Left-axis deviation in patients with nonischemic heart failure and left bundle branch block is a purely electrical
Saer Abu-Alrub1, Marc Strik2, Peter Huntjens3
1Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; Cardiology Department, CHU Clermont-Ferrand, Clermont-Ferrand, France.
Background:
Possible mechanisms of left-axis deviation (LAD) in the setting of left bundle branch block (LBBB) include differences in cardiac electrophysiology, structure, or anatomic axis.
Objective:
The purpose of this study was to clarify the mechanism(s) responsible for LAD in patients with LBBB.
Methods:
Twenty-nine patients with nonischemic cardiomyopathies and LBBB underwent noninvasive electrocardiographic imaging (ECGi), cardiac computed tomography, and magnetic resonance imaging in order to define ventricular electrical activation, characterize cardiac structure, and determine the cardiac anatomic axis.
Results:
Sixteen patients had a normal QRS axis (NA) (mean axis 8° ± 23°), whereas 13 patients had LAD (mean axis -48° ± 13°; P <.001). Total activation times were longer in the LAD group (112 ± 25 ms vs 91 ± 14 ms; P = .01) due to delayed activation of the basal anterolateral region (107 ± 10 ms vs 81 ± 17 ms; P <.001). Left ventricular (LV) activation in patients with LAD was from apex to base, in contrast to a circumferential pattern of activation in patients with NA. Apex-to-base delay was longer in the LA group (95 ± 13 ms vs 64 ± 21 ms; P <.001) and correlated with QRS frontal axis (R2 = 0.67; P <.001). Both groups were comparable with regard to LV end-diastolic volume (295 ± 84 mL vs LAD 310 ± 91 mL; P = .69), LV mass (177 ± 33 g vs LAD 180 ± 37 g; P = .83), and anatomic axis.
Conclusion:
LAD in LBBB appears to be due to electrophysiological abnormalities rather than structural factors or cardiac anatomic axis.
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