Prolongation of LAS40 (duration of the low amplitude electric potential component (<40 microV) of the terminal portion of the QRS) induced by isoproterenol in 11 patients with Brugada syndrome.

The electrophysiological mechanism of Brugada syndrome is unclear, but transmural dispersion of repolarization in the right ventricle is believed to be the most likely mechanism. On the other hand, the presence of a conduction delay region is considered to be related to the occurrence of ventricular fibrillation; that is, a relationship between the presence of a ventricular late potential (LP) and arrhythmogenic right ventricular cardiomyopathy. In this study, the LP from signal-averaged electrocardiography during isoproterenol (ISP) administration in patients with Brugada syndrome is discussed. The subjects were 11 patients with Brugada syndrome and 6 healthy individuals. In all subjects, the total filtered QRS duration (fQRS), root mean square voltage of the 40 ms terminal portion of the QRS (RMS(40)), duration of the low amplitude electric potential component (40 microV) of the terminal portion of the QRS (LAS(40)), and time duration of the fQRS-LAS(40) difference were compared between when ISP was prescribed and when it was not. During ISP administration, a peculiar response, which resulted in an LAS(40) prolongation, was observed in the patients with Brugada syndrome. With ISP, the fQRS remained unchanged, but the RMS(40) and the fQRS-LAS(40) decreased. Consequently another 3 patients with a positive LP were diagnosed using the ordinary standard because of the administration of ISP. We believe that the low-amplitude component was unmasked by shortening of the high-amplitude component. In patients with Brugada syndrome, a conduction delay in the ventricle may be present and may be related to the occurrence of ventricular fibrillation.