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Delayed depolarization and histologic abnormalities underlie the Brugada syndrome
Bortolo Martini1, Nicolò Martini2, Luca De Mattia3
1Cardiac Unit, Alto Vicentino Hospital, Santorso, Italy.
Pacing and Clinical Electrophysiology : PACE
|December 21, 2022
Summary
Brugada syndrome (BrS) is a cardiac condition with unclear causes. Research indicates structural changes in the right ventricle, not just functional issues, are key to understanding BrS pathophysiology.
Area of Science:
- Cardiology
- Electrophysiology
- Pathophysiology
Background:
- Brugada syndrome (BrS) pathophysiology remains incompletely understood, with ongoing debate between functional/repolarization and organic/depolarization theories.
- Initial theories focused on functional aspects, but emerging evidence points towards an organic substrate.
Purpose of the Study:
- To review the current understanding of Brugada syndrome pathophysiology.
- To integrate findings from various diagnostic modalities to elucidate the underlying mechanisms of BrS.
Main Methods:
- Review of data from electrocardiography, endocavitary tracings, electroanatomic mapping, and histopathology.
- Integration of findings from echocardiography and cardiac magnetic resonance imaging (CMRI).
Main Results:
- Brugada syndrome is characterized by structural myocardial changes, primarily in the right ventricular outflow tract (RVOT) and right ventricle (RV).
- Delayed conduction is observed at these structural sites, contributing to the arrhythmogenic substrate.
- Conduction disorders at various levels are associated with an increased risk of major arrhythmic events.
Conclusions:
- Brugada syndrome is primarily an organic disorder characterized by structural myocardial abnormalities and conduction disturbances.
- Understanding these structural and electrophysiological features is crucial for risk stratification and management of BrS patients.
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