O'Brien W D, Sagar K B, Warltier D C, Rhyne T L
Department of Electrical and Computer Engineering, University of Illinois, Urbana.
Circulation. 1995 Jan 1;91(1):154-60. doi: 10.1161/01.cir.91.1.154.
Identification of viable but stunned myocardium remains a major problem. Since stunned myocardium results in impairment of myocardial function without any structural damage and infarcted myocardium causes major structural disruption, we postulated that acoustic properties could distinguish between the two insults.
Anesthetized open-chest dogs underwent a total occlusion of the left anterior descending coronary artery for 15 minutes (stunned, n = 7) and 90 minutes (infarcted, n = 8), followed by reperfusion for 3 hours. Circumflex coronary artery perfusion territory (n = 15) served as normal control tissue. Regions of myocardium were quantitatively evaluated with a scanning laser acoustic microscope operating at 100 MHz and a research ultrasound system operating at 4 to 7 MHz. Four ultrasonic parameters were determined: attenuation coefficient (an index of loss per unit distance), speed of propagation, a spatial variation of propagation speed called the heterogeneity index (HI), and ultrasonic backscatter at 5 MHz (IBR5). Myocardial water, lipid, and protein contents of normal, stunned, and infarcted myocardium were also determined. The attenuation coefficient of normal myocardium (179 +/- 20 dB/cm) was significantly greater than that of stunned (136 +/- 7 dB/cm, P < .001) and infarcted (130 +/- 8 dB/cm, P < .001) myocardium. The propagation speed of normal myocardium (1597 +/- 6 m/s) was similar to that of stunned (1600 +/- 6 m/s) and significantly higher than that of infarcted (1575 +/- 7 m/s, P < .001) myocardium. The HI for specimen thicknesses of 75 to 100 microns showed an increase of 33% between normal (5.0 +/- 0.8 m/s) and stunned (7.5 +/- 2.3 m/s, P < .05) myocardium. However, for the infarcted myocardium (5.8 +/- 2.0 m/s), the HI was essentially the same as that of the normal myocardium (5.0 +/- 0.8 m/s). The IBR5 of normal (-47.1 +/- 1.0 dB) was not significantly different from that of stunned myocardium (-46.8 +/- 0.9 dB). The IBR5 of infarcted myocardium (-42.4 +/- 1.0 dB) was significantly greater than that of normal myocardium. Myocardial water and protein contents were similar in the normal and stunned myocardium. Water content in the infarcted myocardium (80.8 +/- 2%) was significantly greater (P < .05) than in the normal (72.7 +/- 1.3%), and protein content of 18.5 +/- 0.7% was significantly lower (P < .05) than the normal (21.4 +/- 0.8%). Lipid content was increased in the stunned (8.5 +/- 0.5%) and virtually absent in the infarcted myocardium (0.8 +/- 0.3%) compared with normal (5.5 +/- 0.6%).
We conclude that acoustic propagation properties can identify stunned and infarcted myocardium and may be related to biochemical/morphological differences.
识别存活但顿抑的心肌仍然是一个主要问题。由于顿抑心肌导致心肌功能受损但无任何结构损伤,而梗死心肌会引起主要的结构破坏,我们推测声学特性可以区分这两种损伤。
对麻醉开胸犬进行左前降支冠状动脉完全闭塞15分钟(顿抑组,n = 7)和90分钟(梗死组,n = 8),随后再灌注3小时。回旋支冠状动脉灌注区域(n = 15)作为正常对照组织。使用工作频率为100 MHz的扫描激光声学显微镜和工作频率为4至7 MHz的研究超声系统对心肌区域进行定量评估。测定了四个超声参数:衰减系数(每单位距离损失的指标)、传播速度、称为异质性指数(HI)的传播速度空间变化以及5 MHz时的超声背向散射(IBR5)。还测定了正常、顿抑和梗死心肌的心肌水、脂质和蛋白质含量。正常心肌的衰减系数(179±20 dB/cm)显著高于顿抑心肌(136±7 dB/cm,P <.001)和梗死心肌(130±8 dB/cm,P <.001)。正常心肌的传播速度(1597±6 m/s)与顿抑心肌(1600±6 m/s)相似,且显著高于梗死心肌(1575±7 m/s,P <.001)。对于厚度为75至100微米的标本,HI在正常心肌(5.0±0.8 m/s)和顿抑心肌(7.5±2.3 m/s,P <.05)之间增加了33%。然而,梗死心肌(5.8±2.0 m/s) 的HI与正常心肌(5.0±0.8 m/s)基本相同。正常心肌的IBR5(-47.1±1.0 dB)与顿抑心肌(-46.8±0.9 dB)无显著差异。梗死心肌的IBR5(-42.4±1.0 dB)显著高于正常心肌。正常和顿抑心肌的心肌水和蛋白质含量相似。梗死心肌中的水含量(80.8±2%)显著高于正常心肌(72.7±1.3%,P <.05),蛋白质含量为18.5±0.7%显著低于正常心肌(21.4±0.8%,P <.05)。与正常心肌(5.5±0.6%)相比,顿抑心肌中的脂质含量增加(8.5±0.5%),而梗死心肌中几乎不存在脂质(0.8±0.3%)。
我们得出结论,声学传播特性可以识别顿抑和梗死心肌,并且可能与生化/形态学差异有关。