Adam Fang1, Sean Studer2, Steven M Kawut3, Vivek N Ahya4, James Lee4, Keith Wille5, Vibha Lama6, Lorraine Ware7, Jonathan Orens8, Ann Weinacker9, Scott M Palmer10, Maria Crespo1, David J Lederer11, Clifford S Deutschman12, Benjamin A Kohl12, Scarlett Bellamy13, Ejigayehu Demissie3, Jason D Christie14. 1. Division of Pulmonary and Critical Care Medicine, University of Pittsburgh, Pittsburgh PA. 2. Division of Pulmonary and Critical Care Medicine, Newark Beth Israel Medical Center, Newark, NJ. 3. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia PA; Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia PA. 4. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia PA. 5. Division of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, Birmingham AL. 6. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Michigan, Nashville TN. 7. Division of Pulmonary, Allergy, and Critical Care Medicine, Vanderbilt University, Nashville TN. 8. Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Johns Hopkins University Hospital, Baltimore MD. 9. Division of Pulmonary and Critical Care Medicine, Stanford University, Durham NC. 10. Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University, Durham NC. 11. Division of Pulmonary and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY. 12. Department of Anesthesia and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, PA. 13. Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia PA. 14. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia PA; Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia PA. Electronic address: jchristi@mail.med.upenn.edu.
Abstract
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is often associated with elevations in pulmonary artery pressures. Although primary pulmonary arterial hypertension (PAH) has been associated with primary graft dysfunction (PGD), the role of secondary PAH in mediating PGD risk in patients with IPF is incompletely understood. The purpose of this study was to evaluate the relationship between mean pulmonary artery pressure (mPAP) and PGD among patients with IPF. METHODS: We performed a multicenter prospective cohort study of 126 lung transplant procedures performed for IPF between March 2002 and August 2007. The primary outcome was grade 3 PGD at 72 h after lung transplant. The mPAP was measured as the initial reading following insertion of the right-sided heart catheter during lung transplant. Multivariable logistic regression was used to adjust for confounding variables. RESULTS: The mPAP for patients with PGD was 38.5 ± 16.3 mm Hg vs 29.6 ± 11.5 mm Hg for patients without PGD (mean difference, 8.9 mm Hg [95% CI, 3.6-14.2]; P = .001). The increase in odds of PGD associated with each 10-mm Hg increase in mPAP was 1.64 (95% CI, 1.18-2.26; P = .003). In multivariable models, this relationship was independent of confounding by other clinical variables, although the use of cardiopulmonary bypass partially attenuated the relationship. CONCLUSIONS: Higher mPAP in patients with IPF is associated with the development of PGD.
BACKGROUND:Idiopathic pulmonary fibrosis (IPF) is often associated with elevations in pulmonary artery pressures. Although primary pulmonary arterial hypertension (PAH) has been associated with primary graft dysfunction (PGD), the role of secondary PAH in mediating PGD risk in patients with IPF is incompletely understood. The purpose of this study was to evaluate the relationship between mean pulmonary artery pressure (mPAP) and PGD among patients with IPF. METHODS: We performed a multicenter prospective cohort study of 126 lung transplant procedures performed for IPF between March 2002 and August 2007. The primary outcome was grade 3 PGD at 72 h after lung transplant. The mPAP was measured as the initial reading following insertion of the right-sided heart catheter during lung transplant. Multivariable logistic regression was used to adjust for confounding variables. RESULTS: The mPAP for patients with PGD was 38.5 ± 16.3 mm Hg vs 29.6 ± 11.5 mm Hg for patients without PGD (mean difference, 8.9 mm Hg [95% CI, 3.6-14.2]; P = .001). The increase in odds of PGD associated with each 10-mm Hg increase in mPAP was 1.64 (95% CI, 1.18-2.26; P = .003). In multivariable models, this relationship was independent of confounding by other clinical variables, although the use of cardiopulmonary bypass partially attenuated the relationship. CONCLUSIONS: Higher mPAP in patients with IPF is associated with the development of PGD.
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