Observational study finds persistent atrial fibrillation independently predicts elevated galectin-3 in ablation candidates, highlighting its role in fibrotic atrial remodeling.
Mechanisms of maintenance of atrial fibrillation are known to include fibrosis. Galectin-3, as a biomarker of fibrosis, may be a valuable marker of atrial remodeling. We sought to find whether there was a link between clinical features and higher galectin-3 levels in patients with atrial fibrillation. Serum concentrations of Galectin-3 were determined in a consecutive series of patients addressed for ablation of atrial fibrillation. One-hundred-and-eighty-seven patients were included, 56% having a paroxysmal type of atrial fibrillation. Mean Galectin-3 concentration was 14.5 ± 5.5 ng/mL. Age, persistent form of atrial fibrillation, underlying cardiac disease, heart failure, decreased left ventricular ejection fraction (LVEF), hypertension, diabetes, treatment with ACEI/ARB, enlarged left atrium and renal insufficiency were associated with higher Galectin-3 levels. Importantly, persistent form of atrial fibrillation, female sex, and LVEF < 45% were independent predictors (OR 13.9, p = 0.01, OR = 11.7, p = 0.03, and OR 54.2, p = 0.04, respectively) of higher Galectin-3 levels (≥ 15 ng/mL). Persistent type of atrial fibrillation is an independent predictor of higher Galectin-3 concentration. This biomarker of fibrosis may be implied in the mechanisms of atrial remodeling and maintenance of atrial fibrillation, and thus be helpful for the design of therapeutic strategy in patients with atrial fibrillation.
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Clémenty et al. (2014) studied this question.
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