In vivo high-density mapping in Brugada syndrome patients demonstrated marked regional endocardial conduction delay and reduced local activation gradient (0.33 vs 0.51 mm/ms; P<0.0005) versus controls.
Case-Control (n=38)
Absolute Event Rate: 0.33% vs 0.51%
p-value: p=<0.0005
Background— Two principal mechanisms are thought to be responsible for Brugada syndrome (BS): (1) right ventricular (RV) conduction delay and (2) RV subepicardial action potential shortening. This in vivo high-density mapping study evaluated the conduction and repolarization properties of the RV in BS subjects. Methods and Results— A noncontact mapping array was positioned in the RV of 18 BS patients and 20 controls. Using a standard S 1 -S 2 protocol, restitution curves of local activation time and activation recovery interval were constructed to determine local maximal restitution slopes. Significant regional conduction delays in the anterolateral free wall of the RV outflow tract of BS patients were identified. The mean increase in delay was 3-fold greater in this region than in control ( P =01 was 3.86 versus controls. Five episodes of provoked ventricular tachycardia arose from wave breaks originating from RV outflow tract slow-conduction zones in 5 BS patients. Conclusions— Marked regional endocardial conduction delay and heterogeneities in repolarization exist in BS. Wave break in areas of maximal conduction delay appears to be critical in the initiation and maintenance of ventricular tachycardia. These data indicate that further studies of mapping BS to identify slow-conduction zones should be considered to determine their role in spontaneous ventricular arrhythmias.
Lambiase et al. (Mon,) conducted a case-control in Brugada syndrome (n=38). In vivo high-density mapping vs. Controls was evaluated on Local activation gradient in the anterolateral free wall of the right ventricular outflow tract (mm/ms) (p=<0.0005). In vivo high-density mapping in Brugada syndrome patients demonstrated marked regional endocardial conduction delay and reduced local activation gradient (0.33 vs 0.51 mm/ms; P<0.0005) versus controls.