(822) - Right Ventricular Recovery After Lung Transplantation for Pulmonary Arterial Hypertension: Impact of Immunosuppressive Regimen - Insights from the ScanCLAD Trial

Purpose: Right ventricular (RV) dysfunction is the key prognostic factor in pulmonary arterial hypertension (PAH). Progression to RV failure involves dilatation, systolic and diastolic impairment, fibrosis, and metabolic changes. Lung transplantation (LTx) normalizes RV afterload, but the extent of recovery and its relation to immunosuppressive therapy remain unclear. We aimed to assess RV function before and after LTx in patients with PAH in the multicenter ScanCLAD trial, describing echocardiographic parameters by immunosuppressive regimen (cyclosporine vs tacrolimus).
Methods: This subgroup analysis included PAH patients from the ScanCLAD trial (ClinicalTrials.gov NCT02936505). Transthoracic echocardiography was performed before and within 12 months after LTx. RV size and function were evaluated using standard and derived parameters (Table 1). Due to the small sample size, statistical testing was not performed; data are presented as mean ± SD or median [IQR].
Results: Of 249 ScanCLAD participants, 11 had PAH. Median time from LTx to follow-up was 3 [9] months. Both treatment groups showed marked RV improvement after LTx. Systolic pulmonary arterial pressure (sPAP) fell from 74 ± 6 to 24 ± 2 mmHg (cyclosporine) and from 80 ± 24 to 26 ± 5 mmHg (tacrolimus), indicating reduced RV afterload. Right atrial area and central venous pressure decreased, while RV performance indices improved. Fractional area change rose from 29 ± 11% to 44 ± 4% and from 18 ± 9% to 46 ± 8%, respectively while RV-PA coupling improved markedly in both groups. Cardiac output increased from 4.7 ± 0.2 to 5.7 ± 0.3 L/min and from 4.1 ± 1.2 to 6.2 ± 1.5 L/min.
Conclusion: Lung transplantation led to marked RV recovery in PAH patients, with similar improvements under cyclosporine and tacrolimus. Post-transplant recovery seemed largely regimen-independent, though tacrolimus reduced chronic lung allograft dysfunction incidence in the "parent study".