PDF(Pubmed)
Abstract：
UNASSIGNED: Obesity is a risk factor for atrial fibrillation (AF) and strongly influences the response to treatment. Atrial fibrosis shows similar associations. Epicardial adipose tissue (EAT) may be a link between these associations. We sought to assess whether EAT is associated with body mass index (BMI), left atrial (LA) fibrosis and volume.
UNASSIGNED: LA fibrosis and EAT were assessed using late gadolinium enhancement, and Dixon MRI sequences, respectively. We derived 3D models incorporating fibrosis and EAT, then measured the distance of fibrotic and non-fibrotic areas to the nearest EAT to assess spatial colocalization.
UNASSIGNED: One hundred and three AF patients (64% paroxysmal, 27% female) were analyzed. LA volume index was 54.9 (41.2, 69.7) mL/m2, LA EAT index was 17.4 (12.7, 22.9) mL/m2, and LA fibrosis was 17.1 (12.4, 23.1)%. LA EAT was significantly correlated with BMI (R = 0.557, p < 0.001); as well as with LA volume and LA fibrosis after BSA adjustment (R = 0.579 and R = 0.432, respectively, p < 0.001 for both). Multivariable analysis showed LA EAT to be independently associated with LA volume and fibrosis. 3D registration of fat and fibrosis around the LA showed no clear spatial overlap between EAT and fibrotic LA regions.
UNASSIGNED: LA EAT is associated with obesity (BMI) as well as LA volume and fibrosis. Regions of LA EAT did not colocalize with fibrotic areas, suggesting a systemic or paracrine mechanism rather than EAT infiltration of fibrotic areas.
UNASSIGNED: LA fibrosis and EAT were assessed using late gadolinium enhancement, and Dixon MRI sequences, respectively. We derived 3D models incorporating fibrosis and EAT, then measured the distance of fibrotic and non-fibrotic areas to the nearest EAT to assess spatial colocalization.
UNASSIGNED: One hundred and three AF patients (64% paroxysmal, 27% female) were analyzed. LA volume index was 54.9 (41.2, 69.7) mL/m2, LA EAT index was 17.4 (12.7, 22.9) mL/m2, and LA fibrosis was 17.1 (12.4, 23.1)%. LA EAT was significantly correlated with BMI (R = 0.557, p < 0.001); as well as with LA volume and LA fibrosis after BSA adjustment (R = 0.579 and R = 0.432, respectively, p < 0.001 for both). Multivariable analysis showed LA EAT to be independently associated with LA volume and fibrosis. 3D registration of fat and fibrosis around the LA showed no clear spatial overlap between EAT and fibrotic LA regions.
UNASSIGNED: LA EAT is associated with obesity (BMI) as well as LA volume and fibrosis. Regions of LA EAT did not colocalize with fibrotic areas, suggesting a systemic or paracrine mechanism rather than EAT infiltration of fibrotic areas.
摘要：
未经证实：肥胖是房颤（AF）的危险因素，并强烈影响对治疗的反应。心房纤维化显示类似的关联。心外膜脂肪组织（EAT）可能是这些关联之间的联系。我们试图评估EAT是否与体重指数(BMI)相关，左心房（LA）纤维化和体积。
未经证实：使用晚期钆增强来评估LA纤维化和EAT，和DixonMRI序列,分别。我们导出了结合纤维化和饮食的3D模型，然后测量纤维化和非纤维化区域到最近的EAT的距离，以评估空间共定位。
未经证实：一百零三例房颤患者（64%阵发性，27%的女性）进行了分析。LA体积指数为54.9（41.2，69.7）mL/m2，LAEAT指数为17.4（12.7，22.9）mL/m2，LA纤维化为17.1（12.4，23.1）％。LAEAT与BMI显著相关(R=0.557,p<0.001);以及与调整BSA后LA体积和LA纤维化显著相关(R=0.579和R=0.432,两者的p<0.001)。多变量分析显示LAEAT与LA体积和纤维化独立相关。LA周围的脂肪和纤维化的3D配准显示EAT和纤维化LA区域之间没有明显的空间重叠。
未经证实：LAEAT与肥胖（BMI）以及LA体积和纤维化有关。LAEAT的区域没有与纤维化区域共定位，提示系统性或旁分泌机制，而不是纤维化区域的EAT浸润。
未经证实：使用晚期钆增强来评估LA纤维化和EAT，和DixonMRI序列,分别。我们导出了结合纤维化和饮食的3D模型，然后测量纤维化和非纤维化区域到最近的EAT的距离，以评估空间共定位。
未经证实：一百零三例房颤患者（64%阵发性，27%的女性）进行了分析。LA体积指数为54.9（41.2，69.7）mL/m2，LAEAT指数为17.4（12.7，22.9）mL/m2，LA纤维化为17.1（12.4，23.1）％。LAEAT与BMI显著相关(R=0.557,p<0.001);以及与调整BSA后LA体积和LA纤维化显著相关(R=0.579和R=0.432,两者的p<0.001)。多变量分析显示LAEAT与LA体积和纤维化独立相关。LA周围的脂肪和纤维化的3D配准显示EAT和纤维化LA区域之间没有明显的空间重叠。
未经证实：LAEAT与肥胖（BMI）以及LA体积和纤维化有关。LAEAT的区域没有与纤维化区域共定位，提示系统性或旁分泌机制，而不是纤维化区域的EAT浸润。
