Delay in right ventricular activation contributes to Brugada syndrome

Area of Science:

• Cardiology
• Electrophysiology
• Cardiac Imaging

Background:

• Brugada syndrome is characterized by ST-segment elevation and ventricular arrhythmias, but its underlying electrophysiological mechanisms are not fully understood.
• Two leading hypotheses involve right ventricular (RV) conduction delay or selective RV subepicardial action potential shortening.
• Both proposed mechanisms predict distinct alterations in RV contraction timing and force.

Purpose of the Study:

• To investigate the electrophysiological mechanisms of Brugada syndrome by examining the timing and force of RV contraction.
• To correlate contractile changes with ECG manifestations during flecainide challenge.

Main Methods:

• Tissue Doppler echocardiography was used to assess RV and left ventricle (LV) contraction.
• Patients underwent flecainide challenge to induce Brugada syndrome ECG patterns.
• Contractile variables were compared between patients with inducible Brugada patterns and controls.

Main Results:

• Flecainide-induced ST elevation in Brugada syndrome correlated with delayed RV contraction onset relative to LV contraction.
• The magnitude of ST elevation was directly proportional to the degree of RV-LV contraction delay.
• RV ejection time was reduced as the Brugada ECG pattern emerged.

Conclusions:

• The findings suggest that both RV conduction delay and RV action potential shortening contribute to Brugada syndrome.
• These electrophysiological abnormalities manifest as distinct changes in RV mechanical function.