Abnormal transmural repolarization process in patients with Brugada syndrome
Received 15 January 2009; accepted 24 April 2009. published online 04 May 2009.
Background
Repolarization abnormality, especially during bradycardia, might be critical for initiation of ventricular fibrillation (VF) in patients with Brugada syndrome (BrS), but the contribution of the rate-dependent repolarization dynamics to the occurrence of VF is still unknown.
Objective
The aim of our study was to determine the differences in rate-dependent repolarization dynamics between BrS with and without spontaneous VF and between BrS with and without SCN5A mutation.
Methods
The subjects were 37 BrS patients with VF (VF(+) group: 10 male subjects) and without VF (VF(−) group: 27 male subjects) and 20 control subjects. Genetic analysis of SCN5A was performed in all 37 BrS patients. The relationships between QT, QTp, Tp-e, and RR intervals were obtained from Holter recordings as first linear regression lines, and the slopes of QT/RR, QTp/RR, and Tp-e/RR linear regression lines as the sensitivity of rate-dependent repolarization dynamics were compared.
Results
QT/RR and Tp-e/RR slopes showed loss of a rate-dependent property in the VF(+) group compared with those in the VF(−) and control groups. There was no significant difference in QTp/RR slope among the VF(+), VF(−) and control groups. The Tp-e interval had a negative correlation with the RR interval in the VF(+) group and a positive correlation with the RR interval in the VF(−) and control groups. There was no significant difference in QT/RR, QTp/RR, and Tp-e/RR slopes between BrS patients with SCN5A mutation and those without SCN5A mutation.
Conclusions
Loss of rate-dependent QT dynamics may be associated with occurrence of VF in BrS.
⁎Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama City, Okayama, Japan
†Department of Cardiovascular Medicine, Kagawa Saiseikai Hospital, Takamatsu City, Kagawa, Japan
‡Department of Medical Technology, Okayama University Graduate School of Medicine and Dentistry, Okayama City, Okayama, Japan
§Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine and Dentistry, Okayama City, Okayama, Japan
Address reprint requests and correspondence: Dr. Hiroshi Morita, Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama City, Okayama, 700-8558, Japan
This work was supported in part by a Grant-in-Aid for Scientific Research (No. 18790501) and a Grant-in-Aid for Young Scientists (No. 17689026) from the Ministry of Education, Culture, Sports, Science and Technology, Japan, and by Health Sciences Research grants (H18 - Research on Human Genome - 002) from the Ministry of Health, Labor and Welfare, Japan. This work was also supported in part by a grant from the Japan Foundation of Cardiovascular Research, Tokyo, Japan.
ABSTRACT