RT Journal Article
SR Electronic
T1 16 Pulmonary arterial stiffness in COPD: pulmonary biomarker or another measure of systemic arteriosclerosis?
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP A6
OP A6
DO 10.1136/heartjnl-2017-311677.16
VO 103
IS Suppl 4
A1 Jonathan R Weir-McCall
A1 Patrick SK Liu-Shiu-Cheong
A1 Allan D Struthers
A1 Brian J Lipworth
A1 JGraeme Houston
YR 2017
UL http://heart.bmj.com/content/103/Suppl_4/A6.1.abstract
AB Introduction Both pulmonary and systemic arterial stiffening have been described in COPD. It is not currently clear whether these reflect separate disease processes within the pulmonary and systemic circulation or whether they are both due to a global arteriosclerosis. The aim of the current study is to assess arterial stiffness using pulse wave velocity (PWV) within these two arterial beds to determine whether they are separate or linked processes.Methods 58 participants with COPD underwent pulmonary function tests, six-minute walk test, and cardiac MRI (CMR), while 21 age and sex matched non-smoking healthy volunteers underwent CMR. CMR was used to quantify right and left ventricular mass and volumes, with phase contrast imaging of the main pulmonary artery and ascending and abdominal aortic aorta performed in order to calculate pulmonary (pPWV) and systemic (sPWV) arterial stiffness using pulse wave velocity (PWV).Results Compared with controls, pPWV (COPD: 2.63±1.3 ms−1 vs. HC: 1.76±0.7ms−1, p=0.006) was significantly elevated with a trend towards higher sPWV (COPD: 8.67±2.7ms−1 vs. HC: 7.35±2.1ms−1, p=0.06). pPWV showed a trend towards an association with smoking pack years (rho=0.22, p=0.053), while sPWV showed a significant association with age (rho=0.47, p<0.001), systolic blood pressure (rho=0.32, p=0.02), and percentage predicted DLCO/VA (rho=0.43, p=0.001). There was no significant association between sPWV and pPWV (rho=–0.004, p=0.97).Conclusion Pulmonary and systemic arterial stiffening were associated with different risk factors and are independent processes in COPD. Further work is warranted to determine if both can be targeted by similar pharmacological therapy or whether different strategies are required for both.