Association of left ventricular diastolic dysfunction with inflammatory activity, renal dysfunction, and liver-related mortality in patients with cirrhosis and ascites.


Journal

European journal of gastroenterology & hepatology
ISSN: 1473-5687
Titre abrégé: Eur J Gastroenterol Hepatol
Pays: England
ID NLM: 9000874

Informations de publication

Date de publication:
19 Mar 2024
Historique:
medline: 25 3 2024
pubmed: 25 3 2024
entrez: 25 3 2024
Statut: aheadofprint

Résumé

Left ventricular diastolic dysfunction (LVDD) is the predominant cardiac abnormality in cirrhosis. We investigated the association of LVDD with systemic inflammation and its impact on renal function, occurrence of hepatorenal syndrome (HRS) and survival in patients with cirrhosis and ascites. We prospectively enrolled 215 patients with cirrhosis and ascites. We evaluated the diagnosis and grading of LVDD by Doppler echocardiography, inflammatory markers, systemic hemodynamics, vasoactive factors, radioisotope-assessed renal function and blood flow, HRS development and liver-related mortality. LVDD was diagnosed in 142 (66%) patients [grade 2/3: n = 61 (43%)]. Serum lipopolysaccharide-binding protein (LBP), plasma renin activity (PRA) and glomerular filtration rate (GFR) were independently associated with the presence of grade 2/3 LVDD and the severity of diastolic dysfunction. Serum tumor necrosis factor-α, cardiac output and plasma noradrenaline were also independently associated with the presence of grade 2/3 LVDD. The diastolic function marker E/e' was strongly correlated with serum LBP (r = 0.731; P < 0.001), PRA (r = 0.714; P < 0.001) and GFR (r = -0.609; P < 0.001) among patients with LVDD. The 5-year risk of HRS development and death was significantly higher in patients with grade 2/3 LVDD compared to those with grade 1 (35.5 vs. 14.4%; P = 0.01 and 53.3 vs. 28.2%; P = 0.03, respectively). The occurrence and severity of LVDD in patients with cirrhosis and ascites is closely related to inflammatory activity. Advanced LVDD is associated with baseline circulatory and renal dysfunction, favoring HRS development, and increased mortality.

Identifiants

pubmed: 38526935
doi: 10.1097/MEG.0000000000002762
pii: 00042737-990000000-00332
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.

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Auteurs

Georgios Kalambokis (G)

First Division of Internal Medicine.

Maria Christaki (M)

First Division of Internal Medicine.

Ilias Tsiakas (I)

First Division of Internal Medicine.

Grigorios Despotis (G)

First Division of Internal Medicine.

Lampros Lakkas (L)

Second Department of Cardiology.

Spiridon Tsiouris (S)

Laboratory of Nuclear Medicine.

Xanthi Xourgia (X)

Laboratory of Nuclear Medicine.

Georgios S Markopoulos (GS)

Hematology Laboratory, Unit of Molecular Biology and Translational Flow Cytometry, Medical School, University of Ioannina, Ioannina, Greece.

Lefkothea Dova (L)

Hematology Laboratory, Unit of Molecular Biology and Translational Flow Cytometry, Medical School, University of Ioannina, Ioannina, Greece.

Haralampos Milionis (H)

First Division of Internal Medicine.

Classifications MeSH