Tobias Opthof1, Veronique M F Meijborg2, Charly N W Belterman3, Ruben Coronel4. 1. Experimental Cardiology Group, Department of Clinical and Experimental Cardiology, Academic Medical Centre, Room K2-112, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands. 2. Experimental Cardiology Group, Department of Clinical and Experimental Cardiology, Academic Medical Centre, Room K2-112, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. 3. Experimental Cardiology Group, Department of Clinical and Experimental Cardiology, Academic Medical Centre, Room K2-112, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands University Bordeaux Segalen, L'Institut de RYthmologie et modélisation Cardiaque (LIRYC), Bordeaux, France. 4. Experimental Cardiology Group, Department of Clinical and Experimental Cardiology, Academic Medical Centre, Room K2-112, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands University Bordeaux Segalen, L'Institut de RYthmologie et modélisation Cardiaque (LIRYC), Bordeaux, France rubencoronel@gmail.com.
Abstract
AIMS: The aim of this study was to evaluate the effect of increase in left ventricular (LV) pressure on repolarization and activation-recovery intervals. METHODS AND RESULTS: Six pig hearts were Langendorff-perfused. A compliant liquid-filled balloon, connected with a pressure transducer, inserted through the mitral orifice, could be filled until the required LV systolic pressure was obtained. A grid of 121 electrodes (11 × 11; 5 mm interelectrode distance) was sutured on the LV free wall. Ventricular pacing at 600 ms and at 400 or 450 ms was either performed from the LV wall or from the ventricular septum. Under all these four conditions, the pressure wave occurred at the same moment relative to the onset of the QRS complex. Consequently, the time relation between local repolarization and the pressure wave differed between the various pacing sites. Repolarization times (RTs) at a cycle length (CL) of 600 ms were prolonged by increased pressure. With stimulation from the LV, when the pressure wave coincides with the action potentials (APs) late in their phase (sites with relatively early repolarization), an increase in pressure from 0 to 100 mmHg delayed repolarization more than with stimulation from the septum, when the pressure wave occurs at a relatively earlier phase of the AP (sites with relatively late repolarization). At pacing at CL 400/450 ms, an increase in pressure caused RT prolongation at the LV free wall during LV stimulation, but less RT prolongation or even shortening during septal stimulation. CONCLUSION: The effect of increased LV pressure is synchronization of repolarization. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: The aim of this study was to evaluate the effect of increase in left ventricular (LV) pressure on repolarization and activation-recovery intervals. METHODS AND RESULTS: Six pig hearts were Langendorff-perfused. A compliant liquid-filled balloon, connected with a pressure transducer, inserted through the mitral orifice, could be filled until the required LV systolic pressure was obtained. A grid of 121 electrodes (11 × 11; 5 mm interelectrode distance) was sutured on the LV free wall. Ventricular pacing at 600 ms and at 400 or 450 ms was either performed from the LV wall or from the ventricular septum. Under all these four conditions, the pressure wave occurred at the same moment relative to the onset of the QRS complex. Consequently, the time relation between local repolarization and the pressure wave differed between the various pacing sites. Repolarization times (RTs) at a cycle length (CL) of 600 ms were prolonged by increased pressure. With stimulation from the LV, when the pressure wave coincides with the action potentials (APs) late in their phase (sites with relatively early repolarization), an increase in pressure from 0 to 100 mmHg delayed repolarization more than with stimulation from the septum, when the pressure wave occurs at a relatively earlier phase of the AP (sites with relatively late repolarization). At pacing at CL 400/450 ms, an increase in pressure caused RT prolongation at the LV free wall during LV stimulation, but less RT prolongation or even shortening during septal stimulation. CONCLUSION: The effect of increased LV pressure is synchronization of repolarization. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Keel Yong Lee; Sung-Jin Park; David G Matthews; Sean L Kim; Carlos Antonio Marquez; John F Zimmerman; Herdeline Ann M Ardoña; Andre G Kleber; George V Lauder; Kevin Kit Parker Journal: Science Date: 2022-02-10 Impact factor: 47.728
Authors: Bastiaan J Boukens; Veronique M F Meijborg; Charly N Belterman; Tobias Opthof; Michiel J Janse; Richard B Schuessler; Ruben Coronel; Igor R Efimov Journal: Physiol Rep Date: 2017-05
Authors: Michele Orini; Peter Taggart; Anish Bhuva; Neil Roberts; Carmelo Di Salvo; Martin Yates; Sveeta Badiani; Stefan Van Duijvenboden; Guy Lloyd; Andrew Smith; Pier D Lambiase Journal: Heart Rhythm Date: 2021-04-29 Impact factor: 6.343