Work

Association of Epicardial Adipose Tissue With Bradyarrhythmias: A Matched Case–Control Study

Year: 2025

Type: article

Abstract: Background Epicardial adipose tissue (EAT) is implicated in exerting potential proarrhythmic effects. The relationship between EAT and tachyarrhythmias is well documented. However, the connection between EAT and bradyarrhythmias has not been comprehensively explored. This study aimed to investigate the association between EAT and bradyarrhythmias. Methods We retrospectively quantified the volume and density of EAT using chest computed tomography scans from patients with bradyarrhythmias and case‐matched controls. Measurements were obtained through manual pericardial contour tracing with a standardized Hounsfield unit threshold of −200 to −50 Hounsfield units. Results A total of 652 patients were included, comprising 326 patients with bradyarrhythmias (age 74.00 [interquartile range, 64.00–81.00] years, 46.01% female) and 326 matched controls (age 72.50 [interquartile range, 63.00–80.00] years, 46.01% female). Compared with the matched control group, the bradyarrhythmia group had a significantly greater volume (119.13 [interquartile range, 87.30–151.68] cm 3 versus 93.00 [interquartile range, 67.87–116.71] cm 3 , P <0.001) and a lower density of EAT (−92.02±4.00 Hounsfield units versus −90.68±3.73 Hounsfield units, P <0.001). Conditional logistic analysis demonstrated that the volume rather than the density of EAT is a significant influencing factor for bradyarrhythmias. Subgroup analysis indicated a progressive increase in average EAT volume from groups with first‐degree to third‐degree atrioventricular block. In participants with first‐degree atrioventricular block, there was a positive correlation between PR interval and EAT volume (Spearman’s correlation coefficient: 0.328, P =0.012). Conclusions Patients with bradyarrhythmia demonstrated significantly higher EAT volumes compared with matched controls, with a progressive increase observed across advancing grades of AVB. This dose‐dependent relationship between EAT burden and conduction system impairment underscores its potential role as a modifiable influencing factor in arrhythmogenesis. Further investigations are warranted to determine whether targeted EAT reduction could mitigate conduction abnormalities. Registration URL: https://www.chictr.org.cn ; Unique Identifier: ChiCTR2400088446.

Source: Journal of the American Heart Association

DOI: 10.1161/jaha.125.044223