基于T1 mapping技术对心外膜脂肪组织与肥厚性心肌病左室重构关系的研究

Study on the relationship between epicardial adipose tissue and left ventricular remodeling in hypertrophic cardiomyopathy based on T1 mapping technology

目的利用T1 mapping技术探究心外膜脂肪组织(epicardial adipose tissue,EAT)对肥厚性心肌病(hypertrophic cardiomyopathy,HCM)左室重构的影响。材料与方法通过心脏磁共振电影序列、对比增强前、后T1 mapping序列对52例于本院确诊为HCM患者的EAT、心肌细胞外容积比率(extracellular volume fraction,ECV)进行测量,通过ECV衡量左室纤维化水平。将EAT以中位数划分为高、低两组,评估EAT及相关临床因素对左室纤维化的影响,采用线性回归分析对上述具有统计学意义的变量进行共线性诊断,并进一步比较不同EAT值发生梗阻性心肌肥厚的差异。结果高量EAT患者心肌ECV值高于低量EAT患者(P=0.003),且高量EAT发生梗阻性肥厚者多于低量EAT(P=0.012)。男性ECV值高于女性(P=0.047),性别与EAT之间不存在多重共线性(容差≥0.1,VIF≤5),其他临床因素与ECV无显著相关(P>0.05)。结论高量EAT发生梗阻性心肌肥厚者增多,是HCM间质纤维化的独立危险因素。

Objective:To investigate the effect of epicardial adipose tissue(EAT)on left ventricular remodeling in hypertrophic cardiomyopathy(HCM)using T1 mapping technology.Materials and Methods:The EAT volume and extracellular volume fraction(ECV)of 52 patients diagnosed with HCM in our hospital were measured by cine-MRI,modified Look-Locker inverse recovery T1 mapping sequence.The level of left ventricular fibrosis was measured by ECV.EAT was divided into high and low groups according to the median,and the influence of EAT and related clinical factors on myocardial ECV value was evaluated.Use linear regression to analyze the collinearity of the above statistically significant variables.In addition,the difference of obstructive myocardial hypertrophy between high and low EAT groups was further compared.Results:The ECV value of myocardium in the high EAT group was higher than that in the low EAT group(P=0.003),and more obstructive hypertrophy occurred in the high EAT group than in the low EAT group(P=0.012).The ECV of male was higher than that of female(P=0.047).There was no multicollinearity between gender and EAT(tolerance≥0.1,VIF≤5).The remaining clinical factors had no significant correlation with ECV(P>0.05).Conclusions:The incidence of obstructive myocardial hypertrophy in patients with high EAT is increased,which is an independent risk factor of HCM interstitial fibrosis.