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. 2021 Nov 4;58(5):2004066.
doi: 10.1183/13993003.04066-2020. Print 2021 Oct.

Outcomes of patients with decreased arterial oxyhaemoglobin saturation on pulmonary arterial hypertension drugs

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Free article

Outcomes of patients with decreased arterial oxyhaemoglobin saturation on pulmonary arterial hypertension drugs

Simon Valentin et al. Eur Respir J. .
Free article

Abstract

Background: Drugs approved for the treatment of pulmonary arterial hypertension (PAH) improve long-term outcomes. These drugs have pulmonary vasodilator properties which may potentially cause a decrease in arterial oxyhaemoglobin saturation (S aO2 ) in some patients. The present retrospective study of the French Pulmonary Hypertension Registry aimed to describe the clinical characteristics and outcomes of patients showing a ≥3% decrease in S aO2 while treated with PAH drugs.

Methods: We reviewed 719 PAH patients. The exclusion criteria were PAH associated with congenital heart disease and PAH with overt features of venous/capillaries involvement.

Results: 173 (24%) patients had a ≥3% decrease in S aO2 . At diagnosis, they were older with a lower diffusing capacity of the lung for carbon monoxide and a shorter 6-min walk distance compared with those who did not display a ≥3% decrease in S aO2 . The percentage of patients meeting the European Society of Cardiology/European Respiratory Society (ESC/ERS) low-risk criteria at re-evaluation was significantly lower in those with a ≥3% decrease in S aO2 and more patients started long-term oxygen therapy in this group (16% versus 5%; p<0.001). A ≥3% decrease in S aO2 was associated with a poorer survival (hazard ratio 1.81, 95% CI 1.43-2.34; p<0.0001). In a multivariate Cox analysis, a ≥3% decrease in S aO2 was a prognostic factor independent of age at diagnosis and ESC/ERS risk stratification at follow-up.

Conclusions: When treated with PAH drugs, a large subset of patients experience a ≥3% decrease in S aO2 , which is associated with worse long-term outcomes and reduced survival.

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Conflict of interest statement

Conflict of interest: S. Valentin has nothing to disclose. Conflict of interest: A. Maurac has nothing to disclose. Conflict of interest: O. Sitbon reports grants, personal fees and non-financial support from Actelion, grants and personal fees from Bayer and MSD, personal fees from Acceleron, Ferrer and Gossamer Bio, grants from GlaxoSmithKline, outside the submitted work. Conflict of interest: A. Beurnier reports personal fees from Sanofi and AstraZeneca, outside the submitted work. Conflict of interest: E. Gomez has nothing to disclose. Conflict of interest: A. Guillaumot reports non-financial support from Actelion, AstraZeneca, Boehringer Ingelheim, MSD and Roche, outside the submitted work. Conflict of interest: L. Textoris has nothing to disclose. Conflict of interest: R. Fay has nothing to disclose. Conflict of interest: L. Savale reports personal fees and non-financial support from Actelion and MSD, grants from Bayer, outside the submitted work. Conflict of interest: X. Jaïs reports grants from Bayer, grants, personal fees and non-financial support from Actelion/Janssen, personal fees from MSD, outside the submitted work. Conflict of interest: D. Montani reports grants and personal fees from Actelion and Bayer, personal fees from GlaxoSmithKline, Pfizer, MSD and Chiesi, outside the submitted work. Conflict of interest: F. Picard reports personal fees from Novartis, outside the submitted work. Conflict of interest: J-F. Mornex reports personal fees and non-financial support from Actelion, grants, personal fees and non-financial support from GlaxoSmithKline, during the conduct of the study; grants, personal fees and non-financial support from LFB and CSL Behring, personal fees from Roche and Chiesi, outside the submitted work. Conflict of interest: G. Prevot has nothing to disclose. Conflict of interest: F. Chabot reports non-financial support from Actelion, AstraZeneca, Boehringer Ingelheim and MSD, outside the submitted work. Conflict of interest: M. Humbert reports grants, personal fees and non-financial support from GlaxoSmithKline, grants and personal fees from Acceleron, Actelion and Bayer, personal fees from AstraZeneca, Novartis, Roche, Sanofi, Teva and Merck, outside the submitted work. Conflict of interest: A. Chaouat has received personal fees for lecturing and/or consulting from Actelion, Boehringer Ingelheim, Novartis, MSD and Chiesi, and research grants from Actelion and GlaxoSmithKline.

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