Influence of further decompensation on survival across clinical stages of decompensated cirrhosis: The role of portal hypertension and HVPG changes

Marta Garcia-Guix; Alba Ardevol; Victor Sapena; Edilmar Alvarado-Tápias; Anna Huertas; Anna Brujats; Javier Fajardo; Berta Cuyas; María Poca; Carlos Guarner; Xavier Torras; Àngels Escorsell; Càndid Villanueva

doi:10.1111/liv.15937

Influence of further decompensation on survival across clinical stages of decompensated cirrhosis: The role of portal hypertension and HVPG changes

Liver Int. 2024 Apr 18. doi: 10.1111/liv.15937. Online ahead of print.

Authors

Marta Garcia-Guix^{1

2}, Alba Ardevol¹, Victor Sapena^{3

4}, Edilmar Alvarado-Tápias^{1

2}, Anna Huertas¹, Anna Brujats^{1

2}, Javier Fajardo¹, Berta Cuyas^{1

2}, María Poca^{1

2}, Carlos Guarner^{1

2}, Xavier Torras^{1

2}, Àngels Escorsell^{1

2}, Càndid Villanueva^{1

2}

Affiliations

¹ Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau (IIB Sant Pau), Universitat Autònoma de Barcelona, Barcelona, Spain.
² Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.
³ Biostatistics Unit, Medical School, Universitat Autònoma de Barcelona, Barcelona, Spain.
⁴ Medical Statistics Core Faculty, IDIBAPS, Hospital Clinic, Barcelona, Spain.

PMID: 38634685
DOI: 10.1111/liv.15937

Abstract

Background and aims: Decompensated-cirrhosis encompasses several stages with different prognosis, such as bleeding, ascites and bleeding-plus-ascites. Development of further-decompensation worsens survival, while non-selective β-blockers (NSBBs) can modify the risk. However, how this applies to each stage is uncertain. We aimed to investigate, in each stage of decompensated-cirrhosis, the influence of further-decompensation on mortality and whether changes in portal-pressure (HVPG) under NSBBs influence these outcomes.

Methods: Patients with variceal bleeding were consecutively included differentiating those with bleeding-alone from those who also had ascites. Patients with ascites and high-risk varices referred for primary-prophylaxis were also investigated. A baseline haemodynamic study was performed and was repeated after 1-3-months under NSBBs. Outcomes were investigated by competing-risk.

Results: Totally 103 patients had bleeding-alone, 186 bleeding-plus-ascites and 187 ascites-alone. Mean follow-up was 32-months (IQR, 12-60). Patients with bleeding-plus-ascites had higher HVPG and were more hyperdynamic than patients with ascites-alone and these than those with bleeding-alone. At each stage, the mortality risk was more than twice in patients developing further-decompensation vs. those without (p < .001). In each stage, HVPG-decrease under NSBBs showed better discrimination to predict further-decompensation than the baseline MELD, Child-Pugh or HVPG, by time-dependent ROC-curves (c-statistic >70%). At each stage, patients without HVPG-decreases, either ≥10% or ≥20% from the baseline, had higher risk of further-decompensation (sHR from 2.43 to 6.73, p < .01) and worse survival.

Conclusions: In each stage of decompensated cirrhosis, mortality risk significantly and very markedly increase with further-decompensation. HVPG-non-response to NSBBs may adequately stratify the risk of further decompensation and death, in each stage. This suggests potential benefit with pre-emptive therapies in HVPG-non-responders at each-stage.

Keywords: HVPG‐changes; clinical stages; decompensated‐cirrhosis; further‐decompensation.