Intestinal fatty acid binding protein is associated with infarct size and cardiac function in acute heart failure following myocardial infarction.
Humans
Male
Fatty Acid-Binding Proteins
/ blood
Female
Heart Failure
/ physiopathology
Middle Aged
Biomarkers
/ blood
Aged
Ventricular Function, Left
/ physiology
Percutaneous Coronary Intervention
/ methods
ST Elevation Myocardial Infarction
/ physiopathology
Stroke Volume
/ physiology
Tomography, Emission-Computed, Single-Photon
Carrier Proteins
/ blood
Echocardiography
/ methods
Acute-Phase Proteins
Membrane Glycoproteins
/ blood
Time Factors
Lipopolysaccharide Receptors
/ blood
Acute Disease
Prospective Studies
Lipopolysaccharides
Ventricular Remodeling
/ physiology
Biomarkers
Heart Failure
Inflammation
Myocardial Infarction
Journal
Open heart
ISSN: 2053-3624
Titre abrégé: Open Heart
Pays: England
ID NLM: 101631219
Informations de publication
Date de publication:
13 Sep 2024
13 Sep 2024
Historique:
received:
29
07
2024
accepted:
24
08
2024
medline:
15
9
2024
pubmed:
15
9
2024
entrez:
14
9
2024
Statut:
epublish
Résumé
In acute heart failure (HF), reduced cardiac output, vasoconstriction and congestion may damage the intestinal mucosa and disrupt its barrier function. This could facilitate the leakage of bacterial products into circulation and contribute to inflammation and adverse cardiac remodelling. We aimed to investigate gut leakage markers and their associations with inflammation, infarct size and cardiac function. We examined 61 ST-elevation myocardial infarction (STEMI) patients who developed acute HF within 48 hours of successful percutaneous coronary intervention (PCI). Serial blood samples were taken to measure lipopolysaccharide (LPS), LPS-binding protein (LBP), soluble cluster of differentiation 14 (sCD14) and intestinal fatty acid binding protein (I-FABP). Cumulative areas under the curve (AUCs) from baseline to day 5 were calculated. Serial echocardiography was performed to assess left ventricular ejection fraction (LVEF), global longitudinal strain (GLS) and wall motion score index (WMSI). Single-photon emission CT (SPECT) was performed at 6 weeks to determine infarct size and LVEF. I-FABP In primary PCI-treated STEMI patients with acute HF, I-FABP, a marker of intestinal epithelial damage, was associated with larger infarct size and worse cardiac function after 6 weeks.
Sections du résumé
BACKGROUND
BACKGROUND
In acute heart failure (HF), reduced cardiac output, vasoconstriction and congestion may damage the intestinal mucosa and disrupt its barrier function. This could facilitate the leakage of bacterial products into circulation and contribute to inflammation and adverse cardiac remodelling. We aimed to investigate gut leakage markers and their associations with inflammation, infarct size and cardiac function.
METHODS
METHODS
We examined 61 ST-elevation myocardial infarction (STEMI) patients who developed acute HF within 48 hours of successful percutaneous coronary intervention (PCI). Serial blood samples were taken to measure lipopolysaccharide (LPS), LPS-binding protein (LBP), soluble cluster of differentiation 14 (sCD14) and intestinal fatty acid binding protein (I-FABP). Cumulative areas under the curve (AUCs) from baseline to day 5 were calculated. Serial echocardiography was performed to assess left ventricular ejection fraction (LVEF), global longitudinal strain (GLS) and wall motion score index (WMSI). Single-photon emission CT (SPECT) was performed at 6 weeks to determine infarct size and LVEF.
RESULTS
RESULTS
I-FABP
CONCLUSIONS
CONCLUSIONS
In primary PCI-treated STEMI patients with acute HF, I-FABP, a marker of intestinal epithelial damage, was associated with larger infarct size and worse cardiac function after 6 weeks.
Identifiants
pubmed: 39277188
pii: openhrt-2024-002868
doi: 10.1136/openhrt-2024-002868
pii:
doi:
Substances chimiques
Fatty Acid-Binding Proteins
0
Biomarkers
0
lipopolysaccharide-binding protein
0
FABP2 protein, human
0
Carrier Proteins
0
Acute-Phase Proteins
0
Membrane Glycoproteins
0
CD14 protein, human
0
Lipopolysaccharide Receptors
0
Lipopolysaccharides
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: The Department of Cardiology, Oslo University Hospital Ullevaal received an unrestricted educational grant from the manufacturer of levosimendan, Orion Pharma in 2005. Orion Pharma did not, however, provide study medication or participate in the design, monitoring or analyses of the present study. The authors declare no conflict of interest.