Several blood biomarkers have been identified which are helpful in supporting atrial fibrillation (AF) diagnosis, prognosis, and outcomes. Because of its involvement in cardiac fibrosis, inflammation, and remodeling processes, galectin-3 is one of the emerging biomarkers in cardiac diseases. Together with NT-proBNP, galectin-3 demonstrated better prognostic value for mortality in general population and in patients with heart failure, although it has been already demonstrated that galectin-3 has a lower specificity and sensitivity to identify patients with acute heart failure than NT-proBNP.

AF is associated with structural remodeling based on proinflammatory and profibrotic changes in atrial tissue, thus suggesting an association between galectin-3 and AF. A recently published analysis of the Framingham Offspring cohort found that greater circulating galectin-3 concentrations were associated with increased risk of developing AF. However, results are not consistent.

Thus, it was with interest that we read the report by Gurses et al on the role of galectin-3 in patients with persistent AF. The investigators analyzed galectin-3 in 76 patients with AF and 1:1 age- and gender-matched controls. For the first time, the investigators reported correlation between left atrial volume index (as accepted echocardiographic marker of left atrial remodeling) and higher galectin-3 levels in patients with persistent AF. Of note, another study published by the same work group demonstrated in smaller cohort similar association between galectin-3 and electroanatomic remodeling in patients with paroxysmal AF undergoing cryoballoon-based ablation.

The investigators should be congratulated for their interesting findings. We concur with the main conclusion that galectin-3 levels are higher in patients with AF compared with AF-free controls; however, we have some comments mainly from our and other studies.

First and of clinical relevance, present study cohort was relatively young (mean age 59 years) and comprised mainly lone AF because patients with co-morbidities (e.g., hypertension, diabetes mellitus, renal dysfunction, coronary artery disease) were excluded. This may complicate interpretation of the results and their implementation in the clinical routine, where patients with CHA ₂ DS ₂ -VASc score ≥2, renal dysfunction, and metabolic syndrome represent typical AF cohort. Although we also found higher galectin-3 levels in patients with AF, this seemed to be mediated by higher body mass index (as a cardiometabolic component) than by heart rhythm itself. Of note, association between galectin-3 with obesity and female gender had been already investigated in several studies ; however, the investigators did not find any differences between body mass index in patients with AF and controls.

Second, the levels of galectin-3 in our study correlated with neither left atrial dimension nor rhythm outcomes after AF catheter ablation. This contradicts reported association between galectin-3 and structural remodeling. Several studies were performed to identify clinical predictors for AF recurrences after catheter ablation. Of those, persistent AF and enlarged left atrial diameter have reproducibly been shown to associate with AF recurrences. Surely, the fact that Gurses et al included patients with lone AF would explain differences between the results found in our study cohort, where the impact of underlying co-morbidity (reflected by the CHADS ₂ and CHA ₂ DS ₂ -VASc scores) was found to be associated with galectin-3 than the rhythm per se. Whether this is an indication of different AF pathogenesis processes in lone versus not-lone AF is still to discuss.

In summary, whether there are differences in AF pathogenesis processes in lone and not-lone AF remains unclear. Further studies are clearly necessary to address this question that would determine next steps toward individualized AF treatment strategies.