025 Determinants of pulmonary arterial remodelling in copd and implications for right ventricular remodelling. (3rd April 2017)

• Record Type: Journal Article
• Authors: Weir-McCall, Jonathan; Liu-Shiu-Cheong, Patrick; Struthers, Allan D; Lipworth, Brian J; Houston, J Graeme
• Is Part Of: Heart. Volume 103(2017)Supplement 1
• Page Start: A21
• Page End: A21
• Publication Date: 2017-04-03
• Subjects: Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2017-311399.25
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Introduction: Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease(COPD). Pulmonary arterial stiffening has been described in COPD both in those with pulmonary hypertension at rest and at exercise. Pulmonary pulse wave velocity (PWV) allows the non-invasive measurement of pulmonary arterial stiffening providing the potential for detection of early pulmonovascular changes before overt pulmonary hypertension sets in, but has not previously been assessed in COPD. The aim of the current study is thus to assess PWV in COPD and its effects on right ventricular(RV) remodelling. Methods: 58 participants with COPD underwent pulmonary function tests, six minute walk test, and cardiac MRI, while 21 age and sex matched healthy volunteers underwent cardiac MRI. 32 of the COPD patients underwent a follow-up MRI at 1 year to assess for longitudinal changes. Phase contrast imaging of the main pulmonary artery was performed in order to calculate pulmonary PWV using the flow-area technique. Results: Those with COPD demonstrated pulmonary arterial stiffening and pulmonary vascular remodelling with higher pulmonary artery area at end diastole (COPD: 2.36±0.56 cm 2 /m 1 .7 vs. HC: 2.14±0.28 cm 2 /m 1 .7, p=0.027), reduced pulsatility (COPD: 24.9±8.8% vs. HC: 30.6%±11.3%, p=0.021), reduced PAT (COPD: 104.0±22.9 ms vs. HC: 128.1±32.2 ms, p<0.001) and higher PWV (COPD: 2.62±1.29 ms -1 vs. HC: 1.78±0.72 ms -1, p=0.001). Pulmonary PWV was not associated with lung function, exercise capacity or right ventricular parameters. Cardiac remodelling in COPD was instead that of a reduced preload with a lower RV end diastolic volume (COPD: 53.6±11.1 ml vs. HC: 59.9±13.0 ml, p=0.037) and RV stroke volume (COPD: 31.9±6.9 ml/m 2 vs. HC: 37.1±6.2 m/m 2 l, p=0.003). At follow-up those with the stiffest pulmonary arteries (top tertile of PWV) experienced no greater increase in RV mass than those with the lowest stiffness (bottom tertile of PWV), p=0.29 for difference. Conclusion: Pulmonary PWV is elevated in COPD, but does not have any significant association with right ventricular function or functional capacity. In fact remodelling in COPD is that of a reduced preload rather than the expected increased afterload.