CILP-1 Is a Biomarker for Backward Failure and Right Ventricular Dysfunction in HFrEF.

CILP1 fibrosis heart failure right heart

Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
13 Dec 2023
Historique:
received: 30 10 2023
revised: 30 11 2023
accepted: 06 12 2023
medline: 22 12 2023
pubmed: 22 12 2023
entrez: 22 12 2023
Statut: epublish

Résumé

CILP-1 regulates myocardial fibrotic response and remodeling and was reported to indicate right ventricular dysfunction (RVD) in pulmonary hypertension (PH) and heart failure (HF). This study examines CILP-1 as a potential biomarker for RVD and prognosis in heart failure with reduced ejection fraction (HFrEF) patients on guideline-directed medical therapy. CILP-1 levels were measured in 610 HFrEF patients from a prospective registry with biobanking (2016-2022). Correlations with echocardiographic and hemodynamic data and its association with RVD and prognosis were analyzed. The median age was 62 years (Q1-Q3: 52-72), 77.7% of patients were male, and the median NT-proBNP was 1810 pg/mL (Q1-Q3: 712-3962). CILP-1 levels increased with HF severity, as indicated by NT-proBNP and NYHA class ( CILP-1 correlates with HFrEF severity and may indicate an elevated risk for all-cause mortality, though it is not independent from NT-proBNP. Increased CILP-1 is associated with backward failure and RVD rather than forward failure. Whether CILP-1 release in this context is based on elevated pulmonary pressures or is specific to RVD needs to be further investigated.

Sections du résumé

BACKGROUND BACKGROUND
CILP-1 regulates myocardial fibrotic response and remodeling and was reported to indicate right ventricular dysfunction (RVD) in pulmonary hypertension (PH) and heart failure (HF). This study examines CILP-1 as a potential biomarker for RVD and prognosis in heart failure with reduced ejection fraction (HFrEF) patients on guideline-directed medical therapy.
METHODS METHODS
CILP-1 levels were measured in 610 HFrEF patients from a prospective registry with biobanking (2016-2022). Correlations with echocardiographic and hemodynamic data and its association with RVD and prognosis were analyzed.
RESULTS RESULTS
The median age was 62 years (Q1-Q3: 52-72), 77.7% of patients were male, and the median NT-proBNP was 1810 pg/mL (Q1-Q3: 712-3962). CILP-1 levels increased with HF severity, as indicated by NT-proBNP and NYHA class (
CONCLUSIONS CONCLUSIONS
CILP-1 correlates with HFrEF severity and may indicate an elevated risk for all-cause mortality, though it is not independent from NT-proBNP. Increased CILP-1 is associated with backward failure and RVD rather than forward failure. Whether CILP-1 release in this context is based on elevated pulmonary pressures or is specific to RVD needs to be further investigated.

Identifiants

pubmed: 38132152
pii: cells12242832
doi: 10.3390/cells12242832
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : FWF Austrian Science Fund
ID : KLI 700-B30

Auteurs

Annika Weidenhammer (A)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Suriya Prausmüller (S)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Clemens Partsch (C)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Georg Spinka (G)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Bianca Luckerbauer (B)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Mirella Larch (M)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Henrike Arfsten (H)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Ramy Abdel Mawgoud (R)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Philipp E Bartko (PE)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Georg Goliasch (G)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Stefan Kastl (S)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Christian Hengstenberg (C)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Martin Hülsmann (M)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Noemi Pavo (N)

Department of Internal Medicine II, Clinical Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.

Classifications MeSH