Beyond conduction impairment: Unveiling the profound myocardial injury in left bundle branch block
Xiaoxian Wang1, Beibei Ge1, Changqing Miao2
1Department of Ultrasound Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, People's Republic of China.
Insights
Left bundle branch block (LBBB) causes significant heart muscle injury and dysfunction. This study reveals LBBB-induced cardiomyopathy involves fibrosis and Purkinje fiber damage, worsening over time.
Area of Science:
- Cardiology
- Pathology
- Medical Imaging
Background:
- Left bundle branch block (LBBB) is a common conduction disorder with unclear links to cardiomyopathy.
- The pathological mechanisms of LBBB-induced cardiomyopathy (LBBB-CM) are not well understood.
Purpose of the Study:
- To investigate the timeline of LBBB leading to left ventricular dysfunction.
- To elucidate the pathological mechanisms underlying LBBB-CM.
Main Methods:
- An LBBB canine model was created via main left bundle branch trunk ablation.
- Serial echocardiography, ECG, and SPECT imaging were performed over 12 months.
- Cardiac tissue analysis included histology, Purkinje fiber staining, and connexin43 expression.
Main Results:
- LBBB induction resulted in myocardial fibrosis and Purkinje fiber degeneration (fatty changes, vacuolization, fibrosis).
- Connexin43 protein expression was downregulated in affected Purkinje fibers.
- Progressive left ventricular dysfunction was observed over 12 months, correlating with myocardial dysfunction, hypoperfusion, and fibrosis.
Conclusions:
- LBBB can cause significant myocardial injury beyond conduction abnormalities.
- The study clarifies the temporal progression and pathological alterations in LBBB-CM.
- Findings provide insights into LBBB-CM mechanisms and clinical relevance.
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 pathologic 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 the pathologic mechanism of LBBB-CM.
Methods:
LBBB model was established through main left bundle branch trunk ablation in 14 canines. All LBBB dogs underwent transesophageal echocardiography and electrocardiography before ablation and at 1 month, 3 months, 6 months, and 12 months after LBBB induction. Single-photon emission computed tomography imaging was performed at 12 months. We then harvested the heart from all LBBB dogs and 14 healthy adult dogs as normal controls for anatomic observation, Purkinje fiber staining, histologic staining, and connexin43 protein expression quantitation.
Results:
LBBB induction caused significant fibrotic changes in the endocardium and mid-myocardium. Purkinje fibers exhibited fatty degeneration, vacuolization, and fibrosis along with downregulated connexin43 protein expression. During a 12-month follow-up, left ventricular 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.
Conclusion:
LBBB may lead to profound myocardial injury beyond its conduction impairment effects. The temporal progression of left ventricular dysfunction and the pathologic 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.
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