Arrhythmogenic evidence for epicardial adipose tissue: heart rate variability and turbulence are influenced by epicardial fat thickness.

Background: Epicardial adipose tissue (EAT) is a local source of various hormones, cytokines, and vasoactive substances affecting the myocardium. EAT contains abundant ganglionic plexi that interact with the autonomic nervous system. Evidence of the association between EAT and arrhythmia is limited, with the exception of atrial fibrillation. This study aimed to investigate the relation between EAT and cardiac autonomic function using heart rate variability (HRV) and heart rate turbulence (HRT) parameters.

Methods: All subjects underwent a 24-hour Holter recording to assess HRV and HRT parameters and a transthoracic echocardiography to measure EAT thickness. Patients were divided into two groups according to the median EAT thickness (3.9 mm). The higher EAT group consisted of 111 patients with a >3.9-mm thickness and the lower EAT group 113 patients with a ≤ 3.9-mm EAT thickness.

Results: HRV and HRT parameters were significantly influenced in the higher EAT group. Moreover, we observed significant correlations between EAT thickness and Holter findings (standard deviation of all NN intervals [SDNN]: r = -0.462, P < 0.001; SDNN index: r = -0.349, P < 0.001; standard deviation of the average NN intervals: r = -0.465, P < 0.001; root mean square of successive differences: r = -0.251, P < 0.001; pNN50: r = -0.354, P < 0.001; turbulence onset: r = 0.172, P = 0.010; turbulence slope: r = -0.279, P < 0.001, HRT category: r = 0.169, P = 0.011). In multivariate regression analysis, EAT thickness was independently associated with all measures of HRV and HRT, with the exception of turbulence onset.

Conclusions: Sympathovagal imbalance, detected by HRV and HRT parameters, is related to EAT thickness. As sympathovagal imbalance is a predictor of arrhythmic events, EAT may play an important arrhythmogenic role not limited to atrial fibrillation.