Published online before print March 1, 2004, doi: 10.1161/01.CIR.0000118467.53182.D1
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(Circulation. 2004;109:1272-1277.)
© 2004 American Heart Association, Inc.
Clinical Investigation and Reports |
Delay in Right Ventricular Activation Contributes to Brugada Syndrome
From the Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands (R.T., J.V., I.K.L.M.d.G., A.A.M.W., H.L.T.), and the Heart Center Aalborg, Aarhus University Hospitals, Aarhus, Denmark (P.S.).
Correspondence to Hanno L. Tan, MD, PhD, Department of Cardiology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail h.l.tan{at}amc.uva.nl
Received September 23, 2003; revision received November 21, 2003; accepted December 5, 2003.
Background— Although Brugada syndrome revolves around reduced net depolarizing force, the electrophysiological mechanisms of its defining features (right precordial ST-segment elevation and ventricular tachyarrhythmias) remain unresolved. Two proposed mechanisms are (1) right ventricular (RV) conduction delay and (2) selective and significant RV subepicardial action potential shortening. Both mechanisms must cause disparate contractile changes: delay in RV contraction and reduction of contractile force, respectively. We aimed to establish the electrophysiological mechanism of Brugada syndrome by studying the timing and force of RV contraction.
Methods and Results— Using tissue Doppler echocardiography, we studied how these contractile variables change on induction of the characteristic ST-segment changes of Brugada syndrome by flecainide challenge. Accordingly, we studied patients in whom flecainide induced these changes (inducible) and those in whom these changes were not induced (control). We found that (1) the occurrence of a positive response (coved-type ST elevation) after flecainide coincides with delay in the onset of contraction between the RV and left ventricle (LV); (2) the extent of contraction delay between RV and LV correlates with the magnitude of ST elevation; and (3) RV ejection time (duration of RV ejection phase) shortens as the Brugada ECG pattern emerges.
Conclusions— These results indicate that both proposed mechanisms of Brugada syndrome may be operative.
Key Words: arrhythmia • Brugada syndrome • conduction • death, sudden • electrophysiology
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