Tsutsui H, Uematsu M, Shimizu H, Yamagishi M, Tanaka N, Matsuda H, Miyatake K
Cardiology Division of Medicine, National Cardiovascular Center, Suita, Osaka, Japan.
J Am Coll Cardiol. 1998 Jan;31(1):89-93. doi: 10.1016/s0735-1097(97)00430-0.
We tested the hypothesis that ischemic myocardium can be sensitively detected using tissue Doppler-derived myocardial velocity gradient (MVG) by a dobutamine challenge.
Although tissue Doppler imaging (TDI) has recently emerged to quantify regional myocardial contraction, increased translational motion during a dobutamine challenge may affect the measurements. MVG is an indicator of regional myocardial contraction independent of the translational motion.
We studied 19 patients with (n = 13) and without (n = 6) confirmed single-vessel coronary artery disease. Left ventricular short-axis tissue Doppler images were obtained along with conventional echocardiograms during a submaximal two-step dobutamine challenge (10 and 30 microg/kg body weight per min). Endocardial velocity as well as MVG were derived from TDI using computer analysis in the anteroseptal and posterior segments and were compared with visual interpretation.
MVG demonstrated a significant dose-responsive increase in the nonischemic segments (anteroseptal: 2.6 +/- 0.8/s to 6.0 +/- 1.0/s [mean +/- SD], p < 0.05; posterior: 3.9 +/- 0.7/s to 7.6 +/- 1.8/s, p < 0.05) but remained unchanged in the ischemic segments (anteroseptal: 2.5 +/- 0.8/s to 2.7 +/- 0.7/s, p = NS; posterior: 3.4 +/- 1.0/s to 4.1 +/- 0.9/s, p = NS). Endocardial velocity failed to clearly demonstrate the differing responses between the nonischemic (anteroseptal: -2.3 +/- 1.2 to -2.7 +/- 1.6 cm/s, p = NS; posterior: 3.8 +/- 1.1 to 73 +/- 2.7 cm/s, p < 0.05) and ischemic segments (anteroseptal: -2.1 +/- 0.5 to -2.8 +/- 0.8 cm/s, p = NS; posterior: 4.2 +/- 0.8 to 6.5 +/- 2.6 cm/s, p = NS). Wall motion abnormality was hardly detectable with visual interpretation (wall motion score range 1.00 to 1.33).
Abnormal segments could be sensitively detected by using MVG in a submaximal dobutamine challenge, even where conventional methods failed to detect the abnormality.
我们检验了如下假设,即通过多巴酚丁胺激发试验,利用组织多普勒衍生的心肌速度梯度(MVG)能够灵敏地检测出缺血心肌。
尽管组织多普勒成像(TDI)最近已用于量化局部心肌收缩,但多巴酚丁胺激发试验期间平移运动的增加可能会影响测量结果。MVG是一种独立于平移运动的局部心肌收缩指标。
我们研究了19例患者,其中13例确诊为单支冠状动脉疾病,6例未患该病。在次极量两步多巴酚丁胺激发试验(每分钟10和30微克/千克体重)期间,获取左心室短轴组织多普勒图像以及传统超声心动图。使用计算机分析从前间隔和后段的TDI得出心内膜速度以及MVG,并与视觉判读结果进行比较。
MVG在非缺血段显示出显著的剂量反应性增加(前间隔:2.6±0.8/s至6.0±1.0/s[平均值±标准差],p<0.05;后段:3.9±0.7/s至7.6±1.8/s,p<0.05),但在缺血段保持不变(前间隔:2.5±0.8/s至2.7±0.7/s,p=无显著性差异;后段:3.4±1.0/s至4.1±0.9/s,p=无显著性差异)。心内膜速度未能清晰显示非缺血段(前间隔:-2.3±1.2至-2.7±1.6厘米/秒,p=无显著性差异;后段:3.8±1.1至73±2.7厘米/秒,p<0.05)和缺血段(前间隔:-2.1±0.5至-2.8±0.8厘米/秒,p=无显著性差异;后段:4.2±0.8至6.5±2.6厘米/秒,p=无显著性差异)之间的不同反应。通过视觉判读很难检测到室壁运动异常(室壁运动评分范围为1.00至1.33)。
在次极量多巴酚丁胺激发试验中,即使传统方法未能检测到异常情况,使用MVG也能灵敏地检测出异常节段。