Weytjens Caroline, Franken Philippe R, D'hooge Jan, Droogmans Steven, Cosyns Bernard, Lahoutte T, Van Camp Guy
Department of Cardiology, In Vivo Cellular and Molecular Imaging Center, University Hospital, Brussels, Belgium.
Eur J Echocardiogr. 2008 May;9(3):326-33. doi: 10.1093/ejechocard/jen123. Epub 2008 Mar 27.
To find out if Doppler myocardial imaging (DMI) can detect early signs of left ventricular (LV) dysfunction in a rat model of diabetic cardiomyopathy.
Eight control and 12 Streptozotocin (STZ)-induced diabetic rats underwent transthoracic echocardiography with high-resolution technology at baseline and 2, 4, 8, 12, and 16 weeks after STZ injection. Radial function was analysed using conventional M-mode, and velocity, strain and strain rate imaging. Longitudinal function was analysed using pulsed Doppler imaging of the mitral annulus.
In the diabetic rats, a significant increase in LV end diastolic and end systolic diameter was measured when compared with controls (P < 0.001). Fractional shortening and LV ejection fraction remained unchanged in both groups. Using DMI, diabetic rats demonstrated a decrease in radial systolic velocity (rate of change: +0.01 vs. -0.003 week(-1); P < 0.01) and radial systolic strain rate (+0.003 vs. -0.205 week(-1); P = 0.08) of the anteroseptal wall. Histologic examination revealed dilated cardiomyopathy with no signs of fibrosis.
Although LV ejection fraction remained preserved, velocity and strain rate imaging was able to detect radial systolic dysfunction in diabetic rats. The absence of histological signs of fibrosis suggests that other mechanisms play a role in the development of diabetic cardiomyopathy.
探究多普勒心肌成像（DMI）能否在糖尿病性心肌病大鼠模型中检测出左心室（LV）功能障碍的早期迹象。
8只对照大鼠和12只链脲佐菌素（STZ）诱导的糖尿病大鼠在基线以及STZ注射后2、4、8、12和16周接受了高分辨率经胸超声心动图检查。使用传统M型、速度、应变和应变率成像分析径向功能。使用二尖瓣环脉冲多普勒成像分析纵向功能。
与对照大鼠相比，糖尿病大鼠的左心室舒张末期和收缩末期直径显著增加（P < 0.001）。两组的缩短分数和左心室射血分数均保持不变。使用DMI检查发现，糖尿病大鼠前间隔壁的径向收缩速度降低（变化率：+0.01对-0.003周-1；P < 0.01），径向收缩应变率降低（+0.003对-0.205周-1；P = 0.08）。组织学检查显示为扩张型心肌病，无纤维化迹象。
尽管左心室射血分数保持正常，但速度和应变率成像能够检测出糖尿病大鼠的径向收缩功能障碍。缺乏纤维化的组织学迹象表明，其他机制在糖尿病性心肌病的发展中起作用。
