity, Coronary Artery Calcification Score (cacs), Systemic Inflammation And Mortality In Patients With Copd

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Basic mechanisms in COPD pathogenesis
S51 Circulating Desmosine Relates To Cardiovascular Comorbidity, Coronary Artery Calcification Score (cacs), Systemic Inflammation And Mortality In Patients With Copd
  1. Roberto A Rabinovich1,
  2. Bruce E Miller2,
  3. Karolina Wrobel3,
  4. Gourab Choudhury1,
  5. Kareshma Ranjit1,
  6. Ellen M Drost1,
  7. Lisa D Edwards3,
  8. David A Lomas4,
  9. Stephen I Rennard5,
  10. Alvar Agusti6,
  11. Ruth Tal-Singer2,
  12. Jørgen Vestbo7,
  13. Emiel Wouters8,
  14. Edwin Van Beek9,
  15. John T Murchison10,
  16. William MacNee1,
  17. Jeffrey TJ Huang3
  1. 1Edinburgh Lung and the Environment Group Initiative (ELEGI), Centre for Inflammation and Research, Queens Medical Research Institute, Edinburgh, Edinburgh, UK
  2. 2GlaxoSmithKline, King of Prussia, Pennsylvania, USA
  3. 3Medical Research Institute, School of Medicine, University of Dundee, Dundee, UK
  4. 4Faculty of Medical Sciences, University College London, London, UK
  5. 55- Division of Pulmonary, Critical Care, Sleep and Allergy, University of Nebraska, Omaha, Nebraska, USA
  6. 6Hospital Clinic, IDIBAPS, Universitat de Barcelona and CIBER Enfermedades Respiratorias, FISIB, Mallorca, Spain
  7. 7Department of Respiratory Medicine, Odense University and University of Southern Denmark, Odense, Denmark
  8. 8Department of Respiratory Medicine, Maastricht University Medical Centre, Maastricht, Maastricht, The Netherlands
  9. 9Clinical Research Imaging Centre, Queens Medical Research Institute, Edinburgh, UK
  10. 10Royal Infirmary of Edinburgh, Scotland, Edinburgh, UK

Abstract

Introduction COPD is a risk factor for cardiovascular comorbidities. Elastin degradation represents a shared mechanism for the pulmonary and vascular features.

Methods and Results Plasma desmosine (pDES), a marker of elastin degradation, was measured in 955 COPD patients (609 male, age 63.1 ± 7.2 years, FEV1 50.6 ± 15.1%predicted) by an isotope dilution LC-MS/MS method. Coronary artery calcification (CACS), a surrogate of atherosclerosis, was assessed in 440 standard CT scan images (low 1000 AU).

Results pDES was elevated in patients with cardiovascular comorbidities (p < 0.01) and correlated with FEV1 (r = 0.39, p < 0.0001), MMRC (r = 0.16, p < 0.0001), 6MWD (r=-0.16, p < 0.0001), BODE index (r = 0.10, p < 0.005), fibrinogen, IL6, IL8, CCL18, and SPD but not with emphysema. These variables showed significant higher values in the patients in the highest pDES quartile. pDES was elevated in patients with very high CACS in comparison with patients with lower CACS (Figure 1) and in patients that died during a 3 year follow-up (p < 0.0001).

Conclusion pDES relates to lung function, systemic inflammation, cardiovascular comorbidities, and CACS in patients with COPD. pDES is a predictor of all cause overall mortality.

Abstract S51 Figure 1
Abstract S51 Figure 1

Differences in pDES between patients with very high CACS and lower CACS levels (* p < 0.01)

The ECLIPSE study (GSK Study No. SCO104960, NCT00292552) was sponsored by GlaxoSmithKline.

https://doi.org/10.1136/thoraxjnl-2014-206260.57

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