Beyond Conduction Impairment: Unveiling the Profound Myocardial Injury in Left Bundle Branch Block

Abstract

BACKGROUND

Left bundle branch block (LBBB) represents a frequently encountered conduction system disorder. Despite its widespread occurrence, a continual dilemma persists regarding its intricate association with underlying cardiomyopathy and its pivotal role in the initiation of dilated cardiomyopathy. The pathological alterations linked to LBBB-induced cardiomyopathy (LBBB-CM) have remained elusive.

OBJECTIVE

This study sought to investigate the chronologic dynamics of LBBB to left ventricular dysfunction and pathological mechanism of LBBB-CM.

METHODS

LBBB model was established through the main left bundle branch trunk ablation in 14 canines. All LBBB dogs underwent transesophageal echocardiography and electrocardiogram before ablation and at 1^st, 3^rd, 6^th and 12^th month following LBBB induction. Single photon emission computed tomography imaging was performed at the 12^th month. Then, we harvested the heart from all LBBB dogs and 14 healthy adult dogs as normal control for anatomical observation, Purkinje fibers staining, histological staining, and Connexin43 (Cx43) protein expression quantitation.

RESULTS

LBBB induction caused significant fibrotic changes in the endocardium and mid-myocardium. Purkinje fibers exhibited fatty degeneration, vacuolization, fibrosis, along with down-regulated Cx43 protein expression. Over a 12-month follow-up, LV dysfunction progressively worsened, peaking at the end of the observation period. The association between myocardial dysfunction, hypoperfusion, and fibrosis was observed in the LBBB-afflicted canines.

CONCLUSIONS

LBBB may lead to profound myocardial injury beyond its conduction impairment effects. The temporal progression of LV dysfunction and the pathological alterations observed shed light on the complex relationship between LBBB and cardiomyopathy. These findings offer insights into potential mechanisms and clinical implications of LBBB-CM.