Resumen
Rationale: Pulmonary hypertension from pulmonary arterial hypertension or parenchymal lung disease is associated with an increased risk for primary graft dysfunction after lung transplantation. Objective: We evaluated the clinical determinants of severe primary graft dysfunction in pulmonary hypertension and developed and validated a prognostic model. Methods: We conducted a retrospective cohort study of patients in the multicenter Lung Transplant Outcomes Group with pulmonary hypertension at transplant listing. Severe primary graft dysfunction was defined as PaO2/FIO2 ≤200 with allograft infiltrates at 48 or 72 hours after transplantation. Donor, recipient, and operative characteristics were evaluated in a multivariable explanatory model. A prognostic model derived using donor and recipient characteristics was then validated in a separate cohort. Results: In the explanatory model of 826 patients with pulmonary hypertension, donor tobacco smoke exposure, higher recipient body mass index, female sex, listing mean pulmonary artery pressure, right atrial pressure and creatinine at transplant, cardiopulmonary bypass use, transfusion volume, and reperfusion fraction of inspired oxygen were associated with primary graft dysfunction. Donor obesity was associated with a lower risk for primary graft dysfunction. Using a 20% threshold for elevated risk, the prognostic model had good negative predictive value in both derivation and validation cohorts (89.1% [95% confidence interval, 85.3–92.8] and 83.3% [95% confidence interval, 78.5–88.2], respectively), but low positive predictive value. Conclusions: Several recipient, donor, and operative characteristics were associated with severe primary graft dysfunction in patients with pulmonary hypertension, including several risk factors not identified in the overall transplant population. A prognostic model with donor and recipient clinical risk factors alone had low positive predictive value, but high negative predictive value, to rule out high risk for primary graft dysfunction.
| Idioma original | English |
|---|---|
| Páginas (desde-hasta) | 1514-1522 |
| Número de páginas | 9 |
| Publicación | Annals of the American Thoracic Society |
| Volumen | 14 |
| N.º | 10 |
| DOI | |
| Estado | Published - oct 2017 |
Nota bibliográfica
Publisher Copyright:Copyright © 2017 by the American Thoracic Society.
Financiación
This study was supported by the National Institutes of Health (Grants T32 HL007891, K24 HL103844, R01 HL087115, R01 HL081619, R01 HL096845, K23: K23 HL121406) and the Actelion Entelligence Grant.
| Financiadores | Número del financiador |
|---|---|
| National Institutes of Health (NIH) | |
| Actelion Entelligence | |
| National Heart, Lung, and Blood Institute (NHLBI) | R01HL096845, K24HL103844, K23HL116656, R03HL135227, K23HL121406, R01HL087115, R01HL081619, T32HL007891 |
ODS de las Naciones Unidas
Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible
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Good health and well being
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
Huella
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