Abstract 2255: Local And Regional Conduction Heterogeneities In Brugada Patients-a Non-Contact Mapping Study.
Objectives: The pathophysiological basis of Brugada syndrome (BS) remains contentious. Studies have focussed on right ventricular epicardial conduction delay and transmural repolarisation differences. To date there has been no report of in vivo high density mapping of the Brugada heart in man. We investigated the hypothesis that significant endocardial conduction delays exist in the right ventricular outflow tract (RVOT) of BS patients.
Methods: 22 patients (Brugada n=12, Normal n=10) were studied using non-contact mapping. Conduction curves were generated in the RVOT, RV body & apex using a standard S1–S2 decremental pacing protocol pacing from RV apex. Local Activation times (AT) and activation recovery intervals (ARI) were measured at these sites. Area under the curve of AT and Mean Increase in Delay (MID) were calculated to quantify the degree of global delay.
Results: Significant differences in conduction delay was found between the RVOT and RV body & apex in BS patients (p=0.027) (Fig.1⇓). Isochronal maps confirmed local conduction delay in the antero-lateral RVOT of patients with Brugada syndrome which was absent in controls. VF was initiated in one BS patient with wavebreak at this RV segment. The ARI restitution slopes in the RVOT and LVOT were <1.
Conclusions: 1. Significant regional and local conduction delays exist in the RVOT of BS patients compared to RV apical sites. 2. The extent of conduction delay and regional heterogeneity in conduction may be a key determinant of risk of lethal arrhythmia in BS-this could be used prospectively to risk stratify these patients. Fig 1⇓. Regional differences in conduction delay in BS and Normals. (BS - Brugada syndrome; N- Normal)