Simultaneous Non-Invasive Epicardial and Endocardial Mapping in Patients With Brugada Syndrome: New Insights Into Arrhythmia Mechanisms

Abstract

Background: The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS.

Methods and results: Local epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi- and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation-recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST-segment elevation >2 mV and T-wave inversions. Negative voltage gradient (-2.5 to -6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls.

Conclusions: Abnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.

Keywords: Brugada syndrome; ajmaline challenge; arrhythmia; depolarization; electrocardiography; endocardium; epicardium; repolarization; right bundle branch block; right ventricular outflow tract; sudden death.

Figure 1

Recordings of local unipolar electrograms are presented (anterior and posterior view). Epicardial model on the left and endocardial model on the right, where calculations were derived from different sites of the left and right ventricle. LV indicates left ventricle; RV, right ventricle; RVOT, right ventricular outflow tract.

Figure 2

Recordings of local unipolar electrograms of a BrS patient with a type 1 ECG are presented. Epicardial model on the left and endocardial model on the right, where calculations were derived from different sites of the left and right ventricle (see text for detailed description). BrS indicates Brugada syndrome; ECG, electrocardiogram; LV, left ventricle; RV, right ventricle; RVOT, right ventricular outflow tract.

Figure 3

Epi‐Endo voltage gradient at end of the ventricular depolarization in a patient with BrS and type‐1 ECG (A), in a patient with RBBB (B) and in a control subject (C). Four of 6 patients with type 1 ECG, 1 of 5 patients with type 2 ECG before ajmaline administration, and 4 of 6 patient after ajmaline administration demonstrated negative Epi‐Endo VG (−2.5 to −6.0 mV) in the anterior‐lateral part of the RVOT (A). In contrast, during the same period, all control subjects had uniform weak negative Epi‐Endo VG in the entire surface of the RV (C). All RBBB patients had uniform weak positive Epi‐Edo VG in the entire surface of the RV (B). ECG, electrocardiogram; Epi‐Endo, epicardial and endocardial; RBBB, right bundle branch block; RV, right ventricle; RVOT, right ventricular outflow tract; VG, voltage gradient.