Evaluation using 87-lead body surface maps and 48-lead signal-averaged ECGs in 15 Brugada patients showed ST segment elevation coincided with longer delayed potential duration in the RVOT.
Case-Control (n=20)
Do repolarization and depolarization abnormalities topographically coincide and relate to ventricular arrhythmia inducibility in patients with Brugada syndrome?
In Brugada syndrome, repolarization and depolarization abnormalities topographically coincide in the right ventricular outflow tract and are associated with ventricular arrhythmia inducibility.
INTRODUCTION: Repolarization and depolarization abnormalities have been reported to be related to Brugada syndrome. METHODS AND RESULTS: We evaluated the relationships between repolarization abnormality and depolarization abnormality using 48-lead unipolar signal-averaged electrocardiograms and 87-lead unipolar body surface maps in 15 patients with Brugada-type ECGs. Data were compared with those from healthy control subjects (n = 5) and within subgroups of Brugada syndrome with (n = 8) and without (n = 7) ventricular arrhythmias (VA) induced by programmed electrical stimulation (PES). Eighty-seven-lead body surface maps were recorded, and potential maps were constructed to evaluate elevation of the ST segment 20 ms after the J point. Forty-eight-lead signal-averaged ECGs were recorded, and isochronal maps of duration of the delayed potential (dDP) were constructed to evaluate the dDP in each lead. Potential maps showed that patients with Brugada-type ECG, especially those with VA induced by programmed electrical stimulation, had greater elevation of the ST segment in the right ventricular outflow tract, especially at E5. Isochronal maps of dDP in the Brugada-type ECG group showed that maximum dDP was located at E5 and that the area with long dDP was larger than that in the control subjects. The dDPs at E7, E5, F7, and F5 in the VA-inducible group were significantly longer than those in the VA-noninducible group. These results showed that the location of greater elevation in the ST segment coincided with the location of longer dDP. CONCLUSION: Repolarization abnormality and depolarization abnormality in the walls of both ventricles, especially in the right ventricular outflow tract, are related to the VA of Brugada syndrome.
Hisamatsu et al. (Sun,) conducted a case-control in Brugada syndrome (n=20). 48-lead unipolar signal-averaged ECGs and 87-lead unipolar body surface maps vs. Healthy control subjects was evaluated on Elevation of the ST segment 20 ms after the J point and duration of the delayed potential (dDP). Evaluation using 87-lead body surface maps and 48-lead signal-averaged ECGs in 15 Brugada patients showed ST segment elevation coincided with longer delayed potential duration in the RVOT.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: