SARS-CoV-2 infection and two-year longitudinal clinical trajectory in pulmonary hypertension: a single-center retrospective exploratory cohort study.

Introduction: SARS-CoV-2 may promote endothelial injury, pulmonary vascular inflammation, and thrombosis, mechanisms relevant to pulmonary hypertension (PH), but longitudinal post-COVID-19 trajectories in established PH remain poorly defined. Methods: We retrospectively analysed 40 PH patients in the prospectively established POTENT registry with a first documented positive SARS-CoV-2 RT-PCR test dated 15 June 2020 to 2 November 2022 (index infection date). No contemporaneous non-infected PH comparator cohort was included; accordingly, the present analysis was uncontrolled and exploratory in intent. Follow-up windows were T0 during infection, T1 < 3 months, T2 3-12 months, T3 1-2 years, and T4 > 2 years. Clinical status, WHO functional class, haemodynamics, ESC/ERS risk category, NT-proBNP, and haemoglobin were evaluated. The primary endpoint was all-cause mortality, lung transplantation, ICU admission, or PH clinical deterioration, analysed using Kaplan-Meier estimation and Cox regression. Results: Median age was 37 years and 75% were female. Aetiologies were CTEPH 28%, CHD-PAH 25%, IPAH 20%, CTD-PAH 18%, and HPAH 10%; CTEPH represented WHO Group 4 PH and the others WHO Group 1 PAH. At T0, 52.5% were low risk and 27.5% intermediate-high risk. Risk profile shifted toward higher-risk categories at T2, followed by partial recovery by T4. Haemoglobin differed descriptively across available records (Kruskal-Wallis Conclusion: In this single-centre retrospective exploratory cohort, SARS-CoV-2 infection was temporally associated with a post-infection worsening signal in PH trajectory, greatest at 3-12 months, with partial longer-term recovery. Findings support risk-stratified surveillance but do not establish causality or definitive COVID-19-mediated progression; controlled prospective validation is required.