Clinical Outcomes in Patients with Advanced Chronic Liver Disease and Hepatic Venous Pressure Gradient ≤ 10mm Hg.

Abstract

Clinically significant portal hypertension (CSPH), defined as hepatic venous pressure gradient (HVPG) ≥ 10mmHg predicts clinical decompensation (CD) in cirrhosis. A proportion of cirrhosis patients have HVPG 6-10mmHg. Their natural history is largely unknown. Consecutive patients with advanced chronic liver disease (aCLD) [histological cirrhosis(n = 196) or liver stiffness measurement (LSM) > 15kPa(n = 65)] and HVPG 6-10mmHg were included. Primary objective was to study their natural course and patterns of CD. We also analyzed the predictors of CD at presentation and on follow-up and response to carvedilol. Of 261patients with HVPG 6-10mmHg,129(49.4%) had CD at first presentation; 78(29.9%) had single and 51(19.5%) had ≥ 2CD. The most common CDs wereascites(n = 77) and jaundice(n = 65).A baseline HVPG ≥ 8mmHg was independently associated with greater risk of CD [HR:1.7; p-0.002, AUROC:0.85(95%CI-0.81-0.91)]. New CD developed in 14.4% patients with compensated aCLD (median duration-23.1months). Despite comparable baseline HVPG, patients developing new CD had higher HVPG on follow-up(15.3 ± 3.7 vs. 8 ± 2.1mmHg; p < 0.001). Baseline LSM > 26.6kPa, portosystemic shunt and serum albumin independently predicted newCD.Overall HVPG response to carvedilol(n = 60)was 23.3%, independent of baseline CD and HVPG. Five-year mortality was higher with ≥ 2CD compared to single or no CD (23.5, 10 and 3%, respectively; p < 0.001). Nearly one-half of aCLD patients with HVPG 6-10mmHg had CD, justifying the need to redefine CSPH. Interventions to reduce portal pressure in patients with HVPG ≥ 8mmHg might improve long-term outcomes.