心脏衰竭的原位兴奋和收缩及心脏再同步化治疗的效果:心电图成像和斑点跟踪超声心动图的应用

Christopher M. Andrews, G. Singh, Y. Rudy
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引用次数: 1

摘要

尽管心脏再同步治疗(CRT)治疗心力衰竭(HF)取得了成功,但无反应率仍为30%。CRT的改进需要了解反向重构以及同步性的电气和机械测量之间的关系。目的是利用心电图成像(ECGI,一种非侵入性心脏电生理标测方法)和斑点跟踪超声心动图(STE)来研究HF的生理学和CRT诱导的反向重构。我们使用ECGI和STE对30名患者(63%为男性,平均年龄63.7岁)进行了纵向成像。我们量化了CRT诱导的机电参数重塑,并评估了一个新的指标,即机电延迟(EMD,从激活到峰值收缩的延迟)。我们还使用ECGI和STE测量了不同步性,并比较了它们预测CRT反应的有效性。与对照组相比,HF患者的EMD值升高。然而,EMD值取决于激活序列(CRT起搏与非起搏),这表明EMD不是局部组织固有的,而是受到诸如相反的壁收缩等因素的影响。CRT治疗6个月后,与基线治疗前相比,患者的自然节律收缩增加(基线:−8.55%,6个月:−10.14%,p=0.008)。他们在左心室起搏导线位置的复极也延长。平均左心室外侧电激活时间和右心室电激活时间之间的CRT前延迟是CRT有益降低左心室收缩末期容积的最佳预测因素(Spearman’s Rho:-0.722,p<0.001);它优于机械指标和12导联心电图标准。HF患者有异常的EMD。EMD取决于激活序列,并且不能预测对CRT的响应。ECGI测量的左心室激活延迟是CRT患者选择的有效指标。CRT使收缩功能持续改善。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Excitation and Contraction of the Failing Human Heart In Situ and Effects of Cardiac Resynchronization Therapy: Application of Electrocardiographic Imaging and Speckle Tracking Echo-Cardiography
Despite the success of cardiac resynchronization therapy (CRT) for treating heart failure (HF), the rate of nonresponders remains 30%. Improvements to CRT require understanding of reverse remodeling and the relationship between electrical and mechanical measures of synchrony. The objective was to utilize electrocardiographic imaging (ECGI, a method for noninvasive cardiac electrophysiology mapping) and speckle tracking echocardiography (STE) to study the physiology of HF and reverse remodeling induced by CRT. We imaged 30 patients (63% male, mean age 63.7 years) longitudinally using ECGI and STE. We quantified CRT-induced remodeling of electromechanical parameters and evaluated a novel index, the electromechanical delay (EMD, the delay from activation to peak contraction). We also measured dyssynchrony using ECGI and STE and compared their effectiveness for predicting response to CRT. EMD values were elevated in HF patients compared to controls. However, the EMD values were dependent on the activation sequence (CRT-paced vs. un-paced), indicating that the EMD is not intrinsic to the local tissue, but is influenced by factors such as opposing wall contractions. After 6 months of CRT, patients had increased contraction in native rhythm compared to baseline pre-CRT (baseline: −8.55%, 6 months: −10.14%, p = 0.008). They also had prolonged repolarization at the location of the LV pacing lead. The pre-CRT delay between mean lateral LV and RV electrical activation time was the best predictor of beneficial reduction in LV end systolic volume by CRT (Spearman’s Rho: −0.722, p < 0.001); it outperformed mechanical indices and 12-lead ECG criteria. HF patients have abnormal EMD. The EMD depends upon the activation sequence and is not predictive of response to CRT. ECGI-measured LV activation delay is an effective index for CRT patient selection. CRT causes persistent improvements in contractile function.
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