The natural history of patients with compensated cirrhosis and elevated hepatic venous pressure gradient

Portal hypertension is a major complication of liver cirrhosis. Hepatic venous pressure gradient (HVPG) appears to be one of the best surrogates of clinical outcomes. However, the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear.We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, non-bleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepato-pulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement.Patients with high HVPG without evidence of clinical decompensation had significantly lower model for end stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, P = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow-up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 mmHg and 18 mmHg, respectively) differentiated patients who remained compensated vs. those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 g/dL vs. 2.6 g/dL, respectively, P = 0.05).A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long term follow-up.