455 Haemodynamic prediction of primary graft dysfunction in lung transplant recipients

Abstract

Abstract Aims Primary graft dysfunction (PGD) is a form of acute lung injury, that occurs after lung transplantation (LTx), characterized by pulmonary oedema and diffuse alveolar damage. Pulmonary hypertension is a well-known risk factor for PGD and some invasive and non-invasive studies showed an association between PGD and altered left heart filling pressure. Despite the cardiopulmonary haemodynamic seems to be mainly involved in the pathogenesis of PGD, no reliable predictive parameter has been demonstrated. The aim of our study is to test whether pulmonary arterial pressure and left diastolic function may be considered in the risk PGD stratification. Methods and results we retrospectively analyzed the results of right heart catheterization (RHC) performed in occasion of the assessment for the LTx eligibility. All patients have been assessed at the Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico of Milan (Italy) from 2006 to 2018. We included all form of respiratory diseases except for cystic fibrosis. PGD was defined as PaO2/FIO2 < 300, with infiltrates at 72 h after reperfusion. We grouped patients in two groups according to the PGD development or absence (PGD+ and PGD−). Ninety patients were analyzed (mean age 55 ± 10; 53 male). Bilateral LTx was performed in 57 cases (63%). The most frequent indications for LTx were Interstitial Lung Disease (38%), Idiopathic Pulmonary Fibrosis (32%) an COPD (16%). Mean pulmonary arterial pressure (mPAP 29.4 ± 11.5 mmHg vs. 24.2 ± 9.7 mmHg, P = 0.016) and PAWP (12.9 ± 4.3 mmHg vs. 10.4 ±.,8 mmHg, P = 0.012) values were significantly higher in the PGD+ than in the PGD− group as well as PAWP values. At the multivariate analysis, both mPAP and PAWP were independent risk factors for PGD development even adjusted for BMI, age, or indication for LTx (mPAP non-adjusted OR: 1.05, 95% CI: 1.01–1.10, P = 0.027; mPAP adjusted OR: 1.06, 95% CI: 1.00–1.12, P = 0.046; PAWP non-adjusted OR: 1.13, 95% CI: 1.02–1.25, P = 0.016; PAWP adjusted OR: 1.14, 95% CI: 1.01–1.29, P = 0.036). No difference was observed between pulmonary vascular resistance (PVR) values. After a sub analysis of the patients with PAWP ≥15 mmHg, we observed that the ratio between PVR and PAWP was significantly higher in the PGD + group (0.18 ± 0.11 vs. 0.09 ± 0.05, P = 0.036). Conclusion s our data confirmed that pulmonary circulation plays a crucial role in the prediction of PGD and elevated mPAP is the one of the main risk factors. Of note, despite in both group PAWP in was within normal values (<15 mmHg), it was determinant in the risk stratification for PGD development. We suppose that the increased PVR due to pulmonary parenchymal diseases may “mask” and “underestimate” the role of the left ventricular diastolic dysfunction creating a sort of vascular barrage witch is overcome after lung transplantation hesitating in pulmonary oedema. This hypothesis is corroborated by the significative difference of PVR/PAWP ratio that can select patients at risk for PGD.