Sylvain Ploux1, Romain Eschalier2, Zachary I Whinnett3, Joost Lumens4, Nicolas Derval2, Frederic Sacher2, Mélèze Hocini2, Pierre Jaïs2, Remi Dubois2, Philippe Ritter2, Michel Haïssaguerre2, Bruce L Wilkoff5, Darrel P Francis3, Pierre Bordachar2. 1. Hôpital Cardiologique du Haut-Lévêque, CHU Bordeaux, Université Bordeaux, IHU LIRYC, Bordeaux, France. Electronic address: sylvain.ploux@gmail.com. 2. Hôpital Cardiologique du Haut-Lévêque, CHU Bordeaux, Université Bordeaux, IHU LIRYC, Bordeaux, France. 3. Imperial College London, London, United Kingdom. 4. Hôpital Cardiologique du Haut-Lévêque, CHU Bordeaux, Université Bordeaux, IHU LIRYC, Bordeaux, France; Maastricht University, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands. 5. Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Abstract
BACKGROUND: Biventricular pacing (BVP) may not achieve complete electrical resynchronization. OBJECTIVE: The purpose of this study was to assess whether the resynchronizing effect of BVP varies among patients depending on the underlying electrical substrate. METHODS: High-resolution electrocardiographic mapping with invasive measurement of the maximal rate of systolic left ventricular (LV) pressure rise (LVdP/dtmax) was performed during baseline activation and during BVP in 61 patients with heart failure with various conduction delays: 13 with narrow QRS duration (<120 ms), 22 with nonspecific intraventricular conduction disturbance, and 26 with left bundle branch block. Electrical dyssynchrony, both during baseline activation and BVP, was quantified by total and LV activation times (TAT and LVTAT) and by ventricular electrical uncoupling (VEU = mean LVTAT - mean right ventricular activation time). Response to BVP was defined as a ≥10% increase in LVdP/dtmax. RESULTS: The electrical activation pattern during BVP was similar for all patient groups and, hence, not dependent on baseline conduction disturbance. During BVP, TAT, LVTAT, and VEU were similar for all groups and were either not correlated or weakly correlated with the change in LVdP/dtmax. In contrast, changes in electrical dyssynchrony correlated significantly with the change in LVdP/dtmax: r=0.71, 0.69, and 0.69 for ∆TAT, ∆LVTAT, and ∆VEU, respectively (all P < .001). Responders showed higher baseline dyssynchrony levels and BVP-induced dyssynchrony reduction than did nonresponders (all P < .001); in nonresponders, BVP worsened activation times than did baseline activation. CONCLUSION: BVP does not eliminate electrical dyssynchrony, but rather brings it to a common level independent of the patient's underlying electrical substrate. Therefore, BVP is of benefit to patients with dyssynchrony but not to patients with insufficient electrical dyssynchrony in whom it induces an iatrogenic electropathy.
BACKGROUND: Biventricular pacing (BVP) may not achieve complete electrical resynchronization. OBJECTIVE: The purpose of this study was to assess whether the resynchronizing effect of BVP varies among patients depending on the underlying electrical substrate. METHODS: High-resolution electrocardiographic mapping with invasive measurement of the maximal rate of systolic left ventricular (LV) pressure rise (LVdP/dtmax) was performed during baseline activation and during BVP in 61 patients with heart failure with various conduction delays: 13 with narrow QRS duration (<120 ms), 22 with nonspecific intraventricular conduction disturbance, and 26 with left bundle branch block. Electrical dyssynchrony, both during baseline activation and BVP, was quantified by total and LV activation times (TAT and LVTAT) and by ventricular electrical uncoupling (VEU = mean LVTAT - mean right ventricular activation time). Response to BVP was defined as a ≥10% increase in LVdP/dtmax. RESULTS: The electrical activation pattern during BVP was similar for all patient groups and, hence, not dependent on baseline conduction disturbance. During BVP, TAT, LVTAT, and VEU were similar for all groups and were either not correlated or weakly correlated with the change in LVdP/dtmax. In contrast, changes in electrical dyssynchrony correlated significantly with the change in LVdP/dtmax: r=0.71, 0.69, and 0.69 for ∆TAT, ∆LVTAT, and ∆VEU, respectively (all P < .001). Responders showed higher baseline dyssynchrony levels and BVP-induced dyssynchrony reduction than did nonresponders (all P < .001); in nonresponders, BVP worsened activation times than did baseline activation. CONCLUSION: BVP does not eliminate electrical dyssynchrony, but rather brings it to a common level independent of the patient's underlying electrical substrate. Therefore, BVP is of benefit to patients with dyssynchrony but not to patients with insufficient electrical dyssynchrony in whom it induces an iatrogenic electropathy.
Authors: David Soto Iglesias; Nicolas Duchateau; Constantine Butakoff Kostantyn Butakov; David Andreu; Juan Fernandez-Armenta; Bart Bijnens; Antonio Berruezo; Marta Sitges; Oscar Camara Journal: IEEE J Transl Eng Health Med Date: 2016-12-16 Impact factor: 3.316
Authors: Nadine Ali; Daniel Keene; Ahran Arnold; Matthew Shun-Shin; Zachary I Whinnett; S M Afzal Sohaib Journal: Arrhythm Electrophysiol Rev Date: 2018-06
Authors: Romain Eschalier; Sylvain Ploux; Bruno Pereira; Nicolas Clémenty; Antoine Da Costa; Pascal Defaye; Stéphane Garrigue; Jean-Baptiste Gourraud; Daniel Gras; Benoît Guy-Moyat; Christophe Leclercq; Pierre Mondoly; Pierre Bordachar Journal: BMJ Open Date: 2016-11-11 Impact factor: 2.692
Authors: Thomas Jackson; Simon Claridge; Jonathan Behar; Cheng Yao; Mark Elliott; Vishal Mehta; Justin Gould; Baldeep Sidhu; Helder Pereira; Steven Niederer; Gerald Carr-White; Christopher A Rinaldi Journal: Heart Rhythm O2 Date: 2021-01-12