Published Online
on December 2, 2008

A more recent version of this article appeared on December 1, 2008

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Original Article

Slow and discontinuous conduction conspire in Brugada syndrome: a right ventricular mapping and stimulation study

Pieter G. Postema; Pascal F.H.M. van Dessel; Jacques M.T. de Bakker; Lukas R.C. Dekker; Andre C. Linnenbank; Mark G. Hoogendijk; Ruben Coronel; Jan G.P. Tijssen; Arthur A.M. Wilde and Hanno L. Tan¹

Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

¹ E-mail: h.l.tan{at}amc.uva.nl

Background—Brugada syndrome (BrS) is associated with lethal arrhythmias which are linked to specific ST-segment changes (type-1 BrS-ECG) and the right ventricle (RV). The pathophysiological basis of the arrhythmias and type-1 BrS-ECG is unresolved. We studied the electrophysiological characteristics of the RV endocardium in BrS.

Methods and Results—RV endocardial electroanatomical mapping and stimulation studies were performed in controls (n=12) and BrS-patients with a type-1 (BrS-1, n=10) or type-2 BrS-ECG (BrS-2, n=12) during the studies. BrS-1 patients had prominent impairment of RV endocardial impulse propagation when compared to controls, as represented by: 1) prolonged activation-duration during sinus rhythm (86±4 vs. 65±3msec), 2) increased electrogram fractionation (1.36±0.04 vs. 1.15±0.01 deflections per electrogram), 3) longer electrogram duration (83±3 vs. 63±2msec), 4) activation delays upon premature stimulation (longitudinal: 160±26 vs. 86±9msec; transversal: 112±5 vs. 58±6msec), and 5) abnormal transversal conduction velocity restitution (42±8 vs. 18±2msec increase in delay at shortest coupling intervals). Wider and more fractionated electrograms were also found in BrS-2 patients. Repolarization was not different between groups.

Conclusions—BrS-1 and BrS-2 patients are characterized by wide and fractionated electrograms at the RV endocardium. BrS-1 patients display additional conduction slowing during sinus rhythm and premature stimulation along with abnormal transversal conduction velocity restitution. These patients may thus exhibit a substrate for slow and discontinuous conduction caused by abnormal active membrane processes and electrical coupling. Our findings support the emerging notion that BrS is not solely due to abnormal electrophysiological properties but requires the conspiring effects of conduction slowing and tissue discontinuities.

Key Words: arrhythmia • death, sudden (if surviving, use heart arrest) • electrophysiology • mapping • Brugada syndrome

This article has been cited by other articles:

				P.D. Lambiase, A.K. Ahmed, E.J. Ciaccio, R. Brugada, E. Lizotte, S. Chaubey, R. Ben-Simon, A.W. Chow, M.D. Lowe, and W.J. McKenna High-Density Substrate Mapping in Brugada Syndrome: Combined Role of Conduction and Repolarization Heterogeneities in Arrhythmogenesis Circulation, July 14, 2009; 120(2): 106 - 117. [Abstract] [Full Text] [PDF]