Abstract
Background: Both pulmonary arterial and systemic arterial stiffening have been described in COPD. The aim of the current study is to assess pulse wave velocity (PWV) within these two arterial beds to determine whether they are separate or linked processes.
Methods: 58 participants with COPD and 21 healthy volunteers(HV) underwent cardiac MRI and a panel of relevant biomarkers. Cardiac MRI was used to quantify ventricular mass, volumes, pulmonary (pPWV) and systemic (sPWV) arterial stiffness.
Results: Those with COPD had higher pPWV (COPD:2.62 vs. HV:1.78 ms-1,p=0.006), right ventricular mass:volume ratio (COPD:0.29 vs. HV:0.25 g/ml,p=0.012) left ventricular mass:volume ratio (COPD:0.78 vs. HV:0.70 g/ml,p=0.009) and a trend towards a higher sPWV (COPD:8.7 vs. HV:7.4 ms-1,p=0.06). Biomarkers were also higher: IL-6 (COPD:1.38 vs. HV:0.58 pg/ml,p=0.02), hsCRP (COPD:6.42 vs. HV:2.49 mg/L,p=0.002), SPD (COPD:16.9 vs. HV:9.13 ng/ml,p=0.001), NT-proBNP (COPD:603 vs. HV:198 pg/ml,p=0.001), hsTrop-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).
Conclusions: Pulmonary and systemic arterial stiffening appear to be disconnected and should therefore be considered independent processes in COPD. Further work is warranted to determine if this stiffening causes an increased morbidity and mortality and whether both can be targeted by similar pharmacological therapy or whether different strategies are required for each.
Methods: 58 participants with COPD and 21 healthy volunteers(HV) underwent cardiac MRI and a panel of relevant biomarkers. Cardiac MRI was used to quantify ventricular mass, volumes, pulmonary (pPWV) and systemic (sPWV) arterial stiffness.
Results: Those with COPD had higher pPWV (COPD:2.62 vs. HV:1.78 ms-1,p=0.006), right ventricular mass:volume ratio (COPD:0.29 vs. HV:0.25 g/ml,p=0.012) left ventricular mass:volume ratio (COPD:0.78 vs. HV:0.70 g/ml,p=0.009) and a trend towards a higher sPWV (COPD:8.7 vs. HV:7.4 ms-1,p=0.06). Biomarkers were also higher: IL-6 (COPD:1.38 vs. HV:0.58 pg/ml,p=0.02), hsCRP (COPD:6.42 vs. HV:2.49 mg/L,p=0.002), SPD (COPD:16.9 vs. HV:9.13 ng/ml,p=0.001), NT-proBNP (COPD:603 vs. HV:198 pg/ml,p=0.001), hsTrop-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).
Conclusions: Pulmonary and systemic arterial stiffening appear to be disconnected and should therefore be considered independent processes in COPD. Further work is warranted to determine if this stiffening causes an increased morbidity and mortality and whether both can be targeted by similar pharmacological therapy or whether different strategies are required for each.
Original language | English |
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Pages (from-to) | 1755-1765 |
Number of pages | 16 |
Journal | International Journal of Chronic Obstructive Pulmonary Disease |
Volume | 13 |
DOIs | |
Publication status | Published - 28 May 2018 |
Keywords
- Pulmonary vascular
- cardiovascular
- COPD
- arterial compliance
- ventricular function