Increasing Level of Interleukin-1β in Epicardial Adipose Tissue Is Associated with Persistent Atrial Fibrillation

Epicardial adipose tissue (EAT) is associated with the pathogenesis of atrial fibrillation (AF). The role of local inflammation in persistent AF is unclear. The purpose of this study was to assess the relationship between regional interleukin-1β (IL-1β) and persistent AF. Thirty-seven persistent AF patients underwent coronary artery bypass grafting surgery were enrolled. Patients without a history of AF (n = 37), but received the same surgery matched by age, gender, and body mass index, were enrolled in the control group. EAT thickness was measured by echocardiography. We obtained blood and EAT samples at open-heart surgery. In each patient, serum and EAT levels of IL-1β and adiponectin were measured. The EAT thickness in patients with persistent AF was significantly greater than that in the control group (5.6 ± 1.1 versus 5.0 ± 1.3 mm, P = 0.02). The mRNA level of IL-1β was higher in persistent AF group than the control group (4.94 ± 1.69 versus 2.93 ± 0.91, P < 0.01). Adiponectin expression decreased in persistent AF patients (7.04 ± 2.21 versus 8.63 ± 2.95, P = 0.01). There were no significant differences in plasma levels of IL-1β and adiponectin between the 2 groups. Multiple logistic regression analysis showed that IL-1β was an independent risk factor of persistent AF. These findings suggested that regional IL-1β in EAT was an independent risk factor of persistent AF, which may promote the persistence of AF. [Figure: see text].