Clinical and Molecular Hepatology (Jan 2025)

Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306)

  • Chuan Liu,
  • 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

DOI
https://doi.org/10.3350/cmh.2024.0198
Journal volume & issue
Vol. 31, no. 1
pp. 105 – 118

Abstract

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Background/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 (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.

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