Journal Article

Clinical Decompensation and Outcomes in Patients With Compensated Cirrhosis and a Hepatic Venous Pressure Gradient ≥20 mm Hg

Sarin, Shiv Kumar, Jindal, Ankur, Kumar, Guresh, Bhardwaj, Ankit

2020

Overview

Hepatic venous pressure gradient (HVPG) of ≥10 mm Hg predicts clinical decompensation (CD) in compensated cirrhosis. A proportion of cirrhotic patients at presentation have high HVPG (≥20 mm Hg) and are compensated. The natural history, spectrum of CD, and mortality in this group is largely unknown. Consecutive compensated cirrhotic patients with HVPG ≥6 mm Hg (n = 741) were followed up for 3-6 months for the development of any CD. Patients were classified based on the baseline HVPG (6 to <12 mm Hg [low HVPG, Gr.A, n = 163], 12 to <20 mm Hg [intermediate HVPG, Gr.B, n = 437] and ≥20 mm Hg [high HVPG, Gr.C, n = 141]). We analyzed the predictors of first CD, HVPG response to carvedilol, and mortality in these groups. CD developed in 217 (29.3%) patients during a mean follow-up of 1.6 ± 0.4 years, and those who developed CD had higher baseline HVPG (17.02 ± 4.79 vs 14.28 ± 4.86; P < 0.001). First CD was seen earlier (1.3 ± 0.7 years vs 1.5 ± 0.6 years and 1.6 ± 0.5 years, P = 0.02) and more frequently (44.7% vs 11% and 31.1%, P < 0.01) in high HVPG groups compared with low and intermediate HVPG groups, with higher mortality rates. Patients in the high HVPG group compared with the low HVPG group more often had NASH-cirrhosis (35.5% vs 19.6%; P 0.001), higher liver stiffness values (45.06 ± 20.46 vs 20.09 ± 5.47 kPa, P < 0.001), and lower platelet counts (113.37 ± 72.57 vs 151.7 ± 87.30/cmm, P < 0.001). Patients with HVPG ≥12 mm Hg received carvedilol, and a repeat HVPG performed in a proportion after 9.3 ± 2.4 months showed response (≥20% reduction in HVPG or <12 mm Hg) in 31.6% patients (Gr. B, 44.9% > Gr. C, 22.2%, P < 0.05). Baseline HVPG (HVPG ≥12 to <20 mm Hg [Hazard ratio: 2.73] and HVPG ≥20 mm Hg [Hazard ratio: 4.48], P < 0.001) independently predicted CD. HVPG ≥20 mm Hg in patients with compensated cirrhosis independently predicts early and more frequent CD and poor outcomes. These patients should be labeled as \"high-risk compensated cirrhosis,\" and early and effective interventions to reduce portal pressure should be initiated to improve long-term outcomes.

• Publisher: Wolters Kluwer,Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
• Subject: Adult / Ascites / Beta blockers / Carcinoma, Hepatocellular - epidemiology / Carcinoma, Hepatocellular - etiology / Catheterization, Peripheral / Catheters / Drug dosages / End Stage Liver Disease / Endoscopy / Esophageal and Gastric Varices - epidemiology / Esophageal and Gastric Varices - etiology / Esophagus / Female / Gastroenterology / Gastrointestinal Hemorrhage - epidemiology / Hepatic Encephalopathy - epidemiology / Hepatic Encephalopathy - etiology / Hepatic Veins / Hepatitis / Humans / Hypertension / Hypertension, Portal - complications / Hypertension, Portal - physiopathology / Hypotension / Jaundice - epidemiology / Jaundice - etiology / Kidneys / Liver cirrhosis / Liver Cirrhosis - complications / Liver Cirrhosis - physiopathology / Liver diseases / Liver Neoplasms - epidemiology / Liver Neoplasms - etiology / Male / Middle Aged / Mortality / Prognosis / Retrospective Studies / Severity of Illness Index / Venous Pressure