The prognostic role of galectin-3 and endothelial function in patients with heart failure.

ejection fraction endothelial function galectin-3 heart failure prognosis

Journal

Cardiology journal
ISSN: 1898-018X
Titre abrégé: Cardiol J
Pays: Poland
ID NLM: 101392712

Informations de publication

Date de publication:
2023
Historique:
received: 01 02 2022
accepted: 06 05 2022
revised: 12 04 2022
medline: 8 11 2023
pubmed: 18 8 2022
entrez: 17 8 2022
Statut: ppublish

Résumé

Heart failure (HF) is nowadays classified as HF with reduced ejection fraction (HFrEF), HF with mildly reduced EF (HFmrEF), and HF with preserved EF (HFpEF). Endothelial dysfunction (assessed by flow-mediated dilatation [FMD]), increased arterial stiffness (assessed by carotid-femoral pulse-wave velocity [PWV]), and galectin-3, a biomarker of myocardial fibrosis, have been linked to major adverse cardiovascular events (MACE) in patients with ischemic HF. In this study we prospectively enrolled 340 patients with stable ischemic HF. We assessed the brachial artery FMD, carotid-femoral PWV, and galectin-3 levels, and patients were followed up for MACE according to HF group. Interestingly, the FMD values exhibited a stepwise improvement according to left ventricular ejection fraction (LVEF) (HFrEF: 4.74 ± 2.35% vs. HFmrEF: 4.97 ± 2.81% vs. HFpEF: 5.94 ± ± 3.46%, p = 0.01), which remained significant after the evaluation of possible confounders including age, sex, cardiovascular risk factors, and number of significantly stenosed epicardial coronary arteries (b coefficient: 0.990, 95% confidence interval: 0.166-1.814, p = 0.019). Single-vessel coronary artery disease was more frequent in the group of HFpEF (HFrEF: 56% vs. HFmrEF: 64% vs. HFpEF: 73%, p = 0.049). PWV did not display any association with LVEF. Patients who presented MACE exhibited worse FMD values (4.51 ± 2.35% vs. 5.32 ± 2.67%, p = 0.02), and the highest tertile of galectin-3 was linked to more MACEs (36% vs. 5.9%, p = 0.01). Flow-mediated dilatation displayed a linear improvement with LVEF in patients with ischemic HF. Deteriorated values are associated with MACE. Higher levels of galectin-3 might be used for risk stratification of patients with ischemic HF.

Sections du résumé

BACKGROUND
Heart failure (HF) is nowadays classified as HF with reduced ejection fraction (HFrEF), HF with mildly reduced EF (HFmrEF), and HF with preserved EF (HFpEF). Endothelial dysfunction (assessed by flow-mediated dilatation [FMD]), increased arterial stiffness (assessed by carotid-femoral pulse-wave velocity [PWV]), and galectin-3, a biomarker of myocardial fibrosis, have been linked to major adverse cardiovascular events (MACE) in patients with ischemic HF.
METHODS
In this study we prospectively enrolled 340 patients with stable ischemic HF. We assessed the brachial artery FMD, carotid-femoral PWV, and galectin-3 levels, and patients were followed up for MACE according to HF group.
RESULTS
Interestingly, the FMD values exhibited a stepwise improvement according to left ventricular ejection fraction (LVEF) (HFrEF: 4.74 ± 2.35% vs. HFmrEF: 4.97 ± 2.81% vs. HFpEF: 5.94 ± ± 3.46%, p = 0.01), which remained significant after the evaluation of possible confounders including age, sex, cardiovascular risk factors, and number of significantly stenosed epicardial coronary arteries (b coefficient: 0.990, 95% confidence interval: 0.166-1.814, p = 0.019). Single-vessel coronary artery disease was more frequent in the group of HFpEF (HFrEF: 56% vs. HFmrEF: 64% vs. HFpEF: 73%, p = 0.049). PWV did not display any association with LVEF. Patients who presented MACE exhibited worse FMD values (4.51 ± 2.35% vs. 5.32 ± 2.67%, p = 0.02), and the highest tertile of galectin-3 was linked to more MACEs (36% vs. 5.9%, p = 0.01).
CONCLUSIONS
Flow-mediated dilatation displayed a linear improvement with LVEF in patients with ischemic HF. Deteriorated values are associated with MACE. Higher levels of galectin-3 might be used for risk stratification of patients with ischemic HF.

Identifiants

pubmed: 35975796
pii: VM/OJS/J/88256
doi: 10.5603/CJ.a2022.0074
pmc: PMC10635724
doi:

Substances chimiques

Galectin 3 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

725-733

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Auteurs

Vasiliki Tsigkou (V)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Gerasimos Siasos (G)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.

Evangelos Oikonomou (E)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece. boikono@gmail.com.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece. boikono@gmail.com.

Marina Zaromitidou (M)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Konstantinos Mourouzis (K)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Stathis Dimitropoulos (S)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Evanthia Bletsa (E)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Nikolaos Gouliopoulos (N)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Panagiota K Stampouloglou (PK)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Maria-Evi Panoilia (ME)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Georgios Marinos (G)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Konstantinos Tsioufis (K)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Manolis Vavuranakis (M)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Department of Cardiology, 'Sotiria' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Dimitris Tousoulis (D)

Department of Cardiology, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

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