action potential duration restitution
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2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Aulia K. Heikhmakhtiar ◽  
Ki M. Lim

Electromechanical delay (EMD) is the time interval between local myocyte depolarization and the onset of myofiber shortening. Previously, researchers measured EMD during sinus rhythm and ectopic pacing in normal and heart failure conditions. However, to our knowledge, there are no reports regarding EMD during another type of rhythms or arrhythmia. The goal of this study was to quantify EMD during sinus rhythm, tachycardia, and ventricular fibrillation conditions. We hypothesized that EMD under sinus rhythm is longer due to isovolumetric contraction which is imprecise during arrhythmia. We used a realistic model of 3D electromechanical ventricles. During sinus rhythm, EMD was measured in the last cycle of cardiac systole under steady conditions. EMD under tachycardia and fibrillation conditions was measured during the entire simulation, resulting in multiple EMD values. We assessed EMD for the following 3 conduction velocities (CVs): 31 cm/s, 51 cm/s, and 69 cm/s. The average EMD during fibrillation condition was the shortest corresponding to 53.45 ms, 55.07 ms, and 50.77 ms, for the CVs of 31 cm/s, 51 cm/s, and 69 cm/s, respectively. The average EMD during tachycardia was 58.61 ms, 58.33 ms, and 52.50 ms for the three CVs. Under sinus rhythm with action potential duration restitution (APDR) slope 0.7, the average EMD was 66.35 ms, 66.41 ms, and 66.60 ms in line with the three CVs. This result supports our hypothesis that EMD under sinus rhythm is longer than that under tachyarrhythmia conditions. In conclusion, this study observed and quantified EMD under tachycardia and ventricular fibrillation conditions. This simulation study has widened our understanding of EMD in 3D ventricles under chaotic conditions.



Author(s):  
Balvinder S. Handa ◽  
Saheed Lawal ◽  
Ian J. Wright ◽  
Xinyang Li ◽  
Javier Cabello-García ◽  
...  


2017 ◽  
Vol 126 (6) ◽  
pp. 1096-1106 ◽  
Author(s):  
Kimberly Howard-Quijano ◽  
Tatsuo Takamiya ◽  
Erica A. Dale ◽  
Kentaro Yamakawa ◽  
Wei Zhou ◽  
...  

Abstract Background Imbalances in the autonomic nervous system, namely, excessive sympathoexcitation, contribute to ventricular tachyarrhythmias. While thoracic epidural anesthesia clinically suppresses ventricular tachyarrhythmias, its effects on global and regional ventricular electrophysiology and electrical wave stability have not been fully characterized. The authors hypothesized that thoracic epidural anesthesia attenuates myocardial excitability and the proarrhythmic effects of sympathetic hyperactivity. Methods Yorkshire pigs (n = 15) had an epidural catheter inserted (T1 to T4) and a 56-electrode sock placed on the heart. Myocardial excitability was measured by activation recovery interval, dispersion of repolarization, and action potential duration restitution at baseline and during programed ventricular extrastimulation or left stellate ganglion stimulation, before and 30 min after thoracic epidural anesthesia (0.25% bupivacaine). Results After thoracic epidural anesthesia infusion, there was no change in baseline activation recovery interval or dispersion of repolarization. During programmed ventricular extrastimulation, thoracic epidural anesthesia decreased the maximum slope of ventricular electrical restitution (0.70 ± 0.24 vs. 0.89 ± 0.24; P = 0.021) reflecting improved electrical wave stability. Thoracic epidural anesthesia also reduced myocardial excitability during left stellate ganglion stimulation–induced sympathoexcitation through attenuated shortening of activation recovery interval (−7 ± 4% vs. −4 ± 3%; P = 0.001), suppression of the increase in dispersion of repolarization (313 ± 293% vs. 185 ± 234%; P = 0.029), and reduction in sympathovagal imbalance as measured by heart rate variability. Conclusions Our study describes the electrophysiologic mechanisms underlying antiarrhythmic effects of thoracic epidural anesthesia during sympathetic hyperactivity. Thoracic epidural anesthesia attenuates ventricular myocardial excitability and induces electrical wave stability through its effects on activation recovery interval, dispersion of repolarization, and the action potential duration restitution slope.



2013 ◽  
Vol 6 (2) ◽  
pp. 410-418 ◽  
Author(s):  
Yu-Cheng Hsieh ◽  
Po-Cheng Chang ◽  
Chia-Hsiang Hsueh ◽  
Young Soo Lee ◽  
Changyu Shen ◽  
...  




2010 ◽  
Vol 74 (4) ◽  
pp. 664-670 ◽  
Author(s):  
Sonoko Ashino ◽  
Ichiro Watanabe ◽  
Masayoshi Kofune ◽  
Koichi Nagashima ◽  
Kimie Ohkubo ◽  
...  


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