Department of Cardiology, University Heart Center Hamburg, Hamburg, Germany.
J Cardiovasc Electrophysiol. 2010 Jan;21(1):70-7. doi: 10.1111/j.1540-8167.2009.01579.x. Epub 2009 Sep 1.
The mechanism of mechanical dyssynchrony in postinfarction patients with a narrow QRS complex is not defined but essential for cardiac resynchronization therapy (CRT).
Left ventricular electrical activation and subsequent wall motion were recorded for 16 patients with ischemic cardiomyopathy during intrinsic rhythm using a modified NOGA electromechanical mapping system. Ten patients presented mechanical dyssynchrony on tissue Doppler imaging, while 6 patients served as control subjects. The local activation time (LAT) was set by the maximum downslope of the unipolar electrogram. Local wall motion time (LMT) was defined as the time needed for the catheter tip to traverse half of its maximum inward deflection during systole. LAT and LMT were measured relative to the onset of the QRS complex. Electrical activation showed a septal-to-lateral pattern in all patients with a mean endocardial activation time of 65 +/- 13 ms. Control subjects exhibited 97.5% of all LMTs <290 +/- 17 ms. Delayed motion areas (cut-off LMT > 300 ms) showed no slowing of conduction. Wall motion time corrected for differences in electrical activation (LMT-LAT) was significantly longer in delayed (289 +/- 34 ms) than in regular (204 +/- 24 ms) motion areas (P = 0.002). Delayed motion segments were hypokinetic on echocardiography and presented a lower maximum inward motion (9.9 +/- 1.1 mm) compared to regular segments (10.9 +/- 1.2 mm) on electromechanical maps (P = 0.004). Viability, however, was preserved with unipolar and bipolar voltage amplitude >7 mV and >1.5 mV for 79% of all delayed motion areas.
Dyssynchronous segments of an ischemic myocardium show unimpaired local activation but slow wall motion, thereby limiting the benefit of ventricular preexcitation via CRT.
在 QRS 波群狭窄的心肌梗死后患者中，机械不同步的机制尚不清楚，但对心脏再同步治疗（CRT）至关重要。
使用改良的诺加电机械映射系统，在 16 例缺血性心肌病患者固有节律时记录左心室电活动和随后的壁运动。10 例患者在组织多普勒成像上表现出机械不同步，而 6 例患者作为对照。局部激活时间（LAT）由单极电图的最大下斜率设定。局部壁运动时间（LMT）定义为导管尖端在收缩期间穿过其最大向内偏移的一半所需的时间。LAT 和 LMT 相对于 QRS 波群的起始进行测量。电激活在所有患者中均显示出从间隔到侧壁的模式，平均心内膜激活时间为 65±13ms。对照受试者的所有 LMT 中有 97.5%<290±17ms。延迟运动区（LMT>300ms 的截止值）没有显示传导减慢。校正电激活差异后的壁运动时间（LMT-LAT）在延迟运动区（289±34ms）明显长于规则运动区（204±24ms）（P=0.002）。延迟运动节段在超声心动图上呈低动力，与规则运动节段（电机械图上的 10.9±1.2mm）相比，最大向内运动较小（9.9±1.1mm）（P=0.004）。然而，在所有延迟运动区域的 79%中，单极和双极电压幅度>7mV 和>1.5mV 保留了活力。
缺血心肌的不同步节段显示局部激活无损伤，但壁运动缓慢，从而限制了 CRT 通过心室预激的获益。
