Plasma galectin-3 predicts clinical outcomes after catheter ablation in persistent atrial fibrillation patients without structural heart disease

Wu, Xiaoyan; Li, Songnan; Wen, Shaojun; Nie, Jungang; Deng, Wen-Ning; Bai, Rong; Liu, Nian; Tang, Ri‐Bo; Zhang, Ting; Du, Xin; Dong, Jianzeng; Ma, Changsheng

doi:10.1093/europace/euv045

Cited by 47 publications

(51 citation statements)

References 26 publications

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“…Fourteen studies compared serum concentrations of galectin‐3 between the sinus rhythm group and AF group . Our meta‐analysis shows that the AF group had higher concentrations of galectin‐3 than the sinus rhythm (SR) group (mean difference [MD] = −0.68 ng/mL, 95% CI: −0.92, −0.44, Z = 5.61, P < .00001) (Figure A).…”

Section: Resultsmentioning

confidence: 98%

“…Among the 38 full‐text articles assessed for eligibility, ten were excluded for the following reasons: One study lacked a control group; one study population was heart failure; four studies lacked available data for further analysis; and four reported duplicate data from studies that later published as full text . Finally, 28 studies involving 10 830 patients were included in our meta‐analysis, with their baseline characteristics shown in Tables and .…”

Section: Resultsmentioning

confidence: 99%

“…Galectin‐3 can itself mediate macrophage activation through both classical and alternative pathways, as well as induce adverse structural and electrophysiological remodeling in the atria . The latter effect may be independent of heart failure, since galectin‐3 is raised in AF patients without structural heart disease . The following mechanisms underlying galectin‐3‐mediated atrial dysfunction have been identified.…”

Section: Discussionmentioning

confidence: 99%

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Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Gong

Cheung

Wang

et al. 2020

Clinical Laboratory Analysis

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Background Galectin‐3 is an inflammatory marker that is raised in myocardial fibrosis and inflammation. Recent studies have explored its role in predicting atrial fibrillation (AF) outcomes. The aim of this systematic review and meta‐analysis is to examine the association between serum concentration of galectin‐3 and AF. Methods PubMed, EMBASE, and the Cochrane Database were searched. A total of 280 studies were identified, of which 28 studies involving 10 830 patients were included in our meta‐analysis. Results Galectin‐3 is present at higher concentrations in patients with AF than those in sinus rhythm (mean difference [MD] = −0.68 ng/mL, 95% CI: −0.92, −0.44, Z = 5.61, P < .00001). Galectin‐3 levels were significantly higher in the persistent AF than in the paroxysmal AF group (MD = −0.94 ng/mL, 95% CI: −1.85, −0.03, Z = 2.04, P = .04). Higher galectin‐3 levels were associated with a 45% increase in the odds of developing AF (odds ratio [OR] = 1.45, 95% CI: 1.15, 1.83, Z = 3.11, P = .002) and risk of AF recurrence (hazard ratio [HR] =1.17, 95% CI: 1.06, 1.29, Z = 3.12, P = .002). Conclusions Our meta‐analysis found that galectin‐3 is significantly higher in patients with persistent AF than in those with paroxysmal AF, and can predict both AF development and recurrence after treatment.

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Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Gong

Cheung

Wang

et al. 2020

Clinical Laboratory Analysis

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“…Clinical studies have suggested a role of increased circulating levels of Gal‐3 in predicting the severity of heart disease or a high risk of major adverse cardiovascular events (MACE) including HF (Ho et al, ; van der Velde et al, ), poor survival (Bayes‐Genis et al, ; Lok et al, ), post‐MI cardiac events (Di Tano et al, ; Grandin et al, ; Maiolino et al, ), as well as diastolic dysfunction (Wu, Li, et al, ) and severity of atrial fibrosis (Hernandez‐Romero et al, ; Takemoto et al, ; Wu, Su, et al, ). French et al reported in HF patients ( n = 1,385) that elevated Gal‐3 level was associated with a greater risk of MACE (hazard ratio = 1.96 for each doubling in Gal‐3) and that such association was most pronounced among patients diagnosed as HF with preserved ejection fraction (hazard ratio = 3.30; French et al, ).…”

Section: Gal‐3 As a Biomarker Of Heart Disease: Influence Of β‐Adrenomentioning

confidence: 99%

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

Zhao

Nguyen

et al. 2019

British J Pharmacology

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Myocardial fibrosis is a key histopathological component that drives the progression of heart disease leading to heart failure and constitutes a therapeutic target. Recent preclinical and clinical studies have implicated galectin‐3 (Gal‐3) as a pro‐fibrotic molecule and a biomarker of heart disease and fibrosis. However, our knowledge is poor on the mechanism(s) that determine the blood level or regulate cardiac expression of Gal‐3. Recent studies have demonstrated that enhanced β‐adrenoceptor activity is a determinant of both circulating concentration and cardiac expression of Gal‐3. Pharmacological or transgenic activation of β‐adrenoceptors leads to increased blood levels of Gal‐3 and up‐regulated cardiac Gal‐3 expression, effect that can be reversed with the use of β‐adrenoceptor antagonists. Conversely, Gal‐3 gene deletion confers protection against isoprenaline‐induced cardiotoxicity and fibrogenesis. At the transcription level, β‐adrenoceptor stimulation activates cardiac mammalian sterile‐20‐like kinase 1, a pivotal kinase of the Hippo signalling pathway, which is associated with Gal‐3 up‐regulation. Recent studies have suggested a role for the β‐adrenoceptor‐Hippo signalling pathway in the regulation of cardiac Gal‐3 expression thereby contributing to the onset and progression of heart disease. This implies a therapeutic potential of the suppression of Gal‐3 expression. In this review, we discuss the effects of β‐adrenoceptor activity on Gal‐3 as a biomarker and causative mediator in the setting of heart disease and point out pivotal knowledge gaps. Linked Articles This article is part of a themed section on Adrenoceptors—New Roles for Old Players. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.14/issuetoc

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“…12,25,26 This study may help to explain why this is the case, as it suggests that systemic (or at least non- help to explain why it has shown more promise. In this study, however, we have shown that ICTP does not appear to be significantly associated with LA fibrosis.…”

Section: Discussionmentioning

confidence: 89%

Intra-cardiac and peripheral levels of biochemical markers of fibrosis in patients undergoing catheter ablation for atrial fibrillation

et al. 2017

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Plasma galectin-3 predicts clinical outcomes after catheter ablation in persistent atrial fibrillation patients without structural heart disease

Abstract: Plasma Gal-3 concentrations are elevated in PsAF patients without structural heart disease and independently predict AF recurrence after ablation. Plasma Gal-3 concentration may be helpful in identifying appropriate candidates for AF ablation.

Cited by 47 publications

References 26 publications

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

Intra-cardiac and peripheral levels of biochemical markers of fibrosis in patients undergoing catheter ablation for atrial fibrillation

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