Comparison of conduction delay in the right ventricular outflow tract between Brugada syndrome and right ventricular cardiomyopathy: investigation of signal average ECG in the precordial leads

doi:10.1093/europace/eum128

Europace Advance Access originally published online on July 17, 2007
Europace 2007 9(10):951-956; doi:10.1093/europace/eum128

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MISCELLANEOUS

Comparison of conduction delay in the right ventricular outflow tract between Brugada syndrome and right ventricular cardiomyopathy: investigation of signal average ECG in the precordial leads

Hiroshi Furushima^*, Masaomi Chinushi, Kazuki Okamura, Kenichi Iijima, Satoru Komura, Yasutaka Tanabe, Shinsuke Okada, Daisuke Izumi and Yoshifusa Aizawa

The First Department of Internal Medicine, Niigata University School of Medicine, 1-754 Asahi-machi-dori, Niigata, 951-8510, Japan

Background In both Brugada syndrome (BS) and arrhythmogenicright ventricular cardiomyopathy (ARVC), electrical abnormalitiesin the right ventricular outflow tract (RVOT) are importantfor arrhythmogenesis.

Objectives The aim of this study was to compare conduction delayin the right ventricular in BS with that in ARVC using the signal-averagedelectrocardiogram.

Methods Twenty patients with BS (18 men and 2 women; 55 ±12 years old; 9 symptomatic and 11 asymptomatic) and eight patientswith ARVC (six men and two women; 53 ± 16 years old)were included. We assessed the presence of late potentials (LPs)and the filtered QRS duration (fQRSd) in V₂ and V₅ using a high-passfilter of 40 Hz (fQRSd:40) and 100 Hz (fQRSd:100).

Results In ARVC, there was no significant difference in fQRSd:40between V2 and V5 (158 ± 19 vs. 145 ± 17 ms,respectively): however, in BS, fQRSd:40 in V2 was significantlylonger than fQRSd:40 in V5 (147 ± 15 vs. 125 ±10 ms, P < 0.001). In ARVC, there was no significantdifference between fQRSd:40 and fQRSd:100 in V₂ and V₅ (158± 19 vs. 142 ± 23 ms and 145 ± 17vs. 132 ± 9 ms, respectively). In contrast, in BS,fQRSd:100 was significantly shorter than fQRSd:40 in V2 (110± 8 ms vs. 147 ± 15, P < 0.001). The relativedecrease in fQRSd:100 compared with fQRSd:40 in V2 was significantlygreater in BS than in ARVC.

Conclusion The dominant prolongation of the fQRSd in the rightprecordial lead in BS was different from the characteristicsof ARVC, which may be caused by the conduction delay due tofibro-fatty replacement in RV.

Key Words: Brugada syndrome, ARVC, Signal-averaged ECG, RV outflow tract, Delayed potential

^* Corresponding author. Tel: +81 25 227 2185; fax: +81 25 227 0774. E-mail address: chimiri{at}med.niigata-u.ac-jp

Manuscript submitted 2 May 2007. Accepted after revision 8 June 2007.

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