Extract
In this journal, Pellinoet al.[1] presented a survival analysis to assess how deprivation affects prognosis in patients with pulmonary arterial hypertension (PAH). Their conclusions were that social deprivation is not a significant referral barrier or prognostic factor for idiopathic (I)PAH or heritable (H)PAH in Scotland. This may appear surprising, given the wider context of literature describing outcomes stratified by social deprivation. The authors were thorough on using both the address at time of diagnosis and at time of censoring to assign deprivation scores and compare the two, finding no significant differences between the two approaches. They also compared deprivation assigned to PAH cases to expected deprivation based on Scottish citizenry as a whole, and found that PAH patients are more socially deprived than expected. Finally, they used the same survival univariate analysis adjusting for age and sex to assess how several clinical variables are associated with prognosis.
Abstract
No association was found between deprivation and mortality for PAH patients in England and Wales. The association found between risk stratification at baseline and deprivation suggests that the issue of deprivation and outcomes in PAH may be more nuanced.https://bit.ly/2y8WgqB
Footnotes
Conflict of interest: E. Sofianopoulou has nothing to disclose.
Conflict of interest: C. Church has nothing to disclose.
Conflict of interest: G. Coghlan reports grants and personal fees for conference attendance from Johnson & Johnson, personal fees for lectures from GlaxoSmithKline, Bayer andMSD, outside the submitted work.
Conflict of interest: L. Howard has nothing to disclose.
Conflict of interest: M. Johnson reports grants and personal fees for meeting attendance, lectures and advisory board work from Actelion and MSD, outside the submitted work.
Conflict of interest: D.G. Kiely has nothing to disclose.
Conflict of interest: A. Lawrie reports grants from British Heart Foundation and Medical Research Council, grants, personal fees and travel support from Actelion Pharmaceuticals Ltd, grants and personal fees from GlaxoSmithKline, outside the submitted work.
Conflict of interest: J. Lordan has nothing to disclose.
Conflict of interest: M.R. Wilkins has nothing to disclose.
Conflict of interest: S.J. Wort has nothing to disclose.
Conflict of interest: N.W. Morrell has nothing to disclose.
Conflict of interest: M.R. Toshner reports personal fees from GSK, grants and personal fees from J&J/Actelion, grants from Merck and Bayer, outside the submitted work.
Support statement: This work was supported by the Medical Research Council (grant: RG67444), the British Heart Foundation (grant: RG68204) and the NIHR Cambridge Biomedical Research Centre. Funding information for this article has been deposited with theCrossref Funder Registry.
- ReceivedDecember 5, 2019.
- AcceptedMarch 20, 2020.
- Copyright ©ERS 2020.
This version is distributed under the terms of the Creative Commons Attribution Licence 4.0.