Dohi Kaoru, Pinsky Michael R, Kanzaki Hideaki, Severyn Donald, Gorcsan John
Division of Cardiovascular Disease, Critical Care Medicine Department, University of Pittsburgh, Pittsburgh, Pennsylvania 15213-2582, USA.
J Am Soc Echocardiogr. 2006 May;19(5):475-82. doi: 10.1016/j.echo.2005.10.017.
Our objective was to test the hypothesis that novel angle-corrected radial strain imaging can quantify left ventricular dyssynchrony associated with contractile impairment and improved with biventricular pacing. Eight open-chest dogs were studied by novel angle-corrected color-coded radial strain imaging and high-fidelity pressure-conductance catheters recording pressure-volume loops. Heart rate was controlled by right atrial pacing and all timing intervals were corrected by R-R interval (corrected interval = measured interval/(R-R interval)(1/2)). Left bundle branch block, simulated by right ventricular free wall pacing, resulted in marked radial dyssynchrony, which we defined as maximal time difference between peak segmental strain, from 39 +/- 17 to 354 +/- 49 milliseconds and stroke work decreased from 157 +/- 40 to 60 +/- 37 mJ, (P < .005 vs baseline). Depression of contractility by high-dose esmolol (end-systolic pressure-volume relationship from 5.7 +/- 2.4 to 3.6 +/- 1.0 mm Hg/mL) was associated with augmented dyssynchrony to 388 +/- 53 milliseconds (P < .05 vs baseline right ventricular pacing). Biventricular pacing improved dyssynchrony to 55 +/- 19 milliseconds and stroke work to 143 +/- 33 mJ (P < .05 vs right ventricular pacing). Changes in radial dyssynchrony correlated significantly with 6-site average regional strain (r = -0.93 +/- 0.05 individually, r = 0.80 overall) and stroke work (r = -0.88 +/- 0.12 individually, r = -0.82 overall). Angle-corrected radial strain imaging has clinical potential to quantify mechanical dyssynchrony and effects of biventricular pacing.
新型角度校正径向应变成像能够量化与收缩功能受损相关的左心室不同步，并通过双心室起搏得到改善。我们使用新型角度校正彩色编码径向应变成像和记录压力-容积环的高保真压力-电导导管对8只开胸犬进行了研究。通过右心房起搏控制心率，所有时间间期均通过R-R间期进行校正（校正间期=测量间期/（R-R间期）^(1/2)）。通过右心室游离壁起搏模拟左束支传导阻滞，导致明显的径向不同步，我们将其定义为节段峰值应变之间的最大时间差，从39±17毫秒增加到354±49毫秒，每搏功从157±40毫焦降低到60±37毫焦（与基线相比，P<0.005）。高剂量艾司洛尔降低收缩力（收缩末期压力-容积关系从5.7±2.4毫米汞柱/毫升降至3.6±1.0毫米汞柱/毫升）与不同步增加至388±53毫秒相关（与基线右心室起搏相比，P<0.05）。双心室起搏使不同步改善至55±19毫秒，每搏功增加至143±33毫焦（与右心室起搏相比，P<0.05）。径向不同步的变化与6个部位的平均区域应变显著相关（个体r=-0.93±0.05，总体r=0.80）和每搏功（个体r=-0.88±0.12，总体r=-0.82）。角度校正径向应变成像在量化机械不同步和双心室起搏效果方面具有临床应用潜力。
