Veronique M F Meijborg1, Samuel Chauveau2, Michiel J Janse3, Evgeny P Anyukhovsky2, Peter R Danilo2, Michael R Rosen4, Tobias Opthof5, Ruben Coronel6. 1. Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands. Electronic address: veromeijborg@gmail.com. 2. Department of Physiology and Biophysics, Institute for Molecular Cardiology, Stony Brook University, Stony Brook, New York. 3. Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands. 4. Departments of Pharmacology and Pediatrics, Columbia University, New York, New York. 5. Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands; Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands. 6. Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands; L'Institut de RYthmologie et de modélisation Cardiaque (LIRYC), Université Bordeaux Segalen, Bordeaux, France.
Abstract
BACKGROUND: Long QT2 (LQT2) syndrome is characterized by bifid (or notched) T waves, whose mechanism is not understood. OBJECTIVE: The purpose of this study was to test whether increased interventricular dispersion of repolarization induces bifid T waves. METHODS: We simultaneously recorded surface ECG and unipolar electrograms at baseline and after dofetilide in a canine model of dofetilide-induced LQT2 (6 male mongrel dogs). Standard ECG variables, T-wave duration, and moments of peaks of bifid T waves (Tp1 and Tp2) were correlated with moments of local repolarization. Epicardial electrograms were recorded over the left ventricular (LV) and right ventricular (RV) anterior walls (11 × 11 electrode grid, 5-mm interelectrode distance). In 5 of the 6 hearts, we also recorded intramural unipolar electrograms (n = 4-7 needles per heart). In each unipolar recording, we determined activation time, repolarization time (RTs), and activation-recovery interval. In addition, we studied RT response to heart rate changes. RESULTS: Dofetilide prolonged QT and QTc, induced bifid T waves in 4 of 6 animals, and prolonged RT heterogeneously in LV and RV, resulting in increased interventricular and LV intraventricular RT dispersion. Dofetilide did not induce a disparate response in activation-recovery interval across the transmural axis. Dofetilide-induced separation of RT across the RV-LV interface concurred with the moments of T-wave peaks. Dofetilide-induced steepening of restitution slopes was larger in LV than RV. CONCLUSION: Dofetilide-induced bifid T waves result from interventricular RT dispersion.
BACKGROUND: Long QT2 (LQT2) syndrome is characterized by bifid (or notched) T waves, whose mechanism is not understood. OBJECTIVE: The purpose of this study was to test whether increased interventricular dispersion of repolarization induces bifid T waves. METHODS: We simultaneously recorded surface ECG and unipolar electrograms at baseline and after dofetilide in a canine model of dofetilide-induced LQT2 (6 male mongrel dogs). Standard ECG variables, T-wave duration, and moments of peaks of bifid T waves (Tp1 and Tp2) were correlated with moments of local repolarization. Epicardial electrograms were recorded over the left ventricular (LV) and right ventricular (RV) anterior walls (11 × 11 electrode grid, 5-mm interelectrode distance). In 5 of the 6 hearts, we also recorded intramural unipolar electrograms (n = 4-7 needles per heart). In each unipolar recording, we determined activation time, repolarization time (RTs), and activation-recovery interval. In addition, we studied RT response to heart rate changes. RESULTS:Dofetilide prolonged QT and QTc, induced bifid T waves in 4 of 6 animals, and prolonged RT heterogeneously in LV and RV, resulting in increased interventricular and LV intraventricular RT dispersion. Dofetilide did not induce a disparate response in activation-recovery interval across the transmural axis. Dofetilide-induced separation of RT across the RV-LV interface concurred with the moments of T-wave peaks. Dofetilide-induced steepening of restitution slopes was larger in LV than RV. CONCLUSION:Dofetilide-induced bifid T waves result from interventricular RT dispersion.
Authors: Jason A Thomas; Erick A Perez-Alday; Allison Junell; Kelley Newton; Christopher Hamilton; Yin Li-Pershing; David German; Aron Bender; Larisa G Tereshchenko Journal: Ann Noninvasive Electrocardiol Date: 2018-11-07 Impact factor: 1.468
Authors: Marianna Meo; Pietro Bonizzi; Laura R Bear; Matthijs Cluitmans; Emma Abell; Michel Haïssaguerre; Olivier Bernus; Rémi Dubois Journal: Front Physiol Date: 2020-08-13 Impact factor: 4.566
Authors: Valerie Y H van Weperen; Albert Dunnink; Alexandre Bossu; Jet D M Beekman; Veronique M F Meijborg; Jacques M T de Bakker; Ruben Coronel; Rosanne Varkevisser; Marcel A G van der Heyden; Marc A Vos Journal: Front Physiol Date: 2021-04-26 Impact factor: 4.566
Authors: Daniel Romero; Nathalie Behar; Bertrand Petit; Vincent Probst; Frederic Sacher; Philippe Mabo; Alfredo I Hernández Journal: PLoS One Date: 2020-03-03 Impact factor: 3.240