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.
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.
Authors: Stephen Zicha; Victor A Maltsev; Stanley Nattel; Hani N Sabbah; Albertas I Undrovinas Journal: J Mol Cell Cardiol Date: 2004-07 Impact factor: 5.000
Authors: Alexey V Zaitsev; Natalia S Torres; Keiko M Cawley; Amira D Sabry; Junco S Warren; Mark Warren Journal: Am J Physiol Heart Circ Physiol Date: 2019-03-15 Impact factor: 4.733
Authors: Anne-Laure Leoni; Bruno Gavillet; Jean-Sébastien Rougier; Céline Marionneau; Vincent Probst; Solena Le Scouarnec; Jean-Jacques Schott; Sophie Demolombe; Patrick Bruneval; Christopher L H Huang; William H Colledge; Andrew A Grace; Hervé Le Marec; Arthur A Wilde; Peter J Mohler; Denis Escande; Hugues Abriel; Flavien Charpentier Journal: PLoS One Date: 2010-02-19 Impact factor: 3.240