Department of Cardiology, Motol University Hospital and 2nd Faculty of Medicine, Charles University, Prague, Czech Republic.
Department of Radiology, Motol University Hospital and 2nd Faculty of Medicine, Charles University, Prague, Czech Republic.
Pacing Clin Electrophysiol. 2020 May;43(5):486-494. doi: 10.1111/pace.13914. Epub 2020 Apr 28.
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).
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.
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.
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.
目前,通过 QRS 复合波形态和宽度来评估心室失同步的存在和程度。然而,相似的心电图(ECG)模式可能是由不同的心室激活顺序引起的。这可能会导致心脏再同步治疗(CRT)的个体间反应不同。
对 11 例左束支传导阻滞(LBBB,QRS 波 170±14ms)伴心力衰竭的患者进行了电解剖标测和磁共振成像扫描,心力衰竭的病因包括缺血性(冠状动脉疾病(CAD),n=2)和非缺血性(扩张型心肌病(DCM),n=9)。在 LBBB 期间和最终 CRT 编程时研究心室激活顺序。在 17 节段的左心室(LV)模型中分析瘢痕的存在和程度。
无论病因如何,典型 LBBB 的存在与冲动传导的弥漫性延长和从右向左的激活顺序相关。基底外侧壁是迟发激活的恒定部位。这种激活模式存在于“真正的 LBBB”中,但也存在于 LBBB 样模式(V5-6 导联持续 S 波)和左轴偏离。在左轴偏离的患者中,激活始于右心室(RV)心尖,而在正常轴的 RV 游离壁则始于 RV 心尖。CAD 和 DCM 患者表现为局灶性瘢痕。尽管他们表现出典型的 LBBB 和激活顺序与其他 LBBB 患者的发现相吻合。10 例患者在 6 个月后出现 LVESV 减少>15%的逆重构。
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顺序相关。RV 心尖的激活起始,而不是 LV 的激活顺序,可以作为左轴偏离的替代指标。CRT 导致室间和室内 LV 再同步,而 RV 激活顺序和持续时间没有明显改变。