Delayed Afterdepolarization-Mediated Triggered Activity Associated with Slow Calcium Sequestration Near the Endocardium

2005 ◽  
Vol 16 (4) ◽  
pp. 418-424 ◽  
Author(s):  
KENNETH R. LAURITA ◽  
RODOLPHE P. KATRA
Keyword(s):  
Triggered Activity ◽  
Calcium Sequestration ◽  
Delayed Afterdepolarization

Electrophysiological Characteristics of Arterially-Perfused Canine Pulmonary Veins: Role of the Delayed Afterdepolarization-Induced Triggered Activity

2005 ◽  
Vol 35 (9) ◽  
pp. 643 ◽  
Author(s):  
Gi Byoung Nam ◽  
Kee Joon Choi ◽  
Duk Woo Park ◽  
Jun Kim ◽  
Kyung Suk Rhee ◽  
...  
Keyword(s):  
Pulmonary Veins ◽  
Triggered Activity ◽  
Delayed Afterdepolarization

scholarly journals Stochastic initiation and termination of calcium-mediated triggered activity in cardiac myocytes

2017 ◽  
Vol 114 (3) ◽  
pp. E270-E279 ◽  
Author(s):  
Zhen Song ◽  
Zhilin Qu ◽  
Alain Karma
Keyword(s):  
Action Potential ◽  
Cardiac Myocytes ◽  
Cardiac Arrhythmias ◽  
Action Potentials ◽  
Waiting Times ◽  
Excitation Threshold ◽  
Triggered Activity ◽  
Random Events ◽  
Delayed Afterdepolarization ◽  
A Current

Cardiac myocytes normally initiate action potentials in response to a current stimulus that depolarizes the membrane above an excitation threshold. Aberrant excitation can also occur due to spontaneous calcium (Ca2+) release (SCR) from intracellular stores after the end of a preceding action potential. SCR drives the Na+/Ca2+ exchange current inducing a “delayed afterdepolarization” that can in turn trigger an action potential if the excitation threshold is reached. This “triggered activity” is known to cause arrhythmias, but how it is initiated and terminated is not understood. Using computer simulations of a ventricular myocyte model, we show that initiation and termination are inherently random events. We determine the probability of those events from statistical measurements of the number of beats before initiation and before termination, respectively, which follow geometric distributions. Moreover, we elucidate the origin of randomness by a statistical analysis of SCR events, which do not follow a Poisson process observed in other eukaryotic cells. Due to synchronization of Ca2+ releases during the action potential upstroke, waiting times of SCR events after the upstroke are narrowly distributed, whereas SCR amplitudes follow a broad normal distribution with a width determined by fluctuations in the number of independent Ca2+ wave foci. This distribution enables us to compute the probabilities of initiation and termination of bursts of triggered activity that are maintained by a positive feedback between the action potential upstroke and SCR. Our results establish a theoretical framework for interpreting complex and varied manifestations of triggered activity relevant to cardiac arrhythmias.

ATP promotes development of afterdepolarizations and triggered activity in cardiac myocytes

1994 ◽  
Vol 267 (5) ◽  
pp. H2005-H2011 ◽  
Author(s):  
Y. Song ◽  
L. Belardinelli
Keyword(s):  
Action Potentials ◽  
Ventricular Myocytes ◽  
Extracellular Atp ◽  
Extracellular Medium ◽  
Triggered Activity ◽  
Arrhythmogenic Effect ◽  
Early Afterdepolarization ◽  
Triggered Arrhythmias ◽  
Delayed Afterdepolarization ◽  
Isolated Ventricular Myocytes

The effect of extracellular ATP on transient inward current (Iti), delayed afterdepolarization (DAD), early afterdepolarization (EAD), and triggered activity were investigated in guinea pig isolated ventricular myocytes. ATP alone did not induce afterdepolarizations nor did it significantly alter the resting membrane potentials and action potentials. However, when it was applied with drugs known to increase intracellular Ca2+, ATP facilitated the induction of afterdepolarizations and triggered activity in approximately 60% of the cells. In the presence of isoproterenol, ATP increased the amplitude of Iti and DADs by 55 and 206%, respectively, and caused increases in the amplitude of L-type Ca2+ current (ICa) and EADs, which occasionally led to triggered activity. Similarly, addition of ATP increased the amplitude of Iti and DADs induced by elevated extracellular Ca2+ by 110 and 83%, respectively. Ryanodine inhibited the ATP-induced increase in Iti but not the increase in ICa. In the presence of BAY K 8644 or quinidine, ATP not only further prolonged the action potential durations by 18 +/- 4 and 17 +/- 4%, respectively, but also increased the amplitude of EADs. The present results show a novel arrhythmogenic effect of extracellular ATP, which facilitates the genesis of triggered arrhythmias when Ca2+ influx is increased, probably by further increasing Ca2+ influx from extracellular medium and Ca2+ release from intracellular stores.

scholarly journals Determinants of the Diastolic Calcium-Voltage Coupling Gain for Delayed Afterdepolarization Mediated Triggered Activity

2016 ◽  
Vol 110 (3) ◽  
pp. 586a
Author(s):  
Michael B. Liu ◽  
Christopher Y. Ko ◽  
Zhen Song ◽  
Alan Garfinkel ◽  
James N. Weiss ◽  
...  
Keyword(s):  
Triggered Activity ◽  
Delayed Afterdepolarization

scholarly journals A Dynamical Threshold for Cardiac Delayed Afterdepolarization-Mediated Triggered Activity

2016 ◽  
Vol 111 (11) ◽  
pp. 2523-2533 ◽  
Author(s):  
Michael B. Liu ◽  
Christopher Y. Ko ◽  
Zhen Song ◽  
Alan Garfinkel ◽  
James N. Weiss ◽  
...  
Keyword(s):  
Triggered Activity ◽  
Delayed Afterdepolarization

scholarly journals Effect ofα-Allocryptopine on Delayed Afterdepolarizations and Triggered Activities in Mice Cardiomyocytes Treated with Isoproterenol

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Bin Xu ◽  
Yicheng Fu ◽  
Li Liu ◽  
Kun Lin ◽  
Xiaojing Zhao ◽  
...  
Keyword(s):  
Calcium Current ◽  
Ventricular Myocytes ◽  
Treated Group ◽  
Inactivation Kinetics ◽  
Triggered Activity ◽  
Electrophysiological Properties ◽  
Recovery From Inactivation ◽  
Delayed Afterdepolarizations ◽  
Delayed Afterdepolarization ◽  
All Treatment

Objective. To investigate the effect ofα-allocryptopine (ALL) on delayed afterdepolarization (DAD) incidence and triggered activity (TA) in mice administered isoproterenol (ISO).Methods. Mouse ventricular myocytes were isolated. And the cellular electrophysiological properties of ventricular myocytes were investigated.Results. We found that the incidences of DADs and TA in mouse myocytes were increased by ISO treatment. In sharp contrast, triggered arrhythmia events were rarely observed in myocytes with 10 μM ALL treatment. Transient inward current (Iti) was reduced significantly with ALL treatment, which contributed to DAD-related triggered arrhythmia. Compared to Iso-treated group, the L-type calcium current (ICa,L) densities were decreased after exposure to ALL, along with slower activation, quicker inactivation, and longer time constant of recovery from inactivation kinetics.Conclusion. There is less triggered arrhythmia events in ventricular myocytes treated with ALL. This effect may be associated with the inhibition ofItiandICa,L.

External pH dependency of delayed afterdepolarization in rabbit myocardium

1986 ◽  
Vol 251 (2) ◽  
pp. H324-H330
Author(s):  
T. Kano ◽  
K. Nishi
Keyword(s):  
Action Potentials ◽  
Cycle Length ◽  
Triggered Activity ◽  
Ph Dependency ◽  
Rabbit Myocardium ◽  
Delayed Afterdepolarization ◽  
Electrical Stimuli ◽  
External Ph

Effects of changing external pH on delayed afterdepolarization (DAD) induced by a train of electrical stimuli in the rabbit ventricular papillary muscle fibers were examined using a conventional microelectrode technique in vitro. Preparations were superfused with Tyrode solution containing norepinephrine (3 X 10(-6) M), and the external pH was decreased. After a train of driven action potentials, DAD was induced at pH 7.0 in the presence of norepinephrine. The amplitude of the DAD induced by norepinephrine at pH 7.0 increased as the stimulus cycle length was shortened and as the number of applied stimuli increased. The increase in the amplitude of DAD resulted in yielding one or multiple nondriven action potentials. DAD, thus initiated, was completely suppressed by a further decrease of external pH to 6.7-6.0. Lidocaine and adriamycin depressed the amplitude of DAD, but verapamil did not. The results imply that only slight lowering of the external pH induced by ischemic conditions or by other means would provoke DAD which, in turn, would result in triggered activity in situ.

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