Mary K Porteous1, James C Lee1, David J Lederer2, Scott M Palmer3, Edward Cantu4, Rupal J Shah5, Scarlett L Bellamy6, Vibha N Lama7, Sangeeta M Bhorade8, Maria M Crespo1, John F McDyer9, Keith M Wille10, A Russell Localio6, Jonathan B Orens11, Pali D Shah11, Ann B Weinacker12, Selim Arcasoy2, David S Wilkes13, Lorraine B Ware14,15, Jason D Christie1,6, Steven M Kawut1,6, Joshua M Diamond1,6. 1. 1 Department of Medicine. 2. 2 Department of Medicine, Columbia University Medical Center, New York, New York. 3. 3 Department of Medicine, Duke University, Durham, North Carolina. 4. 4 Department of Surgery, and. 5. 5 Department of Medicine, University of California, San Francisco, California. 6. 6 Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 7. 7 Department of Medicine, University of Michigan Health System, Ann Arbor, Michigan. 8. 8 Department of Medicine, Northwestern University, Chicago, Illinois. 9. 9 Department of Medicine, University of Pittsburgh Medical Center Montefiore Hospital, Pittsburgh, Pennsylvania. 10. 10 Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama. 11. 11 Department of Medicine, Johns Hopkins University, Baltimore, Maryland. 12. 12 Department of Medicine, Stanford University Medical Center, Stanford, California. 13. 13 Department of Medicine, University of Virginia, Charlottesville, Virginia; and. 14. 14 Department of Medicine and. 15. 15 Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee.
Abstract
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.
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, donortobacco 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. Donorobesity 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.
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