When should we measure biomarkers in patients with atrial fibrillation to predict recurrences?

Merino-Merino, Ana; Saez-Maleta, Ruth; Salgado-Aranda, Ricardo; AlKassam-Martinez, Daniel; Pascual-Tejerina, Virginia; Martín‐González, Javier; García-Fernández, Javier; Rivera, Jaime A.

doi:10.1016/j.ajem.2020.05.051

Cited by 7 publications

(6 citation statements)

References 4 publications

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“…In a recent study of our group [41] in which 115 patients with persistent nonvalvular AF who underwent electrical cardioversion were included, seven biomarkers were analyzed (Gal3, ST2, ultrasensitive troponin T, CRP, urate, fibrinogen, and NT-proBNP) at baseline (prior to performing electrical cardioversion) and at the 6-month follow-up, and its possible relationship with electrical recurrence of arrhythmia was evaluated at the 6-month follow-up. The patients were evaluated with a holter-ECG at 3 months, electrocardiogram at 6 months, in addition to other possible eventual records in their clinical history.…”

Section: St2 and Galectin-3 In Atrial Fibrillationmentioning

confidence: 99%

The Role of Galectin-3 and ST2 in Cardiology: A Short Review

Merino-Merino¹,

González-Bernal

Fernandez-Zoppino

et al. 2021

Biomolecules

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Galectin-3 is a lectin that binds beta-galactosides. It is involved in cardiac remodeling and fibrosis through the activation of macrophages and fibroblasts. ST2 is secreted by myocardial cells due to cardiac overload. These two biomarkers have been traditionally studied in the field of heart failure to guide medical therapy and detect the progression of the disease. Nevertheless, there are novel evidences that connect galectin-3 and ST2 with coronary heart disease and, specifically, with atrial fibrillation. The aim of this article is to concisely review the diagnostic and prognostic role of galectin-3 and ST2 in different cardiac diseases.

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Section: St2 and Galectin-3 In Atrial Fibrillationmentioning

confidence: 99%

The Role of Galectin-3 and ST2 in Cardiology: A Short Review

Merino-Merino¹,

González-Bernal

Fernandez-Zoppino

et al. 2021

Biomolecules

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“…In contrast, Begg et al showed that gal-3 concentration is not prognostic for maintaining SR after DCCV [22]. Similarly, Merino-Merino et al showed that gal-3 concentration measured at the time of DCCV and 6 months after DCCV is not prognostic for maintaining sinus rhythm after DCCV [39]. In the group of patients with persistent AF studied by our team, we also did not show that the level of gal-3 was prognostic in terms of maintaining SR after DCCV [28].…”

Section: Discussionmentioning

confidence: 98%

Analysis of the Correlation of Galectin-3 Concentration with the Measurements of Echocardiographic Parameters Assessing Left Atrial Remodeling and Function in Patients with Persistent Atrial Fibrillation

et al. 2021

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Galectin-3 (gal-3) is a fibrosis marker and may play a role in fibrosis of the left atrium (LA). Left atrial wall fibrosis may influence the transition from paroxysmal to non-paroxysmal atrial fibrillation (AF). In this study, we assessed the correlation of gal-3 concentration with the main echocardio-graphic parameters evaluating dimensions, volume, compliance, and left atrial contractility during AF and after successful electrical cardioversion (DCCV). The study included 63 patients with left atrial enlargement who qualified for DCCV due to persistent AF. The procedure recovered sinus rhythm in 43 (68.3%) patients. The concentration of gal-3 was negatively correlated with the echocardiographic parameters of LA including dimensions (LA length pre, rho = −0.38; p = 0.003), volume (LAV pre, rho = −0.39; p = 0.003), compliance (LASr mean post, rho = −0.33) and contractility (pLASRct mean post, rho = −0.33; p = 0.038). Negative correlations of gal-3 concentration were also observed in relation to the volume and contractility of the left ventricle. The concentration of gal-3 significantly negatively correlates with the size, systolic function, and compliance of the LA wall in patients with persistent AF. Determining gal-3 concentration in patients with persistent AF may help in the assessment of remodeling of the LA wall.

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“…Our results indicated that blocking CD98 activity could decrease Gal‐3‐induced cardiac dysregulation and the Gal‐3/CD98 axis might be a promising therapeutic target among patients with AF with increased circulatory Gal‐3. Recent studies have not identified any significant differences in the levels of Gal‐3 in the peripheral blood of patients with AF and those without AF 40 . Because the level of myocardial Gal‐3, but not that of plasma Gal‐3, was correlated with cardiac fibrosis, 41 cardiac Gal‐3 may have a greater effect on the pathogenesis of AF than does Gal‐3 in peripheral blood, consequently leading to disparate outcomes in clinical observations.…”

Section: Discussionmentioning

confidence: 98%

“…Recent studies have not identified any significant differences in the levels of Gal-3 in the peripheral blood of patients with AF and those without AF. 40 Because the level of myocardial Gal-3, but not that of plasma Gal-3, was correlated with cardiac fibrosis, 41 cardiac Gal-3 may have a greater effect on the pathogenesis of AF than does Gal-3 in peripheral blood, consequently leading to disparate outcomes in clinical observations.…”

Section: And Ncx and Increasedmentioning

confidence: 99%

Galectin‐3 enhances atrial remodelling and arrhythmogenesis through CD98 signalling

Cheng

Chen

et al. 2022

Acta Physiologica

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Aim Galectin‐3 (Gal‐3) is a biomarker of atrial fibrillation (AF) that mediates atrial inflammation. CD98 is the membrane surface receptor for Gal‐3. Nevertheless, the role of the Gal‐3/CD98 axis in atrial arrhythmogenesis is unclear. In this study, we investigated the effects of Gal‐3/CD98 signalling on atrial pathogenesis. Methods Whole cell patch clamp and western blotting were used to analyse calcium/potassium homeostasis and calcium‐related signalling in Gal‐3‐administrated HL‐1 atrial cardiomyocytes with/without CD98 neutralized antibodies. Telemetry electrocardiographic recording, Masson's trichrome staining and immunohistochemistry staining of atrium were obtained from mice having received tail‐vein injections with Gal‐3. Results Gal‐3‐treated HL‐1 myocytes had a shorter action potential duration, smaller L‐type calcium current, increased sarcoplasmic reticulum (SR) calcium content, Na+/Ca2+ exchanger (NCX) current, transient outward potassium current, and ultrarapid delayed rectifier potassium current than control cells had. Gal‐3‐treated HL‐1 myocytes had greater levels of SR Ca2+ATPase, NCX, Nav1.5, and NLR family pyrin domain containing 3 (NLRP3) expression and increased calcium/calmodulin‐dependent protein kinase II (CaMKII), ryanodine receptor 2 (RyR2), and nuclear factor kappa B (NF‐κB) phosphorylation than control cells had. Gal‐3‐mediated activation of CaMKII/RyR2 pathway was diminished in the cotreatment of anti‐CD98 antibodies. Mice that were injected with Gal‐3 had more atrial ectopic beats, increased atrial fibrosis, and activated NF‐κB/NLRP3 signalling than did control mice (nonspecific immunoglobulin) or mice treated with Gal‐3 and anti‐CD98 antibodies. Conclusion Gal‐3 recombinant protein administration increases atrial fibrosis and arrhythmogenesis through CD98 signalling. Targeting Gal‐3/CD98 axis might be a novel therapeutic strategy for patients with AF and high Gal‐3 levels.

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When should we measure biomarkers in patients with atrial fibrillation to predict recurrences?

Cited by 7 publications

References 4 publications

The Role of Galectin-3 and ST2 in Cardiology: A Short Review

The Role of Galectin-3 and ST2 in Cardiology: A Short Review

Analysis of the Correlation of Galectin-3 Concentration with the Measurements of Echocardiographic Parameters Assessing Left Atrial Remodeling and Function in Patients with Persistent Atrial Fibrillation

Galectin‐3 enhances atrial remodelling and arrhythmogenesis through CD98 signalling

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