Contribution of Conduction Delay within the
Right Ventricular Outflow Tract or Bundle Branch to Arrhythmogenesis in the Brugada Syndrome;
A 3-D Computer Simulation Study

Masahiko Kondo, Charles Antzelevitch, Takeshi Tsutsumi, Youichi Takeyama,
and Kenichi Harumi

Showa University Fujigaoka Hospital, Devision of Cardiology, Yokohama, Kanagawa, Japan

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Abstract. The Brugada syndrome (BS) is associated with abnormalities in cardiac conduction. The contribution of conduction slowing to arrhythmogenesis in BS is not well defined. The present study uses a 3-dimensional computer model of the human heart and surrounding thoracic volume conductor (Harumi, 1992) to assess the importance of conduction velocity (CV) in arrhythmogenesis in BS.

Methods. Action potential (AP) waveforms incorporating regional differences in duration and notch (phase 1) magnitude previously measured in experimental models of BS were programmed into the model (50000 ventricular cell units). Transmural (Epicardial, M, Endocardial), inter-ventricular, apico-basal and inferior-anterior distinctions were incorporated and a 12 lead ECG was calculated. CV was 2.5m/sec in Bundle Branch and uniform at 0.5 m/sec in ventricular muscle (Group =A Normal heart model). Local slowing of CV within epicardium (Group B) or transmurally (Group C) in the region of the right ventricular outflow tract (RVOT) or Right Bundle Branch (Group D).

Results. In group A, B, C, saddleback and coved-type ST segment elevation in V1-3 were reproduced faithfully with the accentuation of epicardial AP notch in the RVOT. Closely coupled single extrastimuli applied to RVOT epicardium (in the region of loss of the dome) induced ventricular tachycardia or fibrillation (VT/VF) in all groups. In Group A and D, the vulnerable window, during which polymorphic VT could be induced, was 10 msec wide (S1-S2=120-130 msec). VF could not be induced. In Groups B and C, the vulnerable window expanded progressively to 100 msec (S1-S2=120-220 msec) as CV was slowed. VT slowed progressively and VF could be induced as CV was reduced. Neither ST segment elevation, VT nor VF were observed in any group when action potential notch and dome were restored to normal.

Conclusion. Our data suggest that slowing of conduction in the region of the RVOT can facilitate arrhythmogenesis in the Brugada syndrome, but does not form the primary substrate for the development of VT/VF.

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