Pulmonary Vascular Volume by Quantitative CT in Dyspneic Smokers with Minor Emphysema

Abstract

Reduced lung diffusing capacity for carbon monoxide (DL_CO) at rest and increased ventilation (⩒_E)-carbon dioxide output (⩒CO₂) during exercise are frequent findings in dyspneic smokers with largely preserved FEV₁. It remains unclear whether low DL_CO and high ⩒_E-⩒CO₂ are mere reflections of alveolar destruction (i.e. emphysema) or impaired pulmonary perfusion in non-emphysematous tissue contributes to these functional abnormalities. Sixty-four smokers (41 males, FEV₁= 84 ± 13%predicted) underwent pulmonary function tests, an incremental exercise test, and quantitative chest computed tomography. Total pulmonary vascular volume (TPVV) was calculated for the entire segmented vascular tree (VIDA Vision™). Using the median % low attenuation area (-950 HU), participants were dichotomized into “Trace” or “Mild” emphysema (E), each group classified into preserved versus reduced DL_CO. Within each emphysema subgroup, participants with abnormally low DL_CO showed lower TPVV, higher ⩒_E-⩒CO₂, and exertional dyspnea than those with preserved DL_CO (p < 0.05). TPVV (r = 0.34; p = 0.01), but not emphysema (r = −0.05; p = 0.67), correlated with lower DL_CO after adjusting for age and height. Despite lower emphysema burden, Trace-E participants with reduced DL_CO had lower TPVV, higher dyspnea, and lower peak work rate than the Mild-E with preserved DL_CO (p < 0.05). Interestingly, TPVV (but not emphysema) correlated inversely with both dyspnea-work rate (r = −0.36, p = 0.004) and dyspnea-⩒_E slopes (r = −0.40, p = 0.001). Reduced pulmonary vascular volume adjusted by emphysema extent is associated with low DL_CO and heightened exertional ventilation in dyspneic smokers with minor emphysema. Impaired perfusion of non-emphysematous regions of the lungs has greater functional and clinical consequences than hitherto assumed in these subjects.

Keywords:

• Smoking
• pulmonary vascular volume
• DL_CO
• dyspnea
• CT
• emphysema

Acknowledgements

Dr. D.E. O’Donnell has received research funding via Queen’s University from Canadian Institutes of Health Research, the Canadian Respiratory Research Network, AstraZeneca, and Boehringer Ingelheim and has served on speaker bureaus, consultation panels, and advisory boards for AstraZeneca and Boehringer Ingelheim. The funders had no role in the study design, data collection, analysis, or preparation of the manuscript.

Author Contribution

All the authors played a role in the content and writing of the manuscript. D.E.O. was the principal investigator; A.F.E., and D.E.O. provided the original idea for the study and had input into the study design and conduct of the study. A.F.E., and S.G.V. collected the data. A.F.E., S.G.V., and J.V. prepared data for presentation. A.F.E. wrote the first draft of the manuscript. G.P., J.A.N., and D.E.O. had input in the interpretation and writing the final manuscript and all authors accepted the last version.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Funding

Dr. D.E. O’Donnell has received research funding via Queen’s University from Canadian Institutes of Health Research, Canadian Respiratory Research Network, AstraZeneca, and Boehringer Ingelheim and has served on speaker bureaus, consultation panels, and advisory boards for AstraZeneca and Boehringer Ingelheim. Dr G. Parraga acknowledges funding from the Canada Research Chair Program, CIHR, NSERC the Baran Family Foundation for COPD research, Astra Zeneca, Novartis, and GSK, not related to this study. These funders had no role in the study design, data collection, and analysis, or preparation of the manuscript.

Notification of prior abstract presentation

Some of the data herein presented was part of an abstract presented at the European Respiratory Society Annual Meeting 2021: DOI: 10.1183/13993003.congress-2021.OA2555.