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J Am Coll Cardiol, 2002; 40:1437-1444 © 2002 by the American College of Cardiology Foundation |




* Department of Cardiovascular Medicine, Okayama University Graduate School, Okayama, Japan
Department of Cardiovascular Medicine, Fukuyama Cardiovascular Hospital, Fukuyama, Japan
Department of Cardiovascular Medicine, Cardiovascular Center Sakakibara Hospital, Okayama, Japan
Department of Cardiovascular Medicine, Hata Kennmin Hospital, Sukumo, Japan
Manuscript received February 4, 2002; revised manuscript received May 17, 2002, accepted June 7, 2002.
* Reprint requests and correspondence: Dr. Hiroshi Morita, Department of Cardiovascular Medicine, Okayama University Graduate School, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan.
hmorita{at}cc.okayama-u.ac.jp
OBJECTIVES: We sought to study atrial vulnerability in patients with Brugada syndrome.
BACKGROUND: Atrial fibrillation (AF) often occurs in patients with Brugada syndrome, but atrial vulnerability in Brugada syndrome has not been evaluated.
METHODS: The patient group consisted of 18 patients with Brugada syndrome. The control group consisted of 12 age- and gender-matched subjects who had neither organic heart disease nor AF episodes. The incidence and clinical characteristics of AF were evaluated in all 18 patients with Brugada syndrome, and an electrophysiologic study was performed in all 12 control subjects and in 14 of the 18 patients with Brugada syndrome. The atrial effective refractory period of the right atrium (RA-ERP), intra-atrial conduction time (conduction time from the stimulus at the right atrium to atrial deflection at the distal portion of the coronary sinus), duration of local atrial potential, and repetitive atrial firing (occurrence of two or more premature atrial complexes after atrial stimulation) were studied.
RESULTS: Spontaneous AF occurred in 7 of the 18 patients with Brugada syndrome but in none of the control subjects. The RA-ERP was not different between the two groups. The intra-atrial conduction time was increased in the Brugada syndrome group versus the control group (168.4 ± 17.5 vs. 131.8 ± 13.0 ms, p < 0.001). The duration of atrial potential at the RA-ERP was prolonged in the Brugada syndrome group versus the control group (80.3 ± 18.0 vs. 59.3 ± 9.2 ms, p < 0.001). Repetitive atrial firing was induced in nine patients with Brugada syndrome and in six control subjects. Atrial fibrillation was induced in eight patients with Brugada syndrome but in none of the control subjects. In patients with Brugada syndrome without spontaneous AF, the intra-atrial conduction time and duration of atrial potential were also increased.
CONCLUSIONS: Atrial vulnerability is increased in patients with Brugada syndrome. Abnormal atrial conduction may be an electrophysiologic basis for induction of AF in patients with Brugada syndrome.
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