Portal hypertension persistent in over half of HCV patients even after SVR
Clinically significant portal hypertension (CSPH) may persist for weeks in about half of patients with hepatitis C virus (HCV)-related cirrhosis, even after sustained virological response (SVR) has been achieved, a new study has found. This may indicate that risk of decompensation remains.
Researchers conducted a multicentre prospective study of 226 patients with HCV-related cirrhosis and CSPH. In all participants, antiviral therapy led to SVR. CSPH was defined as a hepatic venous pressure gradient (HVPG) ≥10 mm Hg. Those with CSPH at 24 weeks after end of treatment (SVR 24) were offered another measurement opportunity at SVR 96.
At SVR 24, median HVPG was 13.4 mm Hg, down from 15.6 mm Hg at baseline, representing a significant change (p<0.01). At this first follow-up, however, only 50 patients (22 percent) had HVPG <10 mm Hg, and 176 patients still presented with CSPH.
Of those still with CSPH at SVR 24, 117 opted to undergo another haemodynamic measurement at SVR 96 and 59 opted out. The median HVPG among these patients dropped further to 12.0 mm Hg, and an additional 29 patients were able to drop below the CSPH threshold of 10 mm Hg.
In total, 79 patients were without CSPH at the end of follow-up, yielding an overall cumulative CSPH rate of 53 percent at SVR 96. If none of the 59 drop-outs achieved HVPG <10 mm Hg by SVR 96, the resulting cumulative rate of CSPH would have jumped to 65 percent.
Multivariate Cox regression analysis was then performed to determine significant predictors of clinical decompensation. As expected, high HVPG emerged as a significant risk factor (≥16 mm Hg: hazard ratio [HR], 6.3, 95 percent confidence interval [CI], 1.4–28; p<0.01), as did having a history of ascites (HR, 7.7, 95 percent CI, 2.4–24; p<0.01).