ArticlePloS one2012
Mechanisms and determinants of ultralong action potential duration and slow rate-dependence in cardiac myocytes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- APD restitution controls arrhythmia emergence in cardiac tissue with RyR2 dysfunction.The Journal of physiology · 2026Article
- Hydrogen peroxide exposure to bullfrog heart causes ST segment elevation.The Journal of veterinary medical science · 2025Article
- Cardiac electrical abnormalities in a mouse model of left ventricular non-compaction cardiomyopathy.PloS one · 2025Article
- Tensor cardiography: A novel ECG analysis of deviations in collective myocardial action potential transitions based on point processes and cumulative distribution functions.PLOS digital health · 2024Article
- Bifurcations to transient and oscillatory excitations in inhomogeneous excitable media: Insights into arrhythmogenesis in long QT syndrome.Physical review. E · 2023Article
- Cardiac Alternans: From Bedside to Bench and Back.Circulation research · 2023Review
- R-on-T and the initiation of reentry revisited: Integrating old and new concepts.Heart rhythm · 2022Article
- Targeting late ICaL to close the window to ventricular arrhythmias.The Journal of general physiology · 2021Article
- Suppression of ventricular arrhythmias by targeting late L-type Ca2+ current.The Journal of general physiology · 2021Article
- Arrhythmogenic effects of ultra-long and bistable cardiac action potentials.PLoS computational biology · 2021Article
- Spatially Discordant Repolarization Alternans in the Absence of Conduction Velocity Restitution.Biophysical journal · 2020Article
- R-From-T as a Common Mechanism of Arrhythmia Initiation in Long QT Syndromes.Circulation. Arrhythmia and electrophysiology · 2019Article
- Multiple Dynamical Mechanisms of Phase-2 Early Afterdepolarizations in a Human Ventricular Myocyte Model:Frontiers in physiology · 2019Article
- Paradoxical Onset of Arrhythmic Waves from Depolarized Areas in Cardiac Tissue Due to Curvature-Dependent Instability.Physical review. X · 2018Article
- Mechanisms linking T-wave alternans to spontaneous initiation of ventricular arrhythmias in rabbit models of long QT syndrome.The Journal of physiology · 2018Article
- Potassium currents in the heart: functional roles in repolarization, arrhythmia and therapeutics.The Journal of physiology · 2017Review
- Spontaneous initiation of premature ventricular complexes and arrhythmias in type 2 long QT syndrome.American journal of physiology. Heart and circulatory physiology · 2016Article
- Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension.The Journal of physiology · 2016Article
- Targeting the late component of the cardiac L-type Ca2+ current to suppress early afterdepolarizations.The Journal of general physiology · 2015Article
- Calcium-voltage coupling in the genesis of early and delayed afterdepolarizations in cardiac myocytes.Biophysical journal · 2015Article
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2 authors.
Funding
Abstract
In normal cardiac myocytes, the action potential duration (APD) is several hundred milliseconds. However, experimental studies showed that under certain conditions, APD could be excessively long (or ultralong), up to several seconds. Unlike the normal APD, the ultralong APD increases sensitively with pacing cycle length even when the pacing rate is very slow, exhibiting a sensitive slow rate-dependence. In addition, these long action potentials may or may not exhibit early afterdepolarizations (EADs). Although these phenomena are well known, the underlying mechanisms and ionic determinants remain incompletely understood. In this study, computer simulations were performed with a simplified action potential model. Modifications to the L-type calcium current (I(Ca,L)) kinetics and the activation time constant of the delayed rectifier K current were used to investigate their effects on APD. We show that: 1) the ultralong APD and its sensitive slow rate-dependence are determined by the steady-state window and pedestal I(Ca,L) currents and the activation speed and the recovery of the delayed rectifier K current; 2) whether an ultralong action potential exhibits EADs or not depends on the kinetics of I(Ca,L); 3) increasing inward currents elevates the plateau voltage, which in general prolongs APD, however, this can also shorten APD when the APD is already ultralong under certain conditions; and 4) APD alternans occurs at slow pacing rates due to the sensitive slow rate-dependence and the ionic determinants are different from the ones causing APD alternans at fast heart rates.
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