A66-10 Prevalence and Risk Factors of Severe Primary Graft Dysfunction in Patients With Pulmonary Hypertension Associated With Interstitial Lung Disease

Severe primary graft dysfunction (PGD) is a major early contributor to early mortality in patients undergoing lung transplantation. The pathogenesis of PGD is complex, involving interplay among host/recipient inflammatory and immunologic interactions within the first seventy-two hours of transplantation. Treatment options remain sparse and are primarily supportive. An understanding of at-risk populations for severe PGD remain key and are typically divided into (1) donor-specific, (2) recipient-specific, and (3) operative/perioperative risk factors. In particular, donor smoking history, elevated pulmonary arterial pressures, and donor/recipient obesity are a few of previously identified important risk factors for the development of severe PGD. Interstitial lung disease (ILD) remains one of the primary reasons for patients to under lung transplantation. Pulmonary hypertension (PH) is an important sequela of ILD, and so-called pulmonary hypertension associated with interstitial lung disease (PH-ILD) becomes more common with more advanced lung disease, such as when patients are being evaluated and considered for lung transplantation. In this study, we aimed to identify pre-transplant predictors of severe PGD among patients with PH-ILD undergoing lung transplantation. We performed a single-center retrospective analysis of PH-ILD patients who underwent lung transplantation (n = 78) between 2021-2025 to identify predictors of severe PGD seventy-two hours post-transplantation. Of these patients, twenty-eight percent (n = 22) developed severe PGD while seventy-two percent (n = 56) did not develop severe PGD. Between the two groups, there were no significant differences to age (p = 0.36), sex (p = 0.37), race (p = 0.54) and BMI (p = 0.16). Additionally, the proportion of underlying subtypes of ILD were not significantly different (p = 0.71). Additionally, no significant differences were seen in initial spirometry and echocardiographic measurements between the groups. Interestingly, right heart catheterization measurements trended towards significance between the groups, including measured mean (39 mmHg severe PGD versus 35 mmHg without severe PGD, p = 0.08) and diastolic (25 mmHg versus 21 mmHg, p = 0.06) pulmonary arterial pressures. Using a cutoff of mean pulmonary arterial pressure of greater than forty-five mmHg, the odds of severe PGD were about threefold higher (odds ratio 3.27) and trended towards significance (p = 0.05) compared to those who did not develop severe PGD. Higher pre-transplant pulmonary pressures trended toward increased PGD risk, supporting prior evidence that abnormal hemodynamics and right ventricular dysfunction may predispose to early graft reperfusion injury and PGD. This study is limited primarily by its smaller sample size and retrospective analysis. This abstract is funded by: None