高频生物显微镜结合组织多普勒评价扩张型心肌病小鼠心功能的可行性

Feasibility of HFB and tissue Doppler in evaluating cardiac function of DCM mice

目的应用扩张型心肌病(DCM)小鼠模型探讨组织多普勒显像(TDI)评价早期心肌功能障碍的可行性。方法应用Vevo 770超声生物显微镜和30～40 MHz高频探头,分别在小鼠生后第3个月(G1组,n=12)、第6个月(G2组,n=11)和第9个月(G3组,n=10)对携带ZASP4突变的33只DCM小鼠进行M型、二维及TDI超声心动图检查。以M型和二维超声评价整体心脏功能以获取短轴缩短率(FS)和射血分数(EF)。TDI的取样容积置于左心室后壁,并将其分为基底段、中间段和心尖段以获取收缩和舒张峰值速度。结果 M型和二维超声测量G1、G2组的EF与FS之间均无统计学差异(P>0.05),而G3组则明显降低(P<0.01)。以TDI测量的G2组基底段和中间段收缩峰值速度明显低于G1组[(28.6±4.3)mm/s vs(45.8±12.0)mm/s,(26.3±5.3)mm/s vs(38.6±12.6)mm/s,P<0.01];舒张峰值速度也低于G1组[(32.3±6.3)mm/s vs(53.3±12.6)mm/s,(27.3±7.2)mm/svs(41.9±12.0)mm/s,P<0.01)],G3组基底段和中间段的峰值速度相比,G1和G2组减少更为明显(P<0.01)。结论利用高频显微镜进行TDI评测是可行的;并且TDI检测DCM小鼠模型的早期心功能障碍更敏感。

Objective To investigate the feasibility and value of tissue Doppler imaging（TDI） in evaluating early myocardial dysfunction using HFB in a mouse model of dilated cardiomyopathy（DCM）.Methods A total of 33 mice carrying the ZASP4 mutation found in a DCM family were studied by using HFB with a Vevo 770 system and a 40 MHz transducer.The sample volume of TDI was placed on the posterior wall of the left ventricle,which was divided into basal,middle and apical segments to obtain systolic and diastolic peak velocities（S＇,E＇ and A＇）.The mice were di-vided into 3 groups according to ages： Group 1（G1,3 months,n = 12）,Group 2（G2,6 months,n = 11）,and Group 3（G3,9 months,n = 10）.Global cardiac function was evaluated by M-mode and two-dimensional echocardiography to obtain fractional shorting（FS） and ejection fraction（EF）.Results Both FS and EF in B-mode and M-mode echocar-diograms showed no significant difference between G1and G2,but significantly decreased in G3.The TDI S＇ were more significantly decreased in G2 than in G1 in the basal [（28.62 ± 4.32） mm /s vs（45.80 ± 12.04） mm /s,P 0.01] and middle segments [（26.32 ± 5.35） mm /s vs（38.63 ± 12.62） mm /s,P 0.01],and further diminished in G3compared with G1 and G2 in the two segments（P 0.01）.Conclusion TDI using HFB is feasible,and TDI veloci-ties are probably more sensitive to early myocardial dysfunction in the mouse model of DCM.