Disconnection of pulmonary and systemic arterial stiffness in COPD
Received 16 December 2017
Accepted for publication 19 March 2018
Published 28 May 2018 Volume 2018:13 Pages 1755—1765
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Charles Downs
Peer reviewer comments 2
Editor who approved publication: Dr Richard Russell
Jonathan R Weir-McCall,1 Patrick SK Liu-Shiu-Cheong,2 Allan D Struthers,1 Brian J Lipworth,2 J Graeme Houston1
1Division of Molecular and Clinical Medicine, Medical Research Institute, University of Dundee, Dundee, UK; 2Scottish Centre for Respiratory Research, Medical Research Institute, University of Dundee, Dundee, UK
Background: Both pulmonary arterial stiffening and systemic arterial stiffening have been described in COPD. The aim of the current study was to assess pulse wave velocity (PWV) within these two arterial beds to determine whether they are separate or linked processes.
Materials and methods: In total, 58 participants with COPD and 21 healthy volunteers (HVs) underwent cardiac magnetic resonance imaging (MRI) and were tested with a panel of relevant biomarkers. Cardiac MRI was used to quantify ventricular mass, volumes, and pulmonary (pulse wave velocity [pPWV] and systemic pulse wave velocity [sPWV]).
Results: Those with COPD had higher pPWV (COPD: 2.62 vs HV: 1.78 ms-1, p=0.006), higher right ventricular mass/volume ratio (RVMVR; COPD: 0.29 vs HV: 0.25 g/mL, p=0.012), higher left ventricular mass/volume ratio (LVMVR; COPD: 0.78 vs HV: 0.70 g/mL, p=0.009), and a trend toward a higher sPWV (COPD: 8.7 vs HV: 7.4 ms-1, p=0.06). Multiple biomarkers were elevated: interleukin-6 (COPD: 1.38 vs HV: 0.58 pg/mL, p=0.02), high-sensitivity C-reactive protein (COPD: 6.42 vs HV: 2.49 mg/L, p=0.002), surfactant protein D (COPD: 16.9 vs HV: 9.13 ng/mL, p=0.001), N-terminal pro-brain natriuretic peptide (COPD: 603 vs HV: 198 pg/mL, p=0.001), and high-sensitivity troponin I (COPD: 2.27 vs HV: 0.92 pg/mL, p<0.001). There was a significant relationship between sPWV and LVMVR (p=0.01) but not pPWV (p=0.97) nor between pPWV and RVMVR (p=0.27).
Conclusion: Pulmonary arterial stiffening and systemic arterial stiffening appear to be disconnected and should therefore be considered independent processes in COPD. Further work is warranted to determine whether both these cause an increased morbidity and mortality and whether both can be targeted by similar pharmacological therapy or whether different strategies are required for each.
Keywords: pulmonary vascular, cardiovascular, COPD, arterial compliance, ventricular function
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