Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306)
- Author:
Chuan LIU
1
;
Hong YOU
;
Qing-Lei ZENG
;
Yu Jun WONG
;
Bingqiong WANG
;
Ivica GRGUREVIC
;
Chenghai LIU
;
Hyung Joon YIM
;
Wei GOU
;
Bingtian DONG
;
Shenghong JU
;
Yanan GUO
;
Qian YU
;
Masashi HIROOKA
;
Hirayuki ENOMOTO
;
Amr Shaaban HANAFY
;
Zhujun CAO
;
Xiemin DONG
;
Jing LV
;
Tae Hyung KIM
;
Yohei KOIZUMI
;
Yoichi HIASA
;
Takashi NISHIMURA
;
Hiroko IIJIMA
;
Chuanjun XU
;
Erhei DAI
;
Xiaoling LAN
;
Changxiang LAI
;
Shirong LIU
;
Fang WANG
;
Ying GUO
;
Jiaojian LV
;
Liting ZHANG
;
Yuqing WANG
;
Qing XIE
;
Chuxiao SHAO
;
Zhensheng LIU
;
Federico RAVAIOLI
;
Antonio COLECCHIA
;
Jie LI
;
Gao-Jun TENG
;
Xiaolong QI
Author Information
- Publication Type:Original Article
- From:Clinical and Molecular Hepatology 2025;31(1):105-118
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model.
Methods:Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort.
Results:In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM).
Conclusions:Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.