Long-term continuous terlipressin infusion improves cardiac reserve in patients with decompensated cirrhosis.

cardiac function cardiomyopathy cirrhosis portal hypertension terlipressin

Journal

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775

Informations de publication

Date de publication:
27 Aug 2024
Historique:
received: 24 06 2024
revised: 06 08 2024
accepted: 13 08 2024
medline: 31 8 2024
pubmed: 31 8 2024
entrez: 29 8 2024
Statut: aheadofprint

Résumé

Cardiac dysfunction is a key factor in the pathogenesis of hepatorenal syndrome, for which terlipressin is the recommended first-line treatment. This study investigates whether long-term terlipressin can ameliorate the subclinical cardiac dysfunction observed in decompensated cirrhosis. Twenty-two patients with decompensated cirrhosis and ascites enrolled in a prospective study of home continuous terlipressin infusion were included. Cardiac function was assessed using dobutamine stress echocardiogram before and after 12 weeks of terlipressin. The primary outcome was the impact of terlipressin on cardiac reserve; the change in cardiac output (CO) in response to stress. Median age was 61 years (IQR 56-64), median MELD score was 15 (IQR 12.3-17.0) and 72.7% were male. The increase in CO in response to low-dose dobutamine was significantly higher following terlipressin (↑4.0L/min [↑57.8%]) as compared to baseline (↑1.8L/min [21.3%], p=0.0001). The proportion of patients with impaired cardiac reserve (defined by ΔCO <25% after low-dose dobutamine) reduced from 81.8% at baseline to 40.9% after terlipressin, (p=0.02), driven primarily by improvement in inotropic function. Resting cardiac output (CO) decreased significantly after terlipressin from 8.9±2.2L/min to 7.2±1.8 L/min (p<0.001, normal range 5-6L/min), due to a decrease in stroke volume from 108 to 86mL/beat (p=0.006). Long-term continuous terlipressin infusion resulted in a significant increase in cardiac reserve and attenuation of the hyperdynamic state usually observed in decompensated cirrhosis. These data provide important mechanistic insight into the pathogenesis and reversibility of cardiac dysfunction in cirrhosis. Future studies are required to evaluate whether long-term terlipressin can prevent hepatic decompensating events such as hepatorenal syndrome in high-risk individuals. ANZCTR NUMBER: (http://www.anzctr.org.au/): ACTRN12619000891123.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Cardiac dysfunction is a key factor in the pathogenesis of hepatorenal syndrome, for which terlipressin is the recommended first-line treatment. This study investigates whether long-term terlipressin can ameliorate the subclinical cardiac dysfunction observed in decompensated cirrhosis.
METHODS METHODS
Twenty-two patients with decompensated cirrhosis and ascites enrolled in a prospective study of home continuous terlipressin infusion were included. Cardiac function was assessed using dobutamine stress echocardiogram before and after 12 weeks of terlipressin. The primary outcome was the impact of terlipressin on cardiac reserve; the change in cardiac output (CO) in response to stress.
RESULTS RESULTS
Median age was 61 years (IQR 56-64), median MELD score was 15 (IQR 12.3-17.0) and 72.7% were male. The increase in CO in response to low-dose dobutamine was significantly higher following terlipressin (↑4.0L/min [↑57.8%]) as compared to baseline (↑1.8L/min [21.3%], p=0.0001). The proportion of patients with impaired cardiac reserve (defined by ΔCO <25% after low-dose dobutamine) reduced from 81.8% at baseline to 40.9% after terlipressin, (p=0.02), driven primarily by improvement in inotropic function. Resting cardiac output (CO) decreased significantly after terlipressin from 8.9±2.2L/min to 7.2±1.8 L/min (p<0.001, normal range 5-6L/min), due to a decrease in stroke volume from 108 to 86mL/beat (p=0.006).
CONCLUSION CONCLUSIONS
Long-term continuous terlipressin infusion resulted in a significant increase in cardiac reserve and attenuation of the hyperdynamic state usually observed in decompensated cirrhosis. These data provide important mechanistic insight into the pathogenesis and reversibility of cardiac dysfunction in cirrhosis. Future studies are required to evaluate whether long-term terlipressin can prevent hepatic decompensating events such as hepatorenal syndrome in high-risk individuals. ANZCTR NUMBER: (http://www.anzctr.org.au/): ACTRN12619000891123.

Identifiants

pubmed: 39209185
pii: S1542-3565(24)00778-X
doi: 10.1016/j.cgh.2024.08.010
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

Ryma Terbah (R)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM).

Anoop N Koshy (AN)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM); Department of Cardiology, Austin Health, Heidelberg, Victoria, Australia.

Avik Majumdar (A)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM).

Karl Vaz (K)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM).

Adam Testro (A)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM).

Marie Sinclair (M)

The University of Melbourne, Victoria, Australia; Victorian Liver Transplant Unit, Austin Health, Heidelberg, Victoria, Australia; The Australian Centre for Transplantation Excellence and Research (ACTER); Australian Cardiovascular Collaborative in Liver Transplant Medicine (ACCLAIM). Electronic address: marie.sinclair@austin.org.au.

Classifications MeSH