Abstract:
BACKGROUND:The mechanism of ECG changes and arrhythmogenesis in Brugada syndrome (BS) patients is unknown. METHODS AND RESULTS:A BS patient without clinically detected cardiac structural abnormalities underwent cardiac transplantation for intolerable numbers of implantable cardioverter/defibrillator discharges. The patient's explanted heart was studied electrophysiologically and histopathologically. Whole-cell currents were measured in HEK293 cells expressing wild-type or mutated sodium channels from the patient. The right ventricular outflow tract (RVOT) endocardium showed activation slowing and was the origin of ventricular fibrillation without a transmural repolarization gradient. Conduction restitution was abnormal in the RVOT but normal in the left ventricle. Right ventricular hypertrophy and fibrosis with epicardial fatty infiltration were present. HEK293 cells expressing a G1935S mutation in the gene encoding the cardiac sodium channel exhibited enhanced slow inactivation compared with wild-type channels. Computer simulations demonstrated that conduction slowing in the RVOT might have been the cause of the ECG changes. CONCLUSIONS:In this patient with BS, conduction slowing based on interstitial fibrosis, but not transmural repolarization differences, caused the ECG signs and was the origin of ventricular fibrillation.
journal_name
Circulationjournal_title
Circulationauthors
Coronel R,Casini S,Koopmann TT,Wilms-Schopman FJ,Verkerk AO,de Groot JR,Bhuiyan Z,Bezzina CR,Veldkamp MW,Linnenbank AC,van der Wal AC,Tan HL,Brugada P,Wilde AA,de Bakker JMdoi
10.1161/CIRCULATIONAHA.105.532614subject
Has Abstractpub_date
2005-11-01 00:00:00pages
2769-77issue
18eissn
0009-7322issn
1524-4539pii
112/18/2769journal_volume
112pub_type
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