Abstract 2771: Abnormal Atrial Electrophysiological Vulnerability and Structural Atrial Remodeling in High-Risk Patients with Brugada Syndrome: Assessment with Electrophysiology and Echocardiography
Background: Atrial fibrillation (AF) often occurs in patients with Brugada syndrome (BS) and BS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. We have reported that patients with BS had abnormal atrial electrophysiological vulnerability, which provides a substrate for AF, but there are no data regarding the atrial structural attribute. Our objective is to assess the atrial electrophysiological and structural characteristics according to the disease severity and their relations with gene mutations in BS.
Methods: We studied 41 patients with BS: 9 patients with documented VF and spontaneous AF (Group VF+AF+), 7 patients with VF and without AF (Group VF+AF−), and 25 patients without VF and AF (Group VF−AF−). In electrophysiologic study, intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to the atrial deflection at the distal portion of the coronary sinus, and it was measured at constant pacing (CT1) and extrastimuli (CT2). In echocardiographic study, left atrial volume was calculated using the biplane modified Simpson’s method and indexed to body surface area (LA volume index). Mutations of SCN5A gene were examined in all patients.
Results: CTs, especially CT2, were prolonged in both Group VF+AF+ and Group VF+AF− compared to Group VF−AF− (CT2: Group VF−AF−134.1±15.7 vs. Group VF+AF− 152.8±23.6* vs. Group VF+AF+ 173.5±12.4** ms, *p<0.05, ** p<0.01). Group VF+AF+ had larger LA volume index compared to Group VF−AF−.Group VF+AF− also had large LA volume index although this group did not have spontaneous AF (LA volume index: 22±4 vs. 26±4* vs. 34±8** ml/m2, respectively, *p<0.05, ** p<0.01). LA volume index was correlated with CT2 (r=0.58, p<0.01). SCN5A mutation was associated with prolonged CTs (p<0.05) and increased LA volume index (p<0.05), but not with the episode of spontaneous AF and documented VF.
Conclusions: High-risk patients with BS had both abnormal atrial vulnerability and remodeling even if patients did not have AF. Existence of SCN5A also induced both electrophysiological and anatomical remodeling of the atrium. To identify atrial electrophysiological and structural characteristics may be useful for the risk stratification in patients with BS.