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The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis

FUNDING ACKNOWLEDGEMENTS: Type of funding sources: None. INTRODUCTION: Atrial fibrosis is increasingly considered an important part of vulnerable substrates, with an essential function in the induction of left atrial (LA) conduction abnormalities underlying the transition from paroxysmal (PAF) to pe...

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Autores principales: Katic, J, Sikirc, I, Breskovic, T, Jurisic, Z, Borovac, J A, Anic, A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206811/
http://dx.doi.org/10.1093/europace/euad122.062
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author Katic, J
Sikirc, I
Breskovic, T
Jurisic, Z
Borovac, J A
Anic, A
author_facet Katic, J
Sikirc, I
Breskovic, T
Jurisic, Z
Borovac, J A
Anic, A
author_sort Katic, J
collection PubMed
description FUNDING ACKNOWLEDGEMENTS: Type of funding sources: None. INTRODUCTION: Atrial fibrosis is increasingly considered an important part of vulnerable substrates, with an essential function in the induction of left atrial (LA) conduction abnormalities underlying the transition from paroxysmal (PAF) to persistent atrial fibrillation (PeAF), contributing to disease continuation. A substantial number of studies suggest a correlation between atrial fibrosis and low voltage zones (LVZ) (1). Previous studies have shown that catestatin (CST) regulates cardiac remodeling. The CST inhibition of catecholamine inhibits the Ang II-induced cell proliferation, and the extracellular matrix (ECM) downregulation to protect the heart from fibrosis produces similar results inhibition of catecholamine and the regulation of the beta-adrenergic receptors (β-ARs) (2). From the results, it is clear that CST inhibits cardiac fibrosis by regulating nitric oxide (NO) and the reactive oxygen species (ROS) pathways via inhibiting catecholamine release and influencing the production of the downstream molecule (2). PURPOSE: This study investigated the potential association of serum catestatin level and LA fibrosis in AF patients. METHODS: The current study enrolled 18 consecutive patients with PeAF who had undergone bipolar voltage mapping of the left atrium before catheter ablation. The proportion of the mapped LA surface exhibiting low voltage (<0.5mV) was expressed as a percentage of the overall mapped LA surface area. In all participants, fasting laboratory tests were drawn at admission. The primary outcome measure of the current study was the association of serum CST and low-voltage zones (%LVZ ≥ 10% as a reference for severe LVZ). RESULTS: The patient characteristics were summarized in Table 1. The LA was mildly dilated, and the median %LVZ was 4 (IQR 0.75-31.25). The lower degree of cardiac fibrosis (LVZ < 10%) is significantly associated with higher levels of catestatin compared to severe LVZ >10% (8.6 (interquartile range-IQR 4.6 – 25.0) vs. 21.9 (IQR 11.1-100.0), p= 0.040)(Figure 1). CONCLUSION: The higher catestatin level was associated with the lower extension of atrial fibrosis (low LA voltage zones). [Figure: see text] [Figure: see text]
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spelling pubmed-102068112023-05-25 The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis Katic, J Sikirc, I Breskovic, T Jurisic, Z Borovac, J A Anic, A Europace 10.3 - Diagnostic Methods FUNDING ACKNOWLEDGEMENTS: Type of funding sources: None. INTRODUCTION: Atrial fibrosis is increasingly considered an important part of vulnerable substrates, with an essential function in the induction of left atrial (LA) conduction abnormalities underlying the transition from paroxysmal (PAF) to persistent atrial fibrillation (PeAF), contributing to disease continuation. A substantial number of studies suggest a correlation between atrial fibrosis and low voltage zones (LVZ) (1). Previous studies have shown that catestatin (CST) regulates cardiac remodeling. The CST inhibition of catecholamine inhibits the Ang II-induced cell proliferation, and the extracellular matrix (ECM) downregulation to protect the heart from fibrosis produces similar results inhibition of catecholamine and the regulation of the beta-adrenergic receptors (β-ARs) (2). From the results, it is clear that CST inhibits cardiac fibrosis by regulating nitric oxide (NO) and the reactive oxygen species (ROS) pathways via inhibiting catecholamine release and influencing the production of the downstream molecule (2). PURPOSE: This study investigated the potential association of serum catestatin level and LA fibrosis in AF patients. METHODS: The current study enrolled 18 consecutive patients with PeAF who had undergone bipolar voltage mapping of the left atrium before catheter ablation. The proportion of the mapped LA surface exhibiting low voltage (<0.5mV) was expressed as a percentage of the overall mapped LA surface area. In all participants, fasting laboratory tests were drawn at admission. The primary outcome measure of the current study was the association of serum CST and low-voltage zones (%LVZ ≥ 10% as a reference for severe LVZ). RESULTS: The patient characteristics were summarized in Table 1. The LA was mildly dilated, and the median %LVZ was 4 (IQR 0.75-31.25). The lower degree of cardiac fibrosis (LVZ < 10%) is significantly associated with higher levels of catestatin compared to severe LVZ >10% (8.6 (interquartile range-IQR 4.6 – 25.0) vs. 21.9 (IQR 11.1-100.0), p= 0.040)(Figure 1). CONCLUSION: The higher catestatin level was associated with the lower extension of atrial fibrosis (low LA voltage zones). [Figure: see text] [Figure: see text] Oxford University Press 2023-05-24 /pmc/articles/PMC10206811/ http://dx.doi.org/10.1093/europace/euad122.062 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle 10.3 - Diagnostic Methods
Katic, J
Sikirc, I
Breskovic, T
Jurisic, Z
Borovac, J A
Anic, A
The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title_full The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title_fullStr The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title_full_unstemmed The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title_short The relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
title_sort relationship of plasma catestatin concentrations with the extension of left atrial fibrosis
topic 10.3 - Diagnostic Methods
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206811/
http://dx.doi.org/10.1093/europace/euad122.062
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