Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation
Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation
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DOI：
10.1016/j.hrthm.2012.08.043
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发表时间：
2013-01-01
期刊：
影响因子：
5.5
通讯作者：
Sanders, Prashanthan
中科院分区：
文献类型：
--
作者：
Abed, Hany S.;Samuel, Chrishan S.;Sanders, Prashanthan
背景肥胖与心房纤颤（AF），但是，它诱导AF的机制是unknown.Objective检查的效果进行性体重增加的基板上AF.METHODS 30只羊进行了研究，在基线，4个月，8个月后，高热量的饮食。在每个时间点对10只绵羊进行心脏磁共振成像和血流动力学研究。采用高密度多部位双房心外膜标测，在4个起搏周期LRF和AF诱导时量化有效不应期、传导速度和传导异质性指数。对心房纤维化、炎症和心肌内脂质沉积进行组织学检查，并对内皮素A和B受体、内皮素1肽、血小板衍生生长因子、转化生长因子β 1和结缔组织生长因子进行分子分析。（P = .01）、纤维化（P = .02）、炎性浸润（P = .01）和脂质沉积（P = .02）。而有效不应期没有变化（P = .02），传导速度降低（P < .001），传导异质性指数增加（P <0.001），并增加诱导性（P = .001）和自发性（P = 0.001）AF。随着肥胖的增加，心房L心肌细胞内皮素-A和-B受体（P = 0.001）和内皮素-1（P = 0.03）增加。在协会中，有心房间质和细胞质转化生长因子β 1（P = 0.02）和血小板衍生生长因子（P = 0.02）levels.CONCLUSIONS肥胖与心房L电结构重构显着增加。随着进行性肥胖，心房L的大小、传导、组织学和促纤维化介质的表达发生变化。这些变化与自发性和更持久的AF相关。
BACKGROUND Obesity is associated with atria L fibrillation (AF); however, the mechanisms by which it induces AF are unknown.OBJECTIVE To examine the effect of progressive weight gain on the substrate for AF.METHODS Thirty sheep were studied at baseline, 4 months, and 8 months, following a high-calorie diet. Ten sheep were sampled at each time point for cardiac magnetic resonance imaging and hemodynamic studies. High-density multisite biatrial epicardial mapping was used to quantify effective refractory period, conduction velocity, and conduction heterogeneity index at 4 pacing cycle Lengths and AF inducibility. Histology was performed for atrial fibrosis, inflammation, and intramyocardial Lipidosis, and molecular analysis was performed for endothelin-A and -B receptors, endothelin-1 peptide, platelet-derived growth factor, transforming growth factor beta 1, and connective tissue growth factor.RESULTS Increasing weight was associated with increasing Left atria L volume (P = .01), fibrosis (P = .02), inflammatory infiltrates (P = .01), and Lipidosis (P = .02). While there was no change in the effective refractory period (P = .02), there was a decrease in conduction velocity (P < .001), increase in conduction heterogeneity index (P < .001), and increase in inducible (P = .001) and spontaneous (P = .001) AF. There was an increase in atria L cardiomyocyte endothelin-A and -B receptors (P = .001) and endothelin-1 (P = .03) with an increase in adiposity. In association, there was a significant increase in atrial interstitial and cytoplasmic transforming growth factor beta 1 (P = .02) and platelet-derived growth factor (P = .02) levels.CONCLUSIONS Obesity is associated with atria L electrostructural remodeling. With progressive obesity, there were changes in atria L size, conduction, histology, and expression of profibrotic mediators. These changes were associated with spontaneous and more persistent AF.