Abstract Introduction Pulmonary arterial diameter (PAD) is an important marker of pulmonary hypertension (PH). It is detected on computed tomography (CT) imaging and is often used for screening for PH. Less is known about the degree to which PAD evolves over the course of the disease and responds to treatment. In this study, we sought to examine the response of PAD using CT imaging before and after lung transplantation (LuTx). Methods Patients who underwent LuTx and had evidence of PH on right heart catheterization (RHC) were identified. PAD and Aortic diameters were measured on CT scans before and at least 3 months after LuTx in millimeters in Epic PACS system. Wilcoxon Rank-Sum test was used to test differences between pre- and post-transplant imaging. Results are presented as medians, intraquartile ranges with 2-sided p-values 0.05 considered significant. Results 29 subjects were identified for analysis. 15 were female. Of these subjects, 22 received bilateral LuTx, whereas 4 received right and 3 received left lungs. The etiology of transplant was predominantly interstitial lung disease, but also included pulmonary artery hypertension, chronic obstructive pulmonary disease, and bronchiectasis. Median mean pulmonary artery pressure (mPAP) was 3227-42mmHg at the RHC before transplant. The lowest mPAP in the group was 24 mmHg. Prior to transplantation the measured PAD was 35.3mm28-39.2, whereas the Aortic diameter was 33.431.5-35.9, with a main pulmonary artery over aortic ratio (PAA) of 1.030.93-1.13. Post transplantation PAD was 32.128.7-34.6, Aortic diameter was 34.732.4-37.4, while the PAA was 0.50.86-1.02. The Spearman correlation coefficient between PAA and mPAP was 0.6 (p = 0.0006). Pulmonary arterial diameter decreased by 2.4mm0.4 -5.8, p = 0.018 between pre- and post-transplant imaging. The PAA decreased by 0.100.005-0.18, p 0.0001. Prior to transplant, 17 patients had a PAA of 1.0. After the transplant, 8 subjects continued to have PAA 1.0. Discussion PAD responded to LuTx. Interestingly, however, the response was not complete. For example, seven of the subjects with PAA 1.0 continued to have PAA 1.0 post-transplant. This suggests that the size of the pulmonary artery may be an interplay between pressure elevation and remodeling, which may not be as responsive to treatment. This analysis is a small-scale analysis, and many factors alter PAD, which could confound results. Conclusion Examination of PAD in response to treatment may help us better understand the etiology of pulmonary artery dilation. More studies are needed to better characterize this correlation. This abstract is funded by: None
Gogolashvili et al. (Fri,) studied this question.