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Jason D. Christie, MD, FCCP; Steven M. Kawut, MD, FCCP; for the Lung Transplant Outcomes Group
Author and Funding Information

From the Division of Pulmonary and Critical Care Medicine, University of Pennsylvania.

Correspondence to: Jason D. Christie, MD, FCCP, Division of Pulmonary and Critical Care Medicine, University of Pennsylvania, 719 Blockley Hall 423, Guardian Dr, Philadelphia, PA 19104-6021; e-mail: jchristi@mail.med.upenn.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Kawut has received funding for consulting, speaking fees, conferences, travel to conferences, research, and serving on steering committees from Gilead, Actelion, United Therapeutics, Pfizer, Gerson Lehrman, and Clinical Advisors. Dr Christie has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(3):827. doi:10.1378/chest.11-1228
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To the Editor:

We appreciate the interest of Drs Jenks and Uysal in our article.1 We agree that not all the subjects with primary graft dysfunction (PGD) had a mean pulmonary arterial pressure (mPAP) >25 mm Hg and that not all the subjects without PGD had an mPAP <25 mm Hg. It was precisely for this reason that we presented our finding of a higher mPAP in patients with PGD than in those without as a continuous variable. The study was limited to patients with idiopathic pulmonary fibrosis, but not all patients with higher mPAP met the World Health Organization criteria for pulmonary hypertension, leading us to avoid the application of potentially inaccurate phenotypes. We do not have records of whether the subjects were actively being treated for pulmonary hypertension with pharmacologic agents.

Further, we agree that many factors may influence the first recorded pulmonary arterial pressure during the transplant procedure in patients with idiopathic pulmonary fibrosis. In order for intravascular volume or mechanical ventilation to account for our findings, patients at greater underlying risk for PGD would have to have more intravascular volume administered and higher levels of ventilator support before the diagnosis of PGD is made. Although this is unlikely, we see this as an opportunity for future research.

Fang A, Studer S, Kawut SM, et al; for the Lung Transplant Outcomes Group for the Lung Transplant Outcomes Group Elevated pulmonary artery pressure is a risk factor for primary graft dysfunction following lung transplantation for idiopathic pulmonary fibrosis. Chest. 2011;1394:782-787 [CrossRef] [PubMed]
 

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Fang A, Studer S, Kawut SM, et al; for the Lung Transplant Outcomes Group for the Lung Transplant Outcomes Group Elevated pulmonary artery pressure is a risk factor for primary graft dysfunction following lung transplantation for idiopathic pulmonary fibrosis. Chest. 2011;1394:782-787 [CrossRef] [PubMed]
 
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