Galectin-3 in atrial fibrillation: Simple bystander, player or both?

Galectin-3 promotes fibrosis, and cardiac remodeling is a well-established cause of arrhythmias. Therefore, we reviewed current evidence on the epidemiological and biological association between galectin-3 and atrial fibrillation.

We performed an electronic search on Medline, Scopus and Web of Science, using the keywords "galectin" OR "galectin-3" AND "atrial fibrillation" OR "arrhythmia(s)" in the fields "title/abstract/keywords".

Seven cohort studies were identified and reviewed. A significant association between serum galectin-3 values and the risk of atrial fibrillation was found in 4 studies (1 nested case-control, 2 case-control, 1 prospective), whereas the association could not be confirmed in a single case-control investigation. Serum galectin-3 value was also found to be a significant predictor of left atrium fibrosis, reduced left atrial volume, or decreased left ventricle ejection fraction in four studies (2 nested case-control, 2 case-control). A reliable biological explanation may be brought in support of these findings. Activated macrophages release galectin-3, which not only contributes to increase macrophages accumulation in cardiac tissue and perpetuates their activation, but also promotes fibroblast activation and proliferation, thus leading to cardiac fibrosis, cardiac remodeling, myocardiocyte dysfunction and ultimately atrial fibrillation. The onset of atrial fibrillation further amplifies macrophage activation, thus completing a vicious circle that is mirrored by evidence of substantially increased galectin-3 values in patients with persistent atrial fibrillation.

It seems reasonable to suggest that galectin-3 measurement holds promise for stratifying risk and outcome of atrial fibrillation.