Epicardial adipose tissue and atrial fibrillation: pathophysiological mechanisms, clinical implications, and potential therapies.

BACKGROUND

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Epicardial adipose tissue (EAT) serves as a biologically active organ with important endocrine and inflammatory function. Review An accumulating body of evidence suggests that EAT is associated with the initiation, perpetuation, and recurrence of AF, but the precise role of EAT in AF pathogenesis is not completely elucidated. Pathophysiological mechanisms involve adipocyte infiltration, profibrotic and pro-inflammatory paracrine effects, oxidative stress, neural mechanisms, and genetic factors.

CONCLUSIONS

Notably, EAT accumulation seems to be associated with stroke and adverse cardiovascular outcomes in AF. Weight loss, specific medications and ablation of ganglionated plexi (GP) seem to be potential therapies in this setting.