Is left bundle branch block pattern on the ECG caused by variable ventricular activation sequence?

Abstract

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.

Left-axis deviation in patients with nonischemic heart failure and left bundle branch block is a purely electrical phenomenon

“…Instead, the LV was consistently activated through transmyocardial conduction. 18 Our mapping study does not support the hypothesis of residual anterograde Purkinje conduction as the etiology for LAD in patients with LBBB. In patients with NA, activation during spontaneous rhythm and during RVAP differed in terms of pattern but not duration.…”

Value of q waves in lateral and left precordial leads in patients with left bundle branch block to predict the response to cardiac resynchronization therapy

“…Even though scar burden and distribution can be determined more accurately using imaging modalities such as cardiac magnetic resonance late gadolinium enhancement (CMR‐LGE) or SPECT MPI, 17,18 the standard 12‐lead ECG, as a screening tool, is widely applied with the advantage of being easily available. Strauss et al showed that chronic myocardial scars could be quantified using the ECG despite the presence of LBBB 19,20 .…”

Reversible T-wave inversions during left bundle branch area pacing

“…The amplification of repolarization gradients between segments of the left ventricle is the electrophysiological basis for T-wave memory. The LV was activated only through transmyocardial conduction starting after the RV activation onset, and then the activation spread centrifugally over the anterior and inferior wall in patients with LBBB-like patterns [19]. The maximum repolarization gradients in patients with CLBBB are the anterior and inferior walls.…”