Abstract 2251: Right Ventricular Endocardial Mapping in Brugada Syndrome Patients Reveals Cooperative Depolarization and Repolarization Abnormalities
Introduction: Brugada syndrome (BrS) is characterized by specific ST segment elevation in the right precordial ECG leads and may be provoked by sodium channel blockers. The pathophysiology of the specific ECG and ventricular tachyarrhythmias is debated but is believed to include depolarization and/or repolarization abnormalities in the right ventricle (RV). With endocardial catheter mapping (CARTO) and ECG analysis we aimed to study whether RV activation, conduction and repolarization in BrS patients is altered.
Methods: RV CARTO mapping was conducted in 6 BrS patients with a type 1 ECG (type 1 BrS; 4 spontaneous, 2 ajmaline induced), 8 BrS patients with a type 2 ECG (type 2 BrS) and 6 control patients (studied because of supraventricular tachyarrhythmias). We assessed activation and conduction by endocardial RV activation time, endocardial electrogram fragmentation (mean number of intrinsic deflections per electrogram), PQ and QRS interval. RV endocardial repolarization was assessed with CARTO by the mean activation recovery interval corrected for heart rate (ARIc) as a measure of action potential duration.
Results: Both type 1 and 2 BrS patients had more fragmentation throughout the RV, longer PQ intervals and overall shorter ARIc compared to controls (Table⇓). Furthermore, type 1 BrS patients had longer RV activation times and QRS intervals compared to type 2 BrS and controls.
Conclusions: RV CARTO mapping reveals cooperative endocardial RV activation/conduction abnormalities (increased fragmentation) and repolarization abnormalities (shorter ARIc) in both type 1 and 2 BrS patients. In addition, type 1 BrS patients show endocardial RV activation slowing. The combination of increased fragmentation, slowed activation and shortened ARIc in type 1 BrS patients particularly, indicates asynchronous and slowed impulse transmission but fast recovery. This may be an important contributor to the specific ECG and ventricular tachyarrhythmias in BrS.