Stoleriu MG, Pienn M, Joerres RA, Alter P, Fero T, Urschler M, Kovacs G, Olschewski H, Kauczor HU, Wielpütz M, Jobst B, Welte T, Behr J, Trudzinski FC, Bals R, Watz H, Vogelmeier CF, Biederer J, and Kahnert K
Purpose: The aim of this study was to evaluate the association between computed tomography (CT) quantitative pulmonary vessel morphology and lung function, disease severity, and mortality risk in patients with chronic obstructive pulmonary disease (COPD)., Patients and Methods: Participants of the prospective nationwide COSYCONET cohort study with paired inspiratory-expiratory CT were included. Fully automatic software, developed in-house, segmented arterial and venous pulmonary vessels and quantified volume and tortuosity on inspiratory and expiratory scans. The association between vessel volume normalised to lung volume and tortuosity versus lung function (forced expiratory volume in 1 sec [FEV 1 ]), air trapping (residual volume to total lung capacity ratio [RV/TLC]), transfer factor for carbon monoxide (TLCO), disease severity in terms of Global Initiative for Chronic Obstructive Lung Disease (GOLD) group D, and mortality were analysed by linear, logistic or Cox proportional hazard regression., Results: Complete data were available from 138 patients (39% female, mean age 65 years). FEV 1 , RV/TLC and TLCO, all as % predicted, were significantly (p < 0.05 each) associated with expiratory vessel characteristics, predominantly venous volume and arterial tortuosity. Associations with inspiratory vessel characteristics were absent or negligible. The patterns were similar for relationships between GOLD D and mortality with vessel characteristics. Expiratory venous volume was an independent predictor of mortality, in addition to FEV 1 ., Conclusion: By using automated software in patients with COPD, clinically relevant information on pulmonary vasculature can be extracted from expiratory CT scans (although not inspiratory scans); in particular, expiratory pulmonary venous volume predicted mortality., Trial Registration: NCT01245933., Competing Interests: Dr Gabor Kovacs reports grants, personal fees and/or non-financial support from Janssen, Astra Zeneca, Boehringer Ingelheim, Bayer, GSK, MSD, Chiesi, Vitalaire, Ferrer, and AOP, outside the submitted work. Dr Horst Olschewski reports personal fees from Iqvia, MSD, Janssen, Pfizer, Astra Zeneca, GSK, Boehringer; department director for Ludwig Boltzmann Institute for Lung Vascular Research, outside the submitted work. Dr Hans-Ulrich Kauczor reports non-financial support from Bayer and Siemens; grants from BMBF, during the conduct of the study; grants and/or personal fees from Siemens, Philips, Boehringer Ingelheim, Sanofi, Median, outside the submitted work. Dr Mark Wielpütz reports grants from Vertex and Boehringer, outside the submitted work. Professor Tobias Welte reports grants from German Ministry of Research and Education, during the conduct of the study; personal fees from GSK, AstraZeneca, Berlin-Chemie, Boehringer Ingelheim, and Chiesi, outside the submitted work. Professor Jürgen Behr reports personal fees from Astra-Zeneca, Boehringer-Ingelheim, BMS, Ferrer, Novartis, Roche, Sanofi-Genzyme, Janssen, and Johnson&Johnson, outside the submitted work. Dr Robert Bals reports grants from German Ministery of Education and Science (BMBF), during the conduct of the study; grants from DFG, Schwiete Stiftung, Krebshilfe, personal fees from Boehringer Ingelheim, CSL Behring, outside the submitted work. Professor Claus Vogelmeier reports grants and/or personal fees from Aerogen, AstraZeneca, Boehringer Ingelheim, CSL Behring, Chiesi, GlaxoSmithKline, Grifols, Insmed, Menarini, Novartis, Nuvaira, Roche, and Sanofi, outside the submitted work. The authors declare that they have no other known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 Stoleriu et al.)