PT  - JOURNAL ARTICLE
AU  - Jonathan R Weir-McCall
AU  - Patrick SK Liu-Shiu-Cheong
AU  - Allan D Struthers
AU  - Brian J Lipworth
AU  - JGraeme Houston
TI  - 16 Pulmonary arterial stiffness in COPD: pulmonary biomarker or another measure of systemic arteriosclerosis?
AID  - 10.1136/heartjnl-2017-311677.16
DP  - 2017 May 01
TA  - Heart
PG  - A6--A6
VI  - 103
IP  - Suppl 4
4099  - http://heart.bmj.com/content/103/Suppl_4/A6.1.short
4100  - http://heart.bmj.com/content/103/Suppl_4/A6.1.full
SO  - Heart2017 May 01; 103
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.