Electroanatomical differences in ajmaline-induced compared to spontaneous type-1 Brugada phenotype

Brugada syndrome (BrS) is diagnosed in the presence of a 2mm ST-segment coved-type elevation; a type-1 phenotype after drug test (using a class I antiarrhythmic drug) is diagnostic only in the presence of additional clinical criteria. The endocardial electroanatomical differences between spontaneous and drug-induced phenotype have been scarcely investigated.

To evaluate the differences in depolarization, repolarization and voltage detected by endocardial unipolar right ventricular (RV) mapping between Brugada patients with a spontaneous type-1 pattern and ajmaline-induced pattern.

Data from endocardial mapping with the CARTO3 system of 20 BrS with spontaneous type-1 pattern (S-BrS) and 13 BrS undergoing ajmaline test (A-BrS) were retrospectively analysed. A-BrS had a history of spontaneous type-1 but did not present it at baseline at the time of the study; mapping in this cohort was performed after ajmaline-induced type-1 ECG was evident. Data was exported from CARTO and converted into MATLAB format using OpenEP; a region of interest (ROI) including sub-pulmonary RV outflow tract (RVOT) and RV free wall was selected using Paraview. Depolarization was assessed using RV activation time (RVAT), time difference between beginning of surface depolarization and minimum -dV/dt of the latest depolarizing point in RVOT. By dividing RVAT color scale in 5 ms steps (isoSteps), isochronal activation areas were identified. Repolarization was evaluated in each point of the ROI using activation recovery intervals, calculated with a semi-automated algorithm based on the Wyatt method and corrected for heart rate using Bazett formula (ARIc). ARIc values were interpolated to create ARIc maps. Low voltage areas (LVAs) were defined as areas in the ROI with unipolar voltage <5.3 mV.

A-BrS tended to have shorter RVAT and less isoSteps compared to S-BrS, but the differences were not significant (respectively 101[22.5] ms with 10 isoSteps vs 111[44.3] ms with 14 isoSteps; p=0.58). Interestingly, A-BrS had significantly longer ARIc in comparison to S-BrS (332.6±16.6 ms vs 307.0± 6.8 ms; p<0.001). Unipolar LVAs were present in 12 A-BrS (92%) and in 17 S-BrS (85%). Considering patients with LVAs, there were no differences between A-BrS and S-BrS (6.8[5.1] cm2 vs 8.2[13.7] cm2; p=0.80).

Ajmaline-induced type-1 phenotype is associated with significantly prolonged endocardial repolarization compared to spontaneous type-1 phenotype in Brugada patients. Using endocardial mapping, no significant differences between these two groups were observed regarding depolarization and voltage. Such results, which need to be confirmed on larger cohorts, could impact both research designs and clinical management of BrS.

Methods