1 Monash Cardiovascular Research Centre Department of Medicine (Monash Medical Centre), Monash University and Monash Heart Monash Health Clayton Australia.
2 Baker Heart and Diabetes Institute Melbourne Australia.
J Am Heart Assoc. 2018 Dec 4;7(23):e009975. doi: 10.1161/JAHA.118.009975.
Background Epicardial adipose tissue ( EAT ) is in immediate apposition to the underlying myocardium and, therefore, has the potential to influence myocardial systolic and diastolic function or myocardial geometry, through paracrine or compressive mechanical effects. We aimed to review the association between volumetric EAT and markers of myocardial function and geometry. Methods and Results PubMed, Medline, and Embase were searched from inception to May 2018. Studies were included only if complete EAT volume or mass was reported and related to a measure of myocardial function and/or geometry. Meta-analysis and meta-regression were used to evaluate the weighted mean difference of EAT in patients with and without diastolic dysfunction. Heterogeneity of data reporting precluded meta-analysis for systolic and geometric associations. In the 22 studies included in the analysis, there was a significant correlation with increasing EAT and presence of diastolic dysfunction and mean e' (average mitral annular tissue Doppler velocity) and E/e' (early inflow / annular velocity ratio) but not E/A (ratio of peak early (E) and late (A) transmitral inflow velocities), independent of adiposity measures. There was a greater EAT in patients with diastolic dysfunction (weighted mean difference, 24.43 mL; 95% confidence interval, 18.5-30.4 mL; P<0.001), and meta-regression confirmed the association of increasing EAT with diastolic dysfunction ( P=0.001). Reported associations of increasing EAT with increasing left ventricular mass and the inverse correlation of EAT with left ventricular ejection fraction were inconsistent, and not independent from other adiposity measures. Conclusions EAT is associated with diastolic function, independent of other influential variables. EAT is an effect modifier for chamber size but not systolic function.
背景
心外膜脂肪组织(EAT)与下心肌直接相邻,因此通过旁分泌或压缩机械效应,具有影响心肌收缩和舒张功能或心肌几何形状的潜力。我们旨在综述 EAT 体积与心肌功能和几何形状标志物之间的相关性。
方法和结果
从建立到 2018 年 5 月,我们在 PubMed、Medline 和 Embase 上进行了检索。只有当完整的 EAT 体积或质量被报告,并与心肌功能和/或几何形状的测量相关时,我们才纳入研究。使用荟萃分析和荟萃回归来评估舒张功能障碍患者与无舒张功能障碍患者的 EAT 加权均数差异。数据报告的异质性排除了对收缩和几何相关性的荟萃分析。在纳入分析的 22 项研究中,EAT 与舒张功能障碍的存在以及平均 e'(二尖瓣环组织多普勒速度的平均值)和 E/e'(早期流入/环速度比)呈显著相关,但与 E/A(峰值早期(E)和晚期(A)二尖瓣流入速度的比值)无关,而与肥胖指标无关。舒张功能障碍患者的 EAT 更大(加权均数差异,24.43mL;95%置信区间,18.5-30.4mL;P<0.001),荟萃回归证实 EAT 与舒张功能障碍的相关性(P=0.001)。EAT 与左心室质量增加的相关性以及 EAT 与左心室射血分数的负相关与其他肥胖指标不一致,且不是独立的。
结论
EAT 与舒张功能相关,与其他有影响的变量无关。EAT 是心室大小的效应修饰因子,但不是收缩功能的效应修饰因子。