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Changes in HVPG predict hepatic decompensation in patients who achieved SVR to IFN-free therapy.

Sustained virologic response (SVR) to interferon (IFN)-free therapies ameliorates portal hypertension (PH), however it remains unclear whether a decrease in hepatic venous pressure gradient (HVPG) after cure of hepatitis C translates into a clinical benefit. We assessed the impact of pre-treatment HVPG, changes in HVPG, and post-treatment HVPG on the development of hepatic decompensation in patients with PH who achieved SVR to IFN-free therapy. Moreover, we evaluated transient elastography (TE) and von Willebrand factor to platelet ratio (VITRO) as non-invasive methods for monitoring the evolution of PH. The study comprised 90 patients with HVPG≥6mmHg who underwent paired HVPG, TE, and VITRO assessments before (BL) and after (FU) IFN-free therapy. FU-HVPG but not BL-HVPG predicted hepatic decompensation (per mmHg, hazard ratio [HR]:1.18,95% confidence interval [95%CI]:1.08-1.28;P<0.001). Patients with BL-HVPG≤9mmHg or patients who resolved clinically significant PH (CSPH) were protected from hepatic decompensation. In CSPH patients, a HVPG-decrease≥10% was similarly protective (36months:2.5%vs.40.5%;P<0.001), but observed in a substantially higher proportion of patients (60%vs.24%;P<0.001). Importantly, the performance of non-invasive methods such as TE/VITRO for diagnosing a HVPG-reduction≥10% was inadequate for clinical use (area under the receiver operating characteristic curve [AUROC]:<0.8), emphasizing the need for HVPG-measurements. However, TE/VITRO were able to rule-in or rule-out FU-CSPH (AUROC:0.86-0.92) in most patients, especially if assessed in a sequential manner. CONCLUSION: Re-assessment of HVPG after SVR improved prognostication in patients with pre-treatment CSPH. An 'immediate' HVPG-decrease≥10% was observed in the majority of these patients and was associated with a clinical benefit, as it prevented hepatic decompensation. These results support the use of HVPG as a surrogate endpoint for interventions that lower portal pressure by decreasing intrahepatic resistance. This article is protected by copyright. All rights reserved.