Abstract

A hepatic venous pressure gradient (HVPG) decrease of 20% or more (or ≤12mmHg) indicates a good prognosis during propranolol/nadolol treatment but requires two HVPG measurements. We aimed to simplify the risk stratification after variceal bleeding using clinical data and HVPG. A total of 193 patients with cirrhosis (62% with ascites and/or hepatic encephalopathy [HE]) who were within 7 days of bleeding had their HVPG measured before and at 1-3months of treatment with propranolol/nadolol plus endoscopic band ligation. The endpoints were rebleeding and rebleeding/transplantation-free survival for 4 years. Another cohort (n=231) served as the validation set. During follow-up, 45 patients had variceal bleeding and 61 died. The HVPG responders (n=71) had lower rebleeding risk (10% vs. 34%, P=0.001) and better survival than the 122 nonresponders (61% vs. 39%, P=0.001). Patients with HE (n=120) had lower survival than patients without HE (40% vs. 63%, P=0.005). Among the patients with ascites/HE, those with baseline HVPG≤16mmHg (n=16) had a low rebleeding risk (13%). In contrast, among patients with ascites/HE and baseline HVPG>16mmHg, only the HVPG responders (n=32) had a good prognosis, with lower rebleeding risk and better survival than the nonresponders (n=72) (respective proportions: 7% vs. 39%, P=0.018; 56% vs. 30% P=0.010). These findings allowed us to develop a strategy for risk stratification in which HVPG response was measured only in patients with ascites and/or HE and baseline HVPG>16mmHg. This method reduced the "gray zone" (i.e., high-risk patients who had not died on follow-up) from 46% to 35% and decreased the HVPG measurements required by 42%. The validation cohort confirmed these results. Restricting HVPG measurements to patients with ascites/HE and measuring HVPG response only if the patient's baseline HVPG is over 16mmHg improves detection of high-risk patients while markedly reducing the number of HVPG measurements required.

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