Myocardial Fibrosis Distribution and Electrical Activation Patterns in Left Bundle Branch Block: Integration of Non-Invasive Electrocardiographic Activation Mapping and Cardiovascular Magnetic Resonance Imaging Late Gadolinium Enhancement.

BACKGROUND

Left bundle branch block (LBBB) is associated with heterogeneous electrical and structural remodeling; however, the interplay between myocardial fibrosis and conduction abnormalities remains incompletely characterized.

AIMS: To investigate fibrosis distribution and electrical activation patterns in LBBB patients with preserved (LBBB idiopathic [LBBBi]) and reduced (15 cardiac resynchronization therapy [CRT] recipients) systolic function using noninvasive electrocardiographic activation mapping (NEAM) and late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR).

MATERIALS AND

METHODS

Twenty LBBB patients (15 CRT, 5 LBBBi) and five healthy volunteers (HV) underwent NEAM and LGE-CMR. Global and segmental activation times (epicardial/endocardial ATs), fibrosis volume, and latest activation zone (LAZ) localization were analyzed. Segmental correlations between fibrosis and activation parameters were evaluated in the CRT group.

RESULTS

CRT patients demonstrated longer total ATs than LBBBi (176 ± 18 vs. 148 ± 10 ms, p < 0.001). LAZ localized to segments 5-6 in 80% of cases, with displacement in three CRT patients with midwall fibrosis. Fibrosis (17.4 [7.3-53.7] cm³) was present in 86.7% of CRT patients but absent in LBBBi and HV. Global ATs showed no correlation with fibrosis volume (r = -0.159, p = 0.571), but segmental fibrosis volume moderately correlated with epicardial (r = 0.37, p < 0.001) and endocardial (r = 0.307, p < 0.001) ATs. Most segments in both groups demonstrated prolonged epicardial conduction, while endocardial conduction remained near-normal.

CONCLUSION

Integrated NEAM-LGE-CMR analysis demonstrated that myocardial fibrosis modulates local conduction abnormalities without influencing global activation times. All LBBB patients exhibit prolonged epicardial activation time regardless of fibrosis burden, while endocardial activation time remains preserved in most left ventricular segments.