Galectin-3 level predicts response to ablation and outcomes in patients with persistent atrial fibrillation and systolic heart failure

Abstract

IntroductionMechanisms of maintenance of both atrial fibrillation and structural left ventricular disease are known to include fibrosis. Galectin-3, a biomarker of fibrosis, is elevated both in patients with heart failure and persistent atrial fibrillation. We sought to find whether galectin-3 has a prognostic value in patients with heart failure and a reduced left ventricular ejection fraction undergoing ablation of persistent atrial fibrillation.MethodsSerum concentrations of galectin-3 were determined in a consecutive series of patients with an ejection fraction ≤40%, addressed for ablation of persistent atrial fibrillation. Responders to ablation were patients in sinus rhythm and with an ejection fraction ≥50% at 6 months. A combined endpoint of heart failure hospitalization, transplantation and/or death was used at 12 months.ResultsSeventy-five patients were included (81% male, age 63±10 years, ejection fraction 34±7%, galectin-3 21±12 ng/mL). During follow-up, eight patients were hospitalized for decompensated heart failure, 1 underwent heart transplantation, and 4 died; 50 patients were considered as responders to ablation. After adjustment, galectin-3 level independently predicted both 6-month absence of response to ablation (OR = 0.89 per unit increase, p = 0.002). Patients with galectin-3 levels <26 had a 95% 1-year event-free survival versus 46% in patients with galectin-3 ≥26 ng/mL (p<0.0001).ConclusionsGalectin-3 levels independently predict outcomes in patients with reduced left ventricular systolic function addressed for ablation of persistent AF, and may be of interest in defining the therapeutic strategy in this population.

Circulating Galectin-3 and Atrial Fibrillation Recurrence after Catheter Ablation: A Meta-Analysis

“…Our results demonstrate that, despite the role of Gal-3 in AF pathogenesis, baseline circulating Gal-3 levels may predict the response to catheter ablation in AF patients. This is consistent with the results of a previous study that showed that baseline Gal-3 levels independently predict outcomes in patients with reduced left ventricular systolic function attributed to ablation of persistent AF [38]. Taken together, Gal-3 is likely involved in AF pathogenesis and progression, risk stratification for stroke incidence, and treatment response to catheter ablation.…”

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

“…Recently, Gal-3 has been indicated to be involved in the following broad pathological processes: Inflammation [9], fibrosis, cell-to-cell [10,11] or cell-to-matrix [12] contacts, cell proliferation [13,14], and protection from apoptosis [15,16]. Furthermore, many studies have revealed that Gal-3 expression is detected in many disease conditions, such as heart disease [17][18][19][20][21][22][23], kidney disease [24][25][26][27], diabetes mellitus [24,25,28], viral infection [29][30][31][32], autoimmune disease [33][34][35][36], neurodegenerative disorders [37][38][39][40][41][42], and tumor formation [43][44][45][46][47][48][49][50][51][52].…”

Galectin-3 in Cardiovascular Diseases

“…Gal-3 is involved in the pathophysiology of HF [78] mainly because of its role in cardiac ventricular remodeling [71,77]. Normally, Gal-3 expression in the heart is low, whereas its synthesis and secretion increase in HF [63,79,80]. Gal-3 initially plays a protective role in the heart through its anti-apoptotic and anti-necrotic functions, while the prolonged expression of this protein leads to fibrosis and adverse remodeling of the damaged tissue [78].…”

“…Atrial fibrillation (AF) is the most frequent arrhythmia and it is associated with structural, electrical, genomic and hormonal atrial remodeling [79]. More recently, the concept of fibrotic atrial cardiomyopathy was introduced-defined as a progressive invasion of atrial myocardium by fibrosis, which favors initiation and maintenance of AF [83].…”