LAUSR

BACKGROUND Clinically significant portal hypertension (CSPH, HVPG≥10mmHg) persists 24 weeks after sustained virological response (SVR) in up to 78% of patients with HCV-related cirrhosis treated with direct acting antivirals. These patients remain at risk of decompensation. However, long-term paired clinical and hemodynamic data are not available for this population. METHODS Multicenter prospective study including 226 patients with HCV-related cirrhosis and CSPH achieving SVR after antiviral therapy. Patients with CSPH 24 weeks after therapy (SVR24) were offered another hemodynamic assessment 96 weeks after end of treatment (SVR96). RESULTS All patients were clinically evaluated. One-hundred seventeen (66%) of the 176 patients with SVR24-CSPH underwent SVR96-HVPG (this was not done for several reasons in the remaining 59 patients). At SVR96, 55/117 (47%) patients had HVPG < 10mmHg and 53% had CSPH (65% if we assume persistence of CSPH in all 59 non-evaluated patients). The proportion of high-risk patients (HVPG ≥ 16mmHg) diminished from 41% to 15%. Liver stiffness decreased markedly after SVR (median decrease 10.5 ± 13kPa) but did not correlate with HVPG changes (30% of patients with LSM <13.6kPa still had CSPH). Seventeen (7%) patients presented de novo/additional clinical decompensation, which was independently associated with baseline HVPG ≥ 16mmHg and history of ascites. CONCLUSIONS Patients achieving SVR present a progressive reduction in portal pressure during follow-up. However, CSPH may persist in up to 53-65% of patients at SVR96, indicating persistent risk of decompensation. History of ascites and high-risk HVPG values identified patients at higher risk of de novo or further clinical decompensation.