BACKGROUND The presence and extent of ventricular dyssynchrony are currently assessed from the QRS complex morphology and width. However, similar electrocardiography (ECG) pattern may be caused by variable ventricular activation sequence. This may then contribute to interindividually different response to cardiac resynchronization therapy (CRT). METHODS Electroanatomical mapping and magnetic resonance imaging scan were performed in 11 patients with left bundle branch block (LBBB, QRS 170 ± 14 ms) and heart failure of ischemic (coronary artery disease (CAD), n = 2) and nonischemic (dilated cardiomyopathy (DCM), n = 9) etiology. Ventricular activation sequence was studied during LBBB and final CRT programming. Presence and extent of scarring were analyzed in the 17-segment left-ventricular (LV) model. RESULTS Regardless of etiology, presence of typical LBBB was associated with diffuse prolongation of impulse conduction with right-to-left activation sequence. Basal lateral wall was constant site of late activation. This activation pattern was present in "true LBBB," but also in LBBB-like pattern (persistent S wave in V5-6) and left axis deviation. Activation started in right vetricular (RV) apex in patients with left axis deviation at RV free wall in normal axis. Individuals with CAD and DCM patient displayed focal scar. Despite that they exhibited typical LBBB and activation sequence mirrored findings in other LBBB individuals. Reverse remodeling (∆LVESV > 15% after 6 months) was evident in 10 patients. CONCLUSIONS Both typical LBBB and LBBB-like pattern might be associated with constant activation sequence regardless of etiology and scar localization. Activation initiation in RV apex, not LV activation sequence can be surrogate for left axis deviation. CRT caused inter- and intraventricular LV resynchronization without significantly changed RV activation sequence and duration.

中文翻译：

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心电图上的左束支传导阻滞模式是否由可变的心室激活序列引起？

背景技术目前，根据QRS复合体的形态和宽度来评估心室不同步的存在和程度。但是，类似的心电图（ECG）模式可能是由可变的心室激活序列引起的。然后，这可能有助于个体之间对心脏再同步治疗（CRT）的不同反应。方法对11例左束支传导阻滞（LBBB，QRS 170±14 ms），缺血性（冠状动脉疾病（CAD），n = 2）和非缺血性（扩张型心肌病（ DCM），n = 9）病因。在LBBB和最终CRT编程期间研究了心室激活序列。在17段左心室（LV）模型中分析了疤痕的存在和程度。结果无论病因如何，典型LBBB的存在与从右到左激活序列的脉冲传导的弥漫性延长有关。基底侧壁是晚期激活的恒定部位。此激活模式存在于“真实LBBB”中，但也存在于类似LBBB的模式中（V5-6中的持续S波）和左轴偏移。在正常轴右室游离壁处左轴偏离的患者中，右心室（RV）顶点开始激活。患有CAD和DCM的患者表现出局灶性瘢痕。尽管它们表现出典型的LBBB，并且激活序列在其他LBBB个体中也有类似的发现。10例患者出现了逆重塑（6个月后∆LVESV> 15％）。结论无论病因和瘢痕定位如何，典型的LBBB和LBBB样模式都可能与恒定的激活序列有关。RV顶点的激活起始，而不是LV激活序列，可以代替左轴偏移。CRT引起心室内和心室内左室再同步，而RV的激活顺序和持续时间没有明显改变。