Latent class analysis identifies distinct phenotypes of primary graft dysfunction after lung transplantation. Chest Shah, R. J., Diamond, J. M., Cantu, E., Lee, J. C., Lederer, D. J., Lama, V. N., Orens, J., Weinacker, A., Wilkes, D. S., Bhorade, S., Wille, K. M., Ware, L. B., Palmer, S. M., Crespo, M., Localio, A. R., Demissie, E., Kawut, S. M., Bellamy, S. L., Christie, J. D. 2013; 144 (2): 616-622


ABSTRACT BACKGROUND: There is significant heterogeneity within the primary graft dysfunction (PGD) syndrome. We aimed to identify distinct grade 3 PGD phenotypes based on severity of lung dysfunction and patterns of resolution. METHODS: Subjects from the Lung Transplant Outcomes Group (LTOG) cohort study with grade 3 PGD within 72 hours after transplantation were included. Latent Class Analysis (LCA) was used to statistically identify classes based on changes in PGD ISHLT grade over time. Construct validity of the classes was assessed by testing for divergence of recipient, donor, and operative characteristics between classes. Predictive validity was assessed using time to death. RESULTS: 361 of 1255 subjects had grade 3 PGD within the first 72 hours after transplantation. LCA identified 3 distinct phenotypes: 1) severe persistent dysfunction (class 1); 2) complete resolution of dysfunction within 72 hours (class 2); and 3) attenuation, without complete resolution within 72 hours (class 3). Increased use of cardiopulmonary bypass, greater red blood cell transfusion and higher mean pulmonary artery pressure were associated with persistent PGD (class 1). Subjects in class 1 also had the greatest risk of death (HR 2.39, 95% CI: 1.57, 3.63, p<0.001). CONCLUSIONS: There are distinct phenotypes of resolution of dysfunction within the severe PGD syndrome. Subjects with early resolution may represent a different mechanism of lung pathology, such as resolving pulmonary edema, whereas classes with persistent PGD may represent a more severe phenotype. Future studies aimed at PGD mechanism or treatment may focus on phenotypes based on resolution of graft dysfunction.

View details for DOI 10.1378/chest.12-1480

View details for PubMedID 23429890