Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia; Department of Cardiology, Lyell McEwin Hospital, Adelaide, Australia.
Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
JACC Clin Electrophysiol. 2018 Dec;4(12):1529-1540. doi: 10.1016/j.jacep.2018.08.014. Epub 2018 Nov 1.
The aims of the study were to characterize: 1) electrical and electroanatomical remodeling in patients with atrial fibrillation (AF) with obesity; and 2) the impact of epicardial fat depots on adjacent atrial tissue.
Obesity is associated with an increased risk of AF.
A total of 115 patients with AF who underwent AF ablation were screened. After exclusion, 26 patients were divided into 2 groups (obese: body mass index [BMI] ≥27 kg/m and reference: BMI <27 kg/m). They underwent cardiac magnetic resonance (CMR) imaging and electroanatomic mapping of the left atrium (LA) in sinus rhythm before AF ablation. Atrial and ventricular epicardial adipose tissue (EAT) were assessed by CMR. The following electrophysiological parameters were assessed: global and regional voltage, conduction velocity (CV), electrogram fractionation, and CV heterogeneity. In addition, the regional relationship between LA EAT depots and the electrophysiological substrate was evaluated.
The BMIs of the obese and reference groups were 30.2 ± 2.6 and 25.2 ± 1.3 kg/m, respectively (p < 0.001). There was no difference in the left ventricular ejection fraction and a nonsignificant increase in LA size with obesity. Obesity was associated with increase in all measures of EAT (p < 0.05), with a predominant distribution adjacent to the posterior LA and the atrioventricular groove. Obesity was associated with reduced global CV (0.86 ± 0.31 m/s vs. 1.26 ± 0.29 m/s; p < 0.001), with a nonsignificant increase in conduction heterogeneity (p = 0.10), increased fractionation (54 ± 17% vs. 25 ± 10%; p < 0.001), and regional alteration in voltage (p < 0.001). Although the global LA voltage was preserved, there was greater voltage heterogeneity (p = 0.001) and increased low-voltage areas (13.9% vs. 3.4%; p < 0.001) in the obese group compared with the reference group. The low voltage areas were predominantly seen in the posterior and/or inferior LA, which was similar to location of EAT on CMR imaging. Among various measures of obesity, LA EAT volume correlated best with posterior LA fractionation (r = 0.55 for LA EAT volume vs. r = 0.36 for BMI) and CV (r = 0.31 for LA EAT volume vs. r = 0.22 for BMI).
Obesity is associated with electroanatomical remodeling of the atria, with areas of low voltage, conduction slowing, and greater fractionation of electrograms. These changes were more pronounced in regions adjacent to epicardial fat depots, which suggested a role for fat depots in the development of the AF substrate.
本研究旨在：1）描述肥胖症患者心房颤动（AF）中的电和电解剖重塑；2）探讨心外膜脂肪沉积对邻近心房组织的影响。
肥胖与 AF 风险增加相关。
筛选了 115 例接受 AF 消融的 AF 患者，排除后 26 例患者被分为 2 组（肥胖组：体重指数[BMI]≥27 kg/m2和参考组：BMI<27 kg/m2）。在 AF 消融前，他们在窦性心律下接受心脏磁共振（CMR）成像和左心房（LA）电解剖标测。通过 CMR 评估心房和心室心外膜脂肪（EAT）。评估以下电生理参数：整体和局部电压、传导速度（CV）、电图分节和 CV 异质性。此外，还评估了 LA EAT 沉积区与电生理基质之间的区域关系。
肥胖组和参考组的 BMI 分别为 30.2±2.6 和 25.2±1.3 kg/m2（p<0.001）。肥胖组左心室射血分数无差异，左心房大小有非显著性增加。肥胖与所有 EAT 测量值的增加相关（p<0.05），主要分布在 LA 后侧壁和房室沟附近。肥胖与整体 CV 降低相关（0.86±0.31 m/s 与 1.26±0.29 m/s；p<0.001），但 CV 异质性无显著增加（p=0.10），分节增加（54±17% 与 25±10%；p<0.001），以及电压的区域性改变（p<0.001）。尽管整体 LA 电压保持不变，但肥胖组的电压异质性更大（p=0.001），低电压区更多（13.9%与 3.4%；p<0.001）。与 CMR 成像上的 EAT 位置相似，低电压区主要位于 LA 的后侧壁和/或下侧壁。在肥胖的各种测量指标中，LA EAT 体积与 LA 后侧壁分节（LA EAT 体积 r=0.55 与 BMI r=0.36）和 CV（LA EAT 体积 r=0.31 与 BMI r=0.22）相关性最好。
肥胖与心房的电解剖重塑相关，表现为低电压区、传导减慢和电图分节增加。这些变化在邻近心外膜脂肪沉积区更为明显，提示脂肪沉积在心律失常基质形成中发挥作用。
