Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
JACC Cardiovasc Imaging. 2009 Dec;2(12):1350-6. doi: 10.1016/j.jcmg.2009.07.012.
We hypothesize that left ventricular (LV) segmental dyssynchrony, quantified by paradoxical systolic wall thinning, determines changes in global LV performance in a model of canine right ventricular (RV) pacing-induced dyssynchrony and the response to cardiac resynchronization therapy (CRT).
Quantification of LV dyssynchrony is important to assess the impact of CRT.
Seven pentobarbital-anesthetized open-chest dogs had LV pressure-volume relations and mid-LV short-axis echocardiographic speckle tracking radial strain imaging during right atrial (RA) pacing, RV pacing to simulate left bundle branch block, and CRT using RV pacing plus either LV free-wall (CRTfw) and apical (CRTa) pacing. The area under the segmental LV time-radial strain positive and negative curves defined global thickening and thinning, respectively. Dyssynchrony was defined as the maximum time difference between earliest and latest peak segmental positive strain among 6 radial sites.
RA pacing had minimal dyssynchrony (58 + or - 40 ms). RV pacing induced both dyssynchrony (213 + or - 67 ms, p < 0.05) and reduced LV stroke work (SW) (67 + or - 51 mJ, p < 0.05). CRTfw and CRTa decreased dyssynchrony (116 + or - 47 ms and 50 + or - 34 ms, respectively, p < 0.05 vs. RV pacing), but only CRTa restored LV SW to RA pacing levels. RV pacing decreased global thickening (129 + or - 87%.ms) compared with RA pacing (258 + or - 133%.ms, p < 0.05), whereas CRTfw and CRTa restored regional thickening to RA pacing levels (194 + or - 83%.ms and 230 + or - 76%.ms, respectively). The sum of thickening and thinning during RV (230 + or - 88%.ms vs. 258 + or - 133%.ms, p < 0.05) correlated (r = 0.98) with RA thickening, suggesting that all the loss of LV function was due to thinning.
Dyssynchrony causes proportional changes in regional LV wall thinning and global LV SW that were reversed by CRT, suggesting that dyssynchrony impairs LV systolic function by causing paradoxical regional wall thinning and that CRT effectiveness can be monitored by its reversal. Thus, monitoring paradoxical regional thinning reversal may be used to define CRT effectiveness.
我们假设左心室（LV）节段性不同步，通过矛盾性收缩期壁变薄来量化，可以确定犬右心室（RV）起搏诱导不同步模型中整体 LV 性能的变化以及对心脏再同步治疗（CRT）的反应。
量化 LV 不同步对于评估 CRT 的影响很重要。
在七只戊巴比妥麻醉开胸犬中，在右心房（RA）起搏期间进行 LV 压力-容积关系和中 LV 短轴超声心动图斑点追踪径向应变成像，进行 RV 起搏以模拟左束支传导阻滞，以及使用 RV 起搏加 LV 游离壁（CRTfw）和心尖（CRTa）起搏进行 CRT。节段性 LV 时间-径向应变正曲线和负曲线下的面积分别定义为整体增厚和变薄。不同步定义为 6 个径向部位中最早和最晚节段性正向应变之间的最大时间差。
RA 起搏仅有轻微的不同步（58 ± 40 ms）。RV 起搏不仅诱导了不同步（213 ± 67 ms，p < 0.05），还降低了 LV 每搏功（SW）（67 ± 51 mJ，p < 0.05）。CRTfw 和 CRTa 降低了不同步（116 ± 47 ms 和 50 ± 34 ms，分别与 RV 起搏相比，p < 0.05），但只有 CRTa 将 LV SW 恢复到 RA 起搏水平。与 RA 起搏相比，RV 起搏降低了整体增厚（129 ± 87%.ms）（258 ± 133%.ms，p < 0.05），而 CRTfw 和 CRTa 将局部增厚恢复到 RA 起搏水平（194 ± 83%.ms 和 230 ± 76%.ms，分别）。RV 期间的增厚和变薄之和（230 ± 88%.ms 与 258 ± 133%.ms，p < 0.05）与 RA 增厚相关（r = 0.98），表明 LV 功能的所有损失都归因于变薄。
不同步导致区域 LV 壁变薄和整体 LV SW 的比例变化，CRT 逆转了这些变化，这表明不同步通过引起矛盾性的区域性壁变薄来损害 LV 收缩功能，并且 CRT 的有效性可以通过其逆转来监测。因此，监测矛盾性区域性变薄的逆转可能用于定义 CRT 的有效性。
