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Left Ventricular Abnormal Substrate in Brugada Syndrome.

Ghassen Cheniti¹, Michel Haissaguerre¹, Christian Dina²

¹Department of Electrophysiology and Cardiac Stimulation, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France; Institut Hospitalo-Universitaire Liryc, Electrophysiology and Heart Modeling Institute, Pessac, France; Université de Bordeaux, CRCTB, INSERM, U1045, Pessac, France.

JACC. Clinical Electrophysiology

|July 22, 2023

Summary

This summary is machine-generated.

Brugada syndrome (BrS) can involve abnormal electrical substrate in the left ventricle (LV) epicardium, not just the right ventricle (RV). This finding is linked to SCN5A mutations and suggests a broader substrate in BrS patients with arrhythmias.

Keywords:

Brugada syndrome SCN5A mutation ventricular fibrillation

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Area of Science:

Cardiology
Electrophysiology
Genetics

Background:

Brugada syndrome (BrS) is characterized by slow-conductive structural abnormalities in the right ventricle (RV) epicardium.
The presence and extent of similar abnormalities in the left ventricle (LV) epicardium remain largely uninvestigated.

Purpose of the Study:

To investigate and characterize the extent of epicardial substrate abnormalities in patients diagnosed with Brugada syndrome.
To determine if abnormal substrate is present in the left ventricle (LV) of BrS patients.

Main Methods:

Evaluated 22 BrS patients with recurrent ventricular arrhythmias.
Performed high-density biventricular epicardial mapping to identify fragmented electrograms (>70 ms).
Conducted genetic screening for SCN5A mutations and common risk variants.

Main Results:

All patients exhibited abnormal substrate in the anterior RV epicardium.
45% of patients (10/22) showed abnormal LV epicardial substrate, with 4 having severe LV fascicular blocks.
LV substrate was associated with a longer history of arrhythmia, prolonged PR and HV intervals, inferior RV substrate, and SCN5A mutations.

Conclusions:

A significant subset of BrS patients presents with abnormal epicardial substrate extending to the LV.
This extended substrate is associated with specific genetic factors, including SCN5A mutations and multigenic variants.
Findings suggest a more complex arrhythmogenic substrate in BrS than previously recognized.