Liver stiffness as a prognostic parameter and tool for risk stratification in advanced cardiac transthyretin amyloidosis.

Cardiac amyloidosis GLS Liver stiffness NT-proBNP Transthyretin (ATTR) amyloidosis

Journal

Clinical research in cardiology : official journal of the German Cardiac Society
ISSN: 1861-0692
Titre abrégé: Clin Res Cardiol
Pays: Germany
ID NLM: 101264123

Informations de publication

Date de publication:
20 Aug 2024
Historique:
received: 05 12 2023
accepted: 01 08 2024
medline: 21 8 2024
pubmed: 21 8 2024
entrez: 20 8 2024
Statut: aheadofprint

Résumé

In light of increasing therapeutic options, risk stratification of advanced cardiac transthyretin amyloidosis (ATTR-CA) is gaining clinical importance to avoid ineffective treatments. Liver stiffness as a marker of hypervolemia and hepatic congestion might predict mortality in advanced ATTR-CA and allow to identify patients at highest risk. Proven ATTR-CA patients underwent repeated vibration-controlled transient elastography (VTCE) and standardized serial workup within the local amyloidosis cohort study AmyKoS. Spearman correlation analyses and Cox regressions were performed to evaluate the prognostic value. 41 patients with ATTR-CA were included with median age of 76.6 (55.1-89.1) years, of which 90.2% were male and > 92% wild-type ATTR-CA. In total, 85 VCTE examinations were performed. Median follow-up was 43.7 (2.4-75.6) months; 26.8% of the patients died. At the first clinical evaluation, median left ventricular (LV) absolute global longitudinal strain (GLS) was 11.4 (5.2-19.0) % and median liver stiffness was 6.3 (2.4-22.9) kPa, both significantly correlated with mortality. NT-proBNP possessed statistically significant predictive power in ATTR-CA with more preserved LV function (absolute GLS ≥ 10), whereas stiffness seemed to be more discriminative for ATTR-CA with absolute GLS < 10. The use of alternative congestion surrogates such as liver vein dilation and tricuspid regurgitation peak velocity (tr-v Liver stiffness shows prognostic value regarding all-cause mortality and allows risk stratification in advanced ATTR-CA, particularly in those with markedly impaired longitudinal LV function. These results are transferable to other congestion surrogates.

Sections du résumé

BACKGROUND BACKGROUND
In light of increasing therapeutic options, risk stratification of advanced cardiac transthyretin amyloidosis (ATTR-CA) is gaining clinical importance to avoid ineffective treatments. Liver stiffness as a marker of hypervolemia and hepatic congestion might predict mortality in advanced ATTR-CA and allow to identify patients at highest risk.
METHODS METHODS
Proven ATTR-CA patients underwent repeated vibration-controlled transient elastography (VTCE) and standardized serial workup within the local amyloidosis cohort study AmyKoS. Spearman correlation analyses and Cox regressions were performed to evaluate the prognostic value.
RESULTS RESULTS
41 patients with ATTR-CA were included with median age of 76.6 (55.1-89.1) years, of which 90.2% were male and > 92% wild-type ATTR-CA. In total, 85 VCTE examinations were performed. Median follow-up was 43.7 (2.4-75.6) months; 26.8% of the patients died. At the first clinical evaluation, median left ventricular (LV) absolute global longitudinal strain (GLS) was 11.4 (5.2-19.0) % and median liver stiffness was 6.3 (2.4-22.9) kPa, both significantly correlated with mortality. NT-proBNP possessed statistically significant predictive power in ATTR-CA with more preserved LV function (absolute GLS ≥ 10), whereas stiffness seemed to be more discriminative for ATTR-CA with absolute GLS < 10. The use of alternative congestion surrogates such as liver vein dilation and tricuspid regurgitation peak velocity (tr-v
CONCLUSION CONCLUSIONS
Liver stiffness shows prognostic value regarding all-cause mortality and allows risk stratification in advanced ATTR-CA, particularly in those with markedly impaired longitudinal LV function. These results are transferable to other congestion surrogates.

Identifiants

pubmed: 39164508
doi: 10.1007/s00392-024-02513-3
pii: 10.1007/s00392-024-02513-3
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Interdisziplinäres Zentrum für Klinische Forschung, Universitätsklinikum Würzburg
ID : Z-2_CSP-08

Informations de copyright

© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Sandra Michaela Ihne-Schubert (SM)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany. ihne_s@ukw.de.
Department of Internal Medicine II, Hematology, University Hospital of Würzburg, Würzburg, Germany. ihne_s@ukw.de.
Department of Internal Medicine IV, University Hospital of Gießen and Marburg, Gießen, Germany. ihne_s@ukw.de.
CIRCLE-Centre for Innovation Research, Lund University, Lund, Sweden. ihne_s@ukw.de.

Caroline Morbach (C)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Comprehensive Heart Failure Center, University and University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, Cardiology, University Hospital of Würzburg, Würzburg, Germany.

Oliver Goetze (O)

Department of Internal Medicine II, Hepatology, University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine, University Hospital Knappschaftskrankenhaus Bochum GmbH, Bochum, Germany.

Vladimir Cejka (V)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Comprehensive Heart Failure Center, University and University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, Cardiology, University Hospital of Würzburg, Würzburg, Germany.

Maximilian Johannes Steinhardt (MJ)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine II, Hematology, University Hospital of Würzburg, Würzburg, Germany.

Stefan Frantz (S)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Comprehensive Heart Failure Center, University and University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, Cardiology, University Hospital of Würzburg, Würzburg, Germany.

Hermann Einsele (H)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine II, Hematology, University Hospital of Würzburg, Würzburg, Germany.

Claudia Sommer (C)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Department of Neurology, University Hospital of Würzburg, Würzburg, Germany.

Stefan Störk (S)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Comprehensive Heart Failure Center, University and University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, Cardiology, University Hospital of Würzburg, Würzburg, Germany.

Torben Schubert (T)

CIRCLE-Centre for Innovation Research, Lund University, Lund, Sweden.
Fraunhofer Institute for Systems and Innovation Research ISI, Karlsruhe, Germany.
Department of Design Science (LTH), Lund University, Lund, Sweden.

Andreas Geier (A)

Interdisciplinary Amyloidosis Center of Northern Bavaria, University Hospital of Würzburg, Würzburg, Germany.
Department of Internal Medicine II, Hepatology, University Hospital of Würzburg, Würzburg, Germany.

Classifications MeSH