Extract
COPD is frequently associated with mild to moderate pulmonary hypertension (PH). However, a small subset of patients develops severe PH, which is currently haemodynamically defined as mean pulmonary arterial pressure (mPAP) ≥35 mmHg, or mPAP ≥25 mmHg in combination with cardiac index <2.0 L·min−1·m−2 [1, 2]. These cut-offs are, however, arbitrary and mainly based on expert opinion. In this study we aimed to determine prognostically relevant haemodynamic thresholds for severe PH in COPD by using an unbiased approach.
Abstract
PVR >5 WU proved to be the strongest independent haemodynamic predictor of mortality in COPD patients. This threshold may best identify COPD patients with severe pulmonary vascular disease. https://bit.ly/3v4QE96
Acknowledgements
We thank Daniela Kleinschek for excellent assistance. We thank PH Austria Research Association and Self-Help Organization for their support.
Footnotes
This article has an editorial commentary: https://doi.org/10.1183/13993003.02008-2021
Author contributions: K. Zeder: study design and development, data analysis and interpretation, writing the paper, final approval of the submitted version. A. Avian and G. Bachmaier: statistical analysis, final approval of the submitted version. P. Douschan, V. Foris, T. Sassmann, N. Troester, L. Brcic, M. Fuchsjäger, L.M. Marsh and B.A. Maron: data interpretation, final approval of the submitted version. H. Olschewski: study design and development, data analysis and interpretation, final approval of the submitted version. G. Kovacs: study design and development, data analysis and interpretation, writing the paper, final approval of the submitted version. All authors contributed to the writing and editing of the manuscript.
Conflict of interest: K. Zeder has nothing to disclose.
Conflict of interest: A. Avian has nothing to disclose.
Conflict of interest: G. Bachmaier has nothing to disclose.
Conflict of interest: P. Douschan reports personal fees and non-financial support from Actelion and GSK, non-financial support from AstraZeneca, Bayer, MSD, Novartis, Teva and Boehringer Ingelheim, outside the submitted work.
Conflict of interest: V. Foris reports personal fees and non-financial support from Boehringer Ingelheim, GSK and MSD, non-financial support from Actelion, Chiesi, BMS and Menarini, outside the submitted work.
Conflict of interest: T. Sassmann has nothing to disclose.
Conflict of interest: N. Troester has nothing to disclose.
Conflict of interest: L. Brcic has nothing to disclose.
Conflict of interest: M. Fuchsjäger has nothing to disclose.
Conflict of interest: L.M. Marsh has nothing to disclose.
Conflict of interest: B.A. Maron has nothing to disclose.
Conflict of interest: H. Olschewski reports grants from Bayer, Unither Pharmaceuticals, Actelion Pharmaceuticals Ltd, Roche, Boehringer Ingelheim and Pfizer Inc., personal fees from Gilead Sciences Inc., Encysive Pharmaceuticals Ltd and Nebu-Tec, personal fees and non-financial support from Bayer, Unither Pharmaceuticals, Actelion Pharmaceuticals Ltd, Pfizer Inc., Eli Lilly, Novartis, AstraZeneca, Boehringer Ingelheim, Chiesi, Menarini, MSD and GSK, outside the submitted work.
Conflict of interest: G. Kovacs reports personal fees and non-financial support from Actelion, Janssen, Bayer, GSK, MSD, Boehringer Ingelheim, Novartis, Chiesi, Vitalaire, Ferrer and AOP, outside the submitted work.
- Received February 25, 2021.
- Accepted April 14, 2021.
- Copyright ©The authors 2021. For reproduction rights and permissions contact permissions{at}ersnet.org
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